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Unfolded protein response to autophagy as a promising druggable target for anticancer therapy

Identifieur interne : 000185 ( Istex/Corpus ); précédent : 000184; suivant : 000186

Unfolded protein response to autophagy as a promising druggable target for anticancer therapy

Auteurs : Dong Hoon Suh ; Mi-Kyung Kim ; Hee Seung Kim ; Hyun Hoon Chung ; Yong Sang Song

Source :

RBID : ISTEX:8793D12DCDEC3A8743A164DE89DAFD3EC7D7D3F9

English descriptors

Abstract

The endoplasmic reticulum (ER) is responsible for protein processing. In rapidly proliferating tumor cells, the ER tends to be overloaded with unfolded and misfolded proteins due to high metabolic demand. With the limited protein‐folding capacity of the ER, tumor cells often suffer from more ER stress than do normal cells. Thus, cellular stress responses to cope with ER stress, such as the unfolded protein response (UPR) and autophagy, might be more activated in cancer cells than in normal cells. The complex signaling pathways from the UPR to autophagy provide promising druggable targets; a number of UPR/autophagy‐targeted anticancer agents are currently in development in preclinical and clinical studies. In this short review we will discuss the potential anticancer efficacy of modulators of cellular stress responses, especially UPR and autophagy, on the basis of their signaling pathways. In addition, the current developmental status of the UPR/autophagy‐targeted agents will be discussed.

Url:
DOI: 10.1111/j.1749-6632.2012.06739.x

Links to Exploration step

ISTEX:8793D12DCDEC3A8743A164DE89DAFD3EC7D7D3F9

Le document en format XML

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<titleInfo>
<title>Annals of the New York Academy of Sciences</title>
</titleInfo>
<genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre>
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<extent unit="pages">
<start>20</start>
<end>32</end>
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</relatedItem>
<relatedItem type="references" displayLabel="cit1">
<titleInfo>
<title>Endoplasmic reticulum stress response in cancer: molecular mechanism and therapeutic potential</title>
</titleInfo>
<name type="personal">
<namePart type="given">G.</namePart>
<namePart type="family">Wang</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Z.Q.</namePart>
<namePart type="family">Yang</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">K.</namePart>
<namePart type="family">Zhang</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Wang, G., Z.Q. Yang & K. Zhang. 2010. Endoplasmic reticulum stress response in cancer: molecular mechanism and therapeutic potential. Am. J. Trans. Res. 2: 65–74.</note>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>2</number>
</detail>
<extent unit="pages">
<start>65</start>
<end>74</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Am. J. Trans. Res.</title>
</titleInfo>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>2</number>
</detail>
<extent unit="pages">
<start>65</start>
<end>74</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit2">
<titleInfo>
<title>Untangling the unfolded protein response</title>
</titleInfo>
<name type="personal">
<namePart type="given">E. L.</namePart>
<namePart type="family">Davenport</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">G.J.</namePart>
<namePart type="family">Morgan</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">F.E.</namePart>
<namePart type="family">Davies</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Davenport, E. L., G.J. Morgan & F.E. Davies. 2008. Untangling the unfolded protein response. Cell Cycle 7: 865–869.</note>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>7</number>
</detail>
<extent unit="pages">
<start>865</start>
<end>869</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cell Cycle</title>
</titleInfo>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>7</number>
</detail>
<extent unit="pages">
<start>865</start>
<end>869</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit3">
<titleInfo>
<title>Activation of mTOR signaling pathway associated with adverse prognostic factors of epithelial ovarian cancer</title>
</titleInfo>
<name type="personal">
<namePart type="given">J.H.</namePart>
<namePart type="family">No</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">No, J.H. et al . 2011. Activation of mTOR signaling pathway associated with adverse prognostic factors of epithelial ovarian cancer. Gynecol. Oncol. 121: 8–12.</note>
<part>
<date>2011</date>
<detail type="volume">
<caption>vol.</caption>
<number>121</number>
</detail>
<extent unit="pages">
<start>8</start>
<end>12</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Gynecol. Oncol.</title>
</titleInfo>
<part>
<date>2011</date>
<detail type="volume">
<caption>vol.</caption>
<number>121</number>
</detail>
<extent unit="pages">
<start>8</start>
<end>12</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit4">
<titleInfo>
<title>Akt involvement in paclitaxel chemoresistance of human ovarian cancer cells</title>
</titleInfo>
<name type="personal">
<namePart type="given">S.H.</namePart>
<namePart type="family">Kim</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Y.S.</namePart>
<namePart type="family">Juhnn</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Y.S.</namePart>
<namePart type="family">Song</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Kim, S.H., Y.S. Juhnn & Y.S. Song. 2007. Akt involvement in paclitaxel chemoresistance of human ovarian cancer cells. Ann. N.Y. Acad. Sci. 1095: 82–89.</note>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>1095</number>
</detail>
<extent unit="pages">
<start>82</start>
<end>89</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Ann. N.Y. Acad. Sci.</title>
</titleInfo>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>1095</number>
</detail>
<extent unit="pages">
<start>82</start>
<end>89</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit5">
<titleInfo>
<title>Tumor cell metabolism: cancer's Achilles’ heel</title>
</titleInfo>
<name type="personal">
<namePart type="given">G.</namePart>
<namePart type="family">Kroemer</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">J.</namePart>
<namePart type="family">Pouyssegur</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Kroemer, G. & J. Pouyssegur. 2008. Tumor cell metabolism: cancer's Achilles’ heel. Cancer Cell 13: 472–482.</note>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>13</number>
</detail>
<extent unit="pages">
<start>472</start>
<end>482</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cancer Cell</title>
</titleInfo>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>13</number>
</detail>
<extent unit="pages">
<start>472</start>
<end>482</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit6">
<titleInfo>
<title>Targeting the endoplasmic reticulum‐stress response as an anticancer strategy</title>
</titleInfo>
<name type="personal">
<namePart type="given">S.J.</namePart>
<namePart type="family">Healy</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Healy, S.J. et al . 2009. Targeting the endoplasmic reticulum‐stress response as an anticancer strategy. Eur. J. Pharmacol. 625: 234–246.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>625</number>
</detail>
<extent unit="pages">
<start>234</start>
<end>246</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Eur. J. Pharmacol.</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>625</number>
</detail>
<extent unit="pages">
<start>234</start>
<end>246</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit7">
<titleInfo>
<title>Unfolded protein response in cancer: the physician's perspective</title>
</titleInfo>
<name type="personal">
<namePart type="given">X.</namePart>
<namePart type="family">Li</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">K.</namePart>
<namePart type="family">Zhang</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Z.</namePart>
<namePart type="family">Li</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Li, X., K. Zhang & Z. Li. 2011. Unfolded protein response in cancer: the physician's perspective. J. Hematol. Oncol. 4: 8.</note>
<part>
<date>2011</date>
<detail type="volume">
<caption>vol.</caption>
<number>4</number>
</detail>
<extent unit="pages">
<start>8</start>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>J. Hematol. Oncol.</title>
</titleInfo>
<part>
<date>2011</date>
<detail type="volume">
<caption>vol.</caption>
<number>4</number>
</detail>
<extent unit="pages">
<start>8</start>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit8">
<titleInfo>
<title>Signal integration in the endoplasmic reticulum unfolded protein response. Nature reviews</title>
</titleInfo>
<name type="personal">
<namePart type="given">D.</namePart>
<namePart type="family">Ron</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">P.</namePart>
<namePart type="family">Walter</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Ron, D. & P. Walter. 2007. Signal integration in the endoplasmic reticulum unfolded protein response. Nature reviews. Mol. Cell. Biol. 8: 519–529.</note>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>8</number>
</detail>
<extent unit="pages">
<start>519</start>
<end>529</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cell. Biol.</title>
</titleInfo>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>8</number>
</detail>
<extent unit="pages">
<start>519</start>
<end>529</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit9">
<titleInfo>
<title>Endoplasmic reticulum stress triggers autophagy</title>
</titleInfo>
<name type="personal">
<namePart type="given">T.</namePart>
<namePart type="family">Yorimitsu</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Yorimitsu, T. et al . 2006. Endoplasmic reticulum stress triggers autophagy. J. Biol. Chem. 281: 30299–30304.</note>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>281</number>
</detail>
<extent unit="pages">
<start>30299</start>
<end>30304</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>J. Biol. Chem.</title>
</titleInfo>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>281</number>
</detail>
<extent unit="pages">
<start>30299</start>
<end>30304</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit10">
<titleInfo>
<title>The unfolded protein response: controlling cell fate decisions under ER stress and beyond. Nature reviews</title>
</titleInfo>
<name type="personal">
<namePart type="given">C.</namePart>
<namePart type="family">Hetz</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Hetz, C. 2012. The unfolded protein response: controlling cell fate decisions under ER stress and beyond. Nature reviews. Mol. Cell. Biol. 13: 89–102.</note>
<part>
<date>2012</date>
<detail type="volume">
<caption>vol.</caption>
<number>13</number>
</detail>
<extent unit="pages">
<start>89</start>
<end>102</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cell. Biol.</title>
</titleInfo>
<part>
<date>2012</date>
<detail type="volume">
<caption>vol.</caption>
<number>13</number>
</detail>
<extent unit="pages">
<start>89</start>
<end>102</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit11">
<titleInfo>
<title>Increased synthesis of secreted proteins induces expression of glucose‐regulated proteins in butyrate‐treated Chinese hamster ovary cells</title>
</titleInfo>
<name type="personal">
<namePart type="given">A.J.</namePart>
<namePart type="family">Dorner</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">L.C.</namePart>
<namePart type="family">Wasley</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">R.J.</namePart>
<namePart type="family">Kaufman</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Dorner, A.J., L.C. Wasley & R.J. Kaufman. 1989. Increased synthesis of secreted proteins induces expression of glucose‐regulated proteins in butyrate‐treated Chinese hamster ovary cells. J. Biol. Chem. 264: 20602–20607.</note>
<part>
<date>1989</date>
<detail type="volume">
<caption>vol.</caption>
<number>264</number>
</detail>
<extent unit="pages">
<start>20602</start>
<end>20607</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>J. Biol. Chem.</title>
</titleInfo>
<part>
<date>1989</date>
<detail type="volume">
<caption>vol.</caption>
<number>264</number>
</detail>
<extent unit="pages">
<start>20602</start>
<end>20607</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit12">
<titleInfo>
<title>The mammalian unfolded protein response</title>
</titleInfo>
<name type="personal">
<namePart type="given">M.</namePart>
<namePart type="family">Schroder</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">R.J.</namePart>
<namePart type="family">Kaufman</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Schroder, M. & R.J. Kaufman. 2005. The mammalian unfolded protein response. Annu. Rev. Biochem. 74: 739–789.</note>
<part>
<date>2005</date>
<detail type="volume">
<caption>vol.</caption>
<number>74</number>
</detail>
<extent unit="pages">
<start>739</start>
<end>789</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Annu. Rev. Biochem.</title>
</titleInfo>
<part>
<date>2005</date>
<detail type="volume">
<caption>vol.</caption>
<number>74</number>
</detail>
<extent unit="pages">
<start>739</start>
<end>789</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit13">
<titleInfo>
<title>Modulating stress responses by the UPRosome: a matter of life and death</title>
</titleInfo>
<name type="personal">
<namePart type="given">U.</namePart>
<namePart type="family">Woehlbier</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">C.</namePart>
<namePart type="family">Hetz</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Woehlbier, U. & C. Hetz. 2011. Modulating stress responses by the UPRosome: a matter of life and death. Trends Biochem. Sci. 36: 329–337.</note>
<part>
<date>2011</date>
<detail type="volume">
<caption>vol.</caption>
<number>36</number>
</detail>
<extent unit="pages">
<start>329</start>
<end>337</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Trends Biochem. Sci.</title>
</titleInfo>
<part>
<date>2011</date>
<detail type="volume">
<caption>vol.</caption>
<number>36</number>
</detail>
<extent unit="pages">
<start>329</start>
<end>337</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit14">
<titleInfo>
<title>The role of autophagy in cancer: therapeutic implications</title>
</titleInfo>
<name type="personal">
<namePart type="given">Z.J.</namePart>
<namePart type="family">Yang</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Yang, Z.J. et al . 2011. The role of autophagy in cancer: therapeutic implications. Mol. Cancer Ther. 10: 1533–1541.</note>
<part>
<date>2011</date>
<detail type="volume">
<caption>vol.</caption>
<number>10</number>
</detail>
<extent unit="pages">
<start>1533</start>
<end>1541</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cancer Ther.</title>
</titleInfo>
<part>
<date>2011</date>
<detail type="volume">
<caption>vol.</caption>
<number>10</number>
</detail>
<extent unit="pages">
<start>1533</start>
<end>1541</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit15">
<titleInfo>
<title>Perk is essential for translational regulation and cell survival during the unfolded protein response</title>
</titleInfo>
<name type="personal">
<namePart type="given">H.P.</namePart>
<namePart type="family">Harding</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Harding, H.P. et al . 2000. Perk is essential for translational regulation and cell survival during the unfolded protein response. Mol. Cell 5: 897–904.</note>
<part>
<date>2000</date>
<detail type="volume">
<caption>vol.</caption>
<number>5</number>
</detail>
<extent unit="pages">
<start>897</start>
<end>904</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cell</title>
</titleInfo>
<part>
<date>2000</date>
<detail type="volume">
<caption>vol.</caption>
<number>5</number>
</detail>
<extent unit="pages">
<start>897</start>
<end>904</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit16">
<titleInfo>
<title>ER stress induces cleavage of membrane‐bound ATF6 by the same proteases that process SREBPs</title>
</titleInfo>
<name type="personal">
<namePart type="given">J.</namePart>
<namePart type="family">Ye</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Ye, J. et al . 2000. ER stress induces cleavage of membrane‐bound ATF6 by the same proteases that process SREBPs. Mol. Cell 6: 1355–1364.</note>
<part>
<date>2000</date>
<detail type="volume">
<caption>vol.</caption>
<number>6</number>
</detail>
<extent unit="pages">
<start>1355</start>
<end>1364</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cell</title>
</titleInfo>
<part>
<date>2000</date>
<detail type="volume">
<caption>vol.</caption>
<number>6</number>
</detail>
<extent unit="pages">
<start>1355</start>
<end>1364</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit17">
<titleInfo>
<title>XBP‐1 regulates a subset of endoplasmic reticulum resident chaperone genes in the unfolded protein response</title>
</titleInfo>
<name type="personal">
<namePart type="given">A.H.</namePart>
<namePart type="family">Lee</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">N.N.</namePart>
<namePart type="family">Iwakoshi</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">L.H.</namePart>
<namePart type="family">Glimcher</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Lee, A.H., N.N. Iwakoshi & L.H. Glimcher. 2003. XBP‐1 regulates a subset of endoplasmic reticulum resident chaperone genes in the unfolded protein response. Mol. Cell. Biol. 23: 7448–7459.</note>
<part>
<date>2003</date>
<detail type="volume">
<caption>vol.</caption>
<number>23</number>
</detail>
<extent unit="pages">
<start>7448</start>
<end>7459</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cell. Biol.</title>
</titleInfo>
<part>
<date>2003</date>
<detail type="volume">
<caption>vol.</caption>
<number>23</number>
</detail>
<extent unit="pages">
<start>7448</start>
<end>7459</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit18">
<titleInfo>
<title>Coupling endoplasmic reticulum stress to the cell death program. An Apaf‐1‐independent intrinsic pathway</title>
</titleInfo>
<name type="personal">
<namePart type="given">R.V.</namePart>
<namePart type="family">Rao</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Rao, R.V. et al . 2002. Coupling endoplasmic reticulum stress to the cell death program. An Apaf‐1‐independent intrinsic pathway. J. Biol. Chem. 277: 21836–21842.</note>
<part>
<date>2002</date>
<detail type="volume">
<caption>vol.</caption>
<number>277</number>
</detail>
<extent unit="pages">
<start>21836</start>
<end>21842</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>J. Biol. Chem.</title>
</titleInfo>
<part>
<date>2002</date>
<detail type="volume">
<caption>vol.</caption>
<number>277</number>
</detail>
<extent unit="pages">
<start>21836</start>
<end>21842</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit19">
<titleInfo>
<title>Mediators of endoplasmic reticulum stress‐induced apoptosis</title>
</titleInfo>
<name type="personal">
<namePart type="given">E.</namePart>
<namePart type="family">Szegezdi</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Szegezdi, E. et al . 2006. Mediators of endoplasmic reticulum stress‐induced apoptosis. EMBO Reports 7: 880–885.</note>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>7</number>
</detail>
<extent unit="pages">
<start>880</start>
<end>885</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>EMBO Reports</title>
</titleInfo>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>7</number>
</detail>
<extent unit="pages">
<start>880</start>
<end>885</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit20">
<titleInfo>
<title>Growth arrest and DNA damage‐inducible protein GADD34 targets protein phosphatase 1 alpha to the endoplasmic reticulum and promotes dephosphorylation of the alpha subunit of eukaryotic translation initiation factor 2</title>
</titleInfo>
<name type="personal">
<namePart type="given">M.H.</namePart>
<namePart type="family">Brush</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">D.C.</namePart>
<namePart type="family">Weiser</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">S.</namePart>
<namePart type="family">Shenolikar</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Brush, M.H., D.C. Weiser & S. Shenolikar. 2003. Growth arrest and DNA damage‐inducible protein GADD34 targets protein phosphatase 1 alpha to the endoplasmic reticulum and promotes dephosphorylation of the alpha subunit of eukaryotic translation initiation factor 2. Mol. Cell. Biol. 23: 1292–1303.</note>
<part>
<date>2003</date>
<detail type="volume">
<caption>vol.</caption>
<number>23</number>
</detail>
<extent unit="pages">
<start>1292</start>
<end>1303</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cell. Biol.</title>
</titleInfo>
<part>
<date>2003</date>
<detail type="volume">
<caption>vol.</caption>
<number>23</number>
</detail>
<extent unit="pages">
<start>1292</start>
<end>1303</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit21">
<titleInfo>
<title>Induction of glucose‐regulated protein 78 by chronic hypoxia in human gastric tumor cells through a protein kinase C‐epsilon/ERK/AP‐1 signaling cascade</title>
</titleInfo>
<name type="personal">
<namePart type="given">M.S.</namePart>
<namePart type="family">Song</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Song, M.S. et al . 2001. Induction of glucose‐regulated protein 78 by chronic hypoxia in human gastric tumor cells through a protein kinase C‐epsilon/ERK/AP‐1 signaling cascade. Cancer Res. 61: 8322–8330.</note>
<part>
<date>2001</date>
<detail type="volume">
<caption>vol.</caption>
<number>61</number>
</detail>
<extent unit="pages">
<start>8322</start>
<end>8330</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cancer Res.</title>
</titleInfo>
<part>
<date>2001</date>
<detail type="volume">
<caption>vol.</caption>
<number>61</number>
</detail>
<extent unit="pages">
<start>8322</start>
<end>8330</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit22">
<titleInfo>
<title>ASK1 is essential for endoplasmic reticulum stress‐induced neuronal cell death triggered by expanded polyglutamine repeats</title>
</titleInfo>
<name type="personal">
<namePart type="given">H.</namePart>
<namePart type="family">Nishitoh</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Nishitoh, H. et al . 2002. ASK1 is essential for endoplasmic reticulum stress‐induced neuronal cell death triggered by expanded polyglutamine repeats. Genes Development 16: 1345–1355.</note>
<part>
<date>2002</date>
<detail type="volume">
<caption>vol.</caption>
<number>16</number>
</detail>
<extent unit="pages">
<start>1345</start>
<end>1355</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Genes Development</title>
</titleInfo>
<part>
<date>2002</date>
<detail type="volume">
<caption>vol.</caption>
<number>16</number>
</detail>
<extent unit="pages">
<start>1345</start>
<end>1355</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit23">
<titleInfo>
<title>Signal transduction by the JNK group of MAP kinases</title>
</titleInfo>
<name type="personal">
<namePart type="given">R.J.</namePart>
<namePart type="family">Davis</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Davis, R.J. 2000. Signal transduction by the JNK group of MAP kinases. Cell 103: 239–252.</note>
<part>
<date>2000</date>
<detail type="volume">
<caption>vol.</caption>
<number>103</number>
</detail>
<extent unit="pages">
<start>239</start>
<end>252</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cell</title>
</titleInfo>
<part>
<date>2000</date>
<detail type="volume">
<caption>vol.</caption>
<number>103</number>
</detail>
<extent unit="pages">
<start>239</start>
<end>252</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit24">
<titleInfo>
<title>Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1</title>
</titleInfo>
<name type="personal">
<namePart type="given">F.</namePart>
<namePart type="family">Urano</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Urano, F. et al . 2000. Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1. Science 287: 664–666.</note>
<part>
<date>2000</date>
<detail type="volume">
<caption>vol.</caption>
<number>287</number>
</detail>
<extent unit="pages">
<start>664</start>
<end>666</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Science</title>
</titleInfo>
<part>
<date>2000</date>
<detail type="volume">
<caption>vol.</caption>
<number>287</number>
</detail>
<extent unit="pages">
<start>664</start>
<end>666</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit25">
<titleInfo>
<title>Autophagy as a target for anticancer therapy. Nature reviews</title>
</titleInfo>
<name type="personal">
<namePart type="given">F.</namePart>
<namePart type="family">Janku</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Janku, F. et al . 2011. Autophagy as a target for anticancer therapy. Nature reviews. Clin. Oncol. 8: 528–539.</note>
<part>
<date>2011</date>
<detail type="volume">
<caption>vol.</caption>
<number>8</number>
</detail>
<extent unit="pages">
<start>528</start>
<end>539</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Clin. Oncol.</title>
</titleInfo>
<part>
<date>2011</date>
<detail type="volume">
<caption>vol.</caption>
<number>8</number>
</detail>
<extent unit="pages">
<start>528</start>
<end>539</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit26">
<titleInfo>
<title>Self‐eating and self‐killing: crosstalk between autophagy and apoptosis. Nature reviews</title>
</titleInfo>
<name type="personal">
<namePart type="given">M.C.</namePart>
<namePart type="family">Maiuri</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Maiuri, M.C. et al . 2007. Self‐eating and self‐killing: crosstalk between autophagy and apoptosis. Nature reviews. Mol. Cell. Biol. 8: 741–752.</note>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>8</number>
</detail>
<extent unit="pages">
<start>741</start>
<end>752</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cell. Biol.</title>
</titleInfo>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>8</number>
</detail>
<extent unit="pages">
<start>741</start>
<end>752</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit27">
<titleInfo>
<title>ER stress (PERK/eIF2alpha phosphorylation) mediates the polyglutamine‐induced LC3 conversion, an essential step for autophagy formation</title>
</titleInfo>
<name type="personal">
<namePart type="given">Y.</namePart>
<namePart type="family">Kouroku</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Kouroku, Y. et al . 2007. ER stress (PERK/eIF2alpha phosphorylation) mediates the polyglutamine‐induced LC3 conversion, an essential step for autophagy formation. Cell Death Differentiation 14: 230–239.</note>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>14</number>
</detail>
<extent unit="pages">
<start>230</start>
<end>239</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cell Death Differentiation</title>
</titleInfo>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>14</number>
</detail>
<extent unit="pages">
<start>230</start>
<end>239</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit28">
<titleInfo>
<title>Autophagy is activated for cell survival after endoplasmic reticulum stress</title>
</titleInfo>
<name type="personal">
<namePart type="given">M.</namePart>
<namePart type="family">Ogata</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Ogata, M. et al . 2006. Autophagy is activated for cell survival after endoplasmic reticulum stress. Mol. Cell. Biol. 26: 9220–9231.</note>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>26</number>
</detail>
<extent unit="pages">
<start>9220</start>
<end>9231</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cell. Biol.</title>
</titleInfo>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>26</number>
</detail>
<extent unit="pages">
<start>9220</start>
<end>9231</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit29">
<titleInfo>
<title>Connecting endoplasmic reticulum stress to autophagy by unfolded protein response and calcium</title>
</titleInfo>
<name type="personal">
<namePart type="given">M.</namePart>
<namePart type="family">Hoyer‐Hansen</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">M.</namePart>
<namePart type="family">Jaattela</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Hoyer‐Hansen, M. & M. Jaattela. 2007. Connecting endoplasmic reticulum stress to autophagy by unfolded protein response and calcium. Cell Death Differentiation 14: 1576–1582.</note>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>14</number>
</detail>
<extent unit="pages">
<start>1576</start>
<end>1582</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cell Death Differentiation</title>
</titleInfo>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>14</number>
</detail>
<extent unit="pages">
<start>1576</start>
<end>1582</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit30">
<titleInfo>
<title>Role and regulation of autophagy in cancer</title>
</titleInfo>
<name type="personal">
<namePart type="given">N.</namePart>
<namePart type="family">Chen</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">V.</namePart>
<namePart type="family">Karantza‐Wadsworth</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Chen, N. & V. Karantza‐Wadsworth. 2009. Role and regulation of autophagy in cancer. Biochimica et Biophysica Acta 1793: 1516–1523.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>1793</number>
</detail>
<extent unit="pages">
<start>1516</start>
<end>1523</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Biochimica et Biophysica Acta</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>1793</number>
</detail>
<extent unit="pages">
<start>1516</start>
<end>1523</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit31">
<titleInfo>
<title>Autophagy as a mediator of chemotherapy‐induced cell death in cancer</title>
</titleInfo>
<name type="personal">
<namePart type="given">A.</namePart>
<namePart type="family">Notte</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">L.</namePart>
<namePart type="family">Leclere</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">C.</namePart>
<namePart type="family">Michiels</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Notte, A., L. Leclere & C. Michiels. 2011. Autophagy as a mediator of chemotherapy‐induced cell death in cancer. Biochem. Pharmacol. 82: 427–434.</note>
<part>
<date>2011</date>
<detail type="volume">
<caption>vol.</caption>
<number>82</number>
</detail>
<extent unit="pages">
<start>427</start>
<end>434</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Biochem. Pharmacol.</title>
</titleInfo>
<part>
<date>2011</date>
<detail type="volume">
<caption>vol.</caption>
<number>82</number>
</detail>
<extent unit="pages">
<start>427</start>
<end>434</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit32">
<titleInfo>
<title>Bcl‐2 family members: dual regulators of apoptosis and autophagy</title>
</titleInfo>
<name type="personal">
<namePart type="given">B.</namePart>
<namePart type="family">Levine</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">S.</namePart>
<namePart type="family">Sinha</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">G.</namePart>
<namePart type="family">Kroemer</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Levine, B., S. Sinha & G. Kroemer. 2008. Bcl‐2 family members: dual regulators of apoptosis and autophagy. Autophagy 4: 600–606.</note>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>4</number>
</detail>
<extent unit="pages">
<start>600</start>
<end>606</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Autophagy</title>
</titleInfo>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>4</number>
</detail>
<extent unit="pages">
<start>600</start>
<end>606</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit33">
<titleInfo>
<title>The unfolded protein response regulator GRP78/BiP as a novel target for increasing chemosensitivity in malignant gliomas</title>
</titleInfo>
<name type="personal">
<namePart type="given">P.</namePart>
<namePart type="family">Pyrko</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Pyrko, P. et al . 2007. The unfolded protein response regulator GRP78/BiP as a novel target for increasing chemosensitivity in malignant gliomas. Cancer Res. 67: 9809–9816.</note>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>67</number>
</detail>
<extent unit="pages">
<start>9809</start>
<end>9816</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cancer Res.</title>
</titleInfo>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>67</number>
</detail>
<extent unit="pages">
<start>9809</start>
<end>9816</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit34">
<titleInfo>
<title>Stress chaperone GRP78/BiP confers chemoresistance to tumor‐associated endothelial cells</title>
</titleInfo>
<name type="personal">
<namePart type="given">J.J.</namePart>
<namePart type="family">Virrey</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Virrey, J.J. et al . 2008. Stress chaperone GRP78/BiP confers chemoresistance to tumor‐associated endothelial cells. Mol. Cancer Res. 6: 1268–1275.</note>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>6</number>
</detail>
<extent unit="pages">
<start>1268</start>
<end>1275</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cancer Res.</title>
</titleInfo>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>6</number>
</detail>
<extent unit="pages">
<start>1268</start>
<end>1275</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit35">
<titleInfo>
<title>Functional coupling of p38‐induced up‐regulation of BiP and activation of RNA‐dependent protein kinase‐like endoplasmic reticulum kinase to drug resistance of dormant carcinoma cells</title>
</titleInfo>
<name type="personal">
<namePart type="given">A.C.</namePart>
<namePart type="family">Ranganathan</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Ranganathan, A.C. et al . 2006. Functional coupling of p38‐induced up‐regulation of BiP and activation of RNA‐dependent protein kinase‐like endoplasmic reticulum kinase to drug resistance of dormant carcinoma cells. Cancer Res. 66: 1702–1711.</note>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>66</number>
</detail>
<extent unit="pages">
<start>1702</start>
<end>1711</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cancer Res.</title>
</titleInfo>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>66</number>
</detail>
<extent unit="pages">
<start>1702</start>
<end>1711</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit36">
<titleInfo>
<title>Activation of the ATF6, XBP1 and grp78 genes in human hepatocellular carcinoma: a possible involvement of the ER stress pathway in hepatocarcinogenesis</title>
</titleInfo>
<name type="personal">
<namePart type="given">M.</namePart>
<namePart type="family">Shuda</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Shuda, M. et al . 2003. Activation of the ATF6, XBP1 and grp78 genes in human hepatocellular carcinoma: a possible involvement of the ER stress pathway in hepatocarcinogenesis. J. Hepatol. 38: 605–614.</note>
<part>
<date>2003</date>
<detail type="volume">
<caption>vol.</caption>
<number>38</number>
</detail>
<extent unit="pages">
<start>605</start>
<end>614</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>J. Hepatol.</title>
</titleInfo>
<part>
<date>2003</date>
<detail type="volume">
<caption>vol.</caption>
<number>38</number>
</detail>
<extent unit="pages">
<start>605</start>
<end>614</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit37">
<titleInfo>
<title>Targeting XBP‐1 as a novel anti‐cancer strategy</title>
</titleInfo>
<name type="personal">
<namePart type="given">A.C.</namePart>
<namePart type="family">Koong</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">V.</namePart>
<namePart type="family">Chauhan</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">L.</namePart>
<namePart type="family">Romero‐Ramirez</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Koong, A.C., V. Chauhan & L. Romero‐Ramirez. 2006. Targeting XBP‐1 as a novel anti‐cancer strategy. Cancer Biol. Therapy 5: 756–759.</note>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>5</number>
</detail>
<extent unit="pages">
<start>756</start>
<end>759</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cancer Biol. Therapy</title>
</titleInfo>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>5</number>
</detail>
<extent unit="pages">
<start>756</start>
<end>759</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit38">
<titleInfo>
<title>XBP1 is essential for survival under hypoxic conditions and is required for tumor growth</title>
</titleInfo>
<name type="personal">
<namePart type="given">L.</namePart>
<namePart type="family">Romero‐Ramirez</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Romero‐Ramirez, L. et al . 2004. XBP1 is essential for survival under hypoxic conditions and is required for tumor growth. Cancer Res. 64: 5943–5947.</note>
<part>
<date>2004</date>
<detail type="volume">
<caption>vol.</caption>
<number>64</number>
</detail>
<extent unit="pages">
<start>5943</start>
<end>5947</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cancer Res.</title>
</titleInfo>
<part>
<date>2004</date>
<detail type="volume">
<caption>vol.</caption>
<number>64</number>
</detail>
<extent unit="pages">
<start>5943</start>
<end>5947</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit39">
<titleInfo>
<title>The differentiation and stress response factor XBP‐1 drives multiple myeloma pathogenesis</title>
</titleInfo>
<name type="personal">
<namePart type="given">D.R.</namePart>
<namePart type="family">Carrasco</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Carrasco, D.R. et al . 2007. The differentiation and stress response factor XBP‐1 drives multiple myeloma pathogenesis. Cancer Cell 11: 349–360.</note>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>11</number>
</detail>
<extent unit="pages">
<start>349</start>
<end>360</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cancer Cell</title>
</titleInfo>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>11</number>
</detail>
<extent unit="pages">
<start>349</start>
<end>360</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit40">
<titleInfo>
<title>Activation and clinical significance of the unfolded protein response in breast cancer</title>
</titleInfo>
<name type="personal">
<namePart type="given">P.</namePart>
<namePart type="family">Scriven</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Scriven, P. et al . 2009. Activation and clinical significance of the unfolded protein response in breast cancer. Br. J. Cancer 101: 1692–1698.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>101</number>
</detail>
<extent unit="pages">
<start>1692</start>
<end>1698</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Br. J. Cancer</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>101</number>
</detail>
<extent unit="pages">
<start>1692</start>
<end>1698</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit41">
<titleInfo>
<title>ER stress‐regulated translation increases tolerance to extreme hypoxia and promotes tumor growth</title>
</titleInfo>
<name type="personal">
<namePart type="given">M.</namePart>
<namePart type="family">Bi</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Bi, M. et al . 2005. ER stress‐regulated translation increases tolerance to extreme hypoxia and promotes tumor growth. EMBO J. 24: 3470–3481.</note>
<part>
<date>2005</date>
<detail type="volume">
<caption>vol.</caption>
<number>24</number>
</detail>
<extent unit="pages">
<start>3470</start>
<end>3481</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>EMBO J.</title>
</titleInfo>
<part>
<date>2005</date>
<detail type="volume">
<caption>vol.</caption>
<number>24</number>
</detail>
<extent unit="pages">
<start>3470</start>
<end>3481</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit42">
<titleInfo>
<title>Regulation of protein synthesis by hypoxia via activation of the endoplasmic reticulum kinase PERK and phosphorylation of the translation initiation factor eIF2alpha</title>
</titleInfo>
<name type="personal">
<namePart type="given">C.</namePart>
<namePart type="family">Koumenis</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Koumenis, C. et al . 2002. Regulation of protein synthesis by hypoxia via activation of the endoplasmic reticulum kinase PERK and phosphorylation of the translation initiation factor eIF2alpha. Mol. Cell. Biol. 22: 7405–7416.</note>
<part>
<date>2002</date>
<detail type="volume">
<caption>vol.</caption>
<number>22</number>
</detail>
<extent unit="pages">
<start>7405</start>
<end>7416</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cell. Biol.</title>
</titleInfo>
<part>
<date>2002</date>
<detail type="volume">
<caption>vol.</caption>
<number>22</number>
</detail>
<extent unit="pages">
<start>7405</start>
<end>7416</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit43">
<titleInfo>
<title>Perk‐dependent translational regulation promotes tumor cell adaptation and angiogenesis in response to hypoxic stress</title>
</titleInfo>
<name type="personal">
<namePart type="given">J.D.</namePart>
<namePart type="family">Blais</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Blais, J.D. et al . 2006. Perk‐dependent translational regulation promotes tumor cell adaptation and angiogenesis in response to hypoxic stress. Mol. Cell. Biol. 26: 9517–9532.</note>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>26</number>
</detail>
<extent unit="pages">
<start>9517</start>
<end>9532</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cell. Biol.</title>
</titleInfo>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>26</number>
</detail>
<extent unit="pages">
<start>9517</start>
<end>9532</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit44">
<titleInfo>
<title>Autophagy and metabolism</title>
</titleInfo>
<name type="personal">
<namePart type="given">J.D.</namePart>
<namePart type="family">Rabinowitz</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">E.</namePart>
<namePart type="family">White</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Rabinowitz, J.D. & E. White. 2010. Autophagy and metabolism. Science 330: 1344–1348.</note>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>330</number>
</detail>
<extent unit="pages">
<start>1344</start>
<end>1348</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Science</title>
</titleInfo>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>330</number>
</detail>
<extent unit="pages">
<start>1344</start>
<end>1348</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit45">
<titleInfo>
<title>The tumor suppressor gene ARHI regulates autophagy and tumor dormancy in human ovarian cancer cells</title>
</titleInfo>
<name type="personal">
<namePart type="given">Z.</namePart>
<namePart type="family">Lu</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Lu, Z. et al . 2008. The tumor suppressor gene ARHI regulates autophagy and tumor dormancy in human ovarian cancer cells. J. Clin. Invest. 118: 3917–3929.</note>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>118</number>
</detail>
<extent unit="pages">
<start>3917</start>
<end>3929</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>J. Clin. Invest.</title>
</titleInfo>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>118</number>
</detail>
<extent unit="pages">
<start>3917</start>
<end>3929</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit46">
<titleInfo>
<title>Activated Ras requires autophagy to maintain oxidative metabolism and tumorigenesis</title>
</titleInfo>
<name type="personal">
<namePart type="given">J.Y.</namePart>
<namePart type="family">Guo</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Guo, J.Y. et al . 2011. Activated Ras requires autophagy to maintain oxidative metabolism and tumorigenesis. Genes Development 25: 460–470.</note>
<part>
<date>2011</date>
<detail type="volume">
<caption>vol.</caption>
<number>25</number>
</detail>
<extent unit="pages">
<start>460</start>
<end>470</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Genes Development</title>
</titleInfo>
<part>
<date>2011</date>
<detail type="volume">
<caption>vol.</caption>
<number>25</number>
</detail>
<extent unit="pages">
<start>460</start>
<end>470</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit47">
<titleInfo>
<title>Autophagy in cutaneous malignant melanoma</title>
</titleInfo>
<name type="personal">
<namePart type="given">R.</namePart>
<namePart type="family">Lazova</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">V.</namePart>
<namePart type="family">Klump</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">J.</namePart>
<namePart type="family">Pawelek</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Lazova, R., V. Klump & J. Pawelek. 2010. Autophagy in cutaneous malignant melanoma. J. Cutaneous Pathol. 37: 256–268.</note>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>37</number>
</detail>
<extent unit="pages">
<start>256</start>
<end>268</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>J. Cutaneous Pathol.</title>
</titleInfo>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>37</number>
</detail>
<extent unit="pages">
<start>256</start>
<end>268</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit48">
<titleInfo>
<title>Elevated Beclin 1 expression is correlated with HIF‐1alpha in predicting poor prognosis of nasopharyngeal carcinoma</title>
</titleInfo>
<name type="personal">
<namePart type="given">X.B.</namePart>
<namePart type="family">Wan</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Wan, X.B. et al . 2010. Elevated Beclin 1 expression is correlated with HIF‐1alpha in predicting poor prognosis of nasopharyngeal carcinoma. Autophagy 6: 395–404.</note>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>6</number>
</detail>
<extent unit="pages">
<start>395</start>
<end>404</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Autophagy</title>
</titleInfo>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>6</number>
</detail>
<extent unit="pages">
<start>395</start>
<end>404</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit49">
<titleInfo>
<title>The expression of beclin 1 is associated with favorable prognosis in stage IIIB colon cancers</title>
</titleInfo>
<name type="personal">
<namePart type="given">B.X.</namePart>
<namePart type="family">Li</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Li, B.X. et al . 2009. The expression of beclin 1 is associated with favorable prognosis in stage IIIB colon cancers. Autophagy 5: 303–306.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>5</number>
</detail>
<extent unit="pages">
<start>303</start>
<end>306</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Autophagy</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>5</number>
</detail>
<extent unit="pages">
<start>303</start>
<end>306</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit50">
<titleInfo>
<title>Beclin‐1 expression is a predictor of clinical outcome in patients with esophageal squamous cell carcinoma and correlated to hypoxia‐inducible factor (HIF)‐1alpha expression</title>
</titleInfo>
<name type="personal">
<namePart type="given">Y.</namePart>
<namePart type="family">Chen</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Chen, Y. et al . 2009. Beclin‐1 expression is a predictor of clinical outcome in patients with esophageal squamous cell carcinoma and correlated to hypoxia‐inducible factor (HIF)‐1alpha expression. Pathol. Oncol. Res. 15: 487–493.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>15</number>
</detail>
<extent unit="pages">
<start>487</start>
<end>493</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Pathol. Oncol. Res.</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>15</number>
</detail>
<extent unit="pages">
<start>487</start>
<end>493</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit51">
<titleInfo>
<title>Inhibition of MCL‐1 enhances lapatinib toxicity and overcomes lapatinib resistance via BAK‐dependent autophagy</title>
</titleInfo>
<name type="personal">
<namePart type="given">A.P.</namePart>
<namePart type="family">Martin</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Martin, A.P. et al . 2009. Inhibition of MCL‐1 enhances lapatinib toxicity and overcomes lapatinib resistance via BAK‐dependent autophagy. Cancer Biol. Therapy 8: 2084–2096.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>8</number>
</detail>
<extent unit="pages">
<start>2084</start>
<end>2096</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cancer Biol. Therapy</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>8</number>
</detail>
<extent unit="pages">
<start>2084</start>
<end>2096</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit52">
<titleInfo>
<title>Proteasome inhibitors induce a terminal unfolded protein response in multiple myeloma cells</title>
</titleInfo>
<name type="personal">
<namePart type="given">E.A.</namePart>
<namePart type="family">Obeng</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Obeng, E.A. et al . 2006. Proteasome inhibitors induce a terminal unfolded protein response in multiple myeloma cells. Blood 107: 4907–4916.</note>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>107</number>
</detail>
<extent unit="pages">
<start>4907</start>
<end>4916</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Blood</title>
</titleInfo>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>107</number>
</detail>
<extent unit="pages">
<start>4907</start>
<end>4916</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit53">
<titleInfo>
<title>Bortezomib sensitizes pancreatic cancer cells to endoplasmic reticulum stress‐mediated apoptosis</title>
</titleInfo>
<name type="personal">
<namePart type="given">S.T.</namePart>
<namePart type="family">Nawrocki</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Nawrocki, S.T. et al . 2005. Bortezomib sensitizes pancreatic cancer cells to endoplasmic reticulum stress‐mediated apoptosis. Cancer Res. 65: 11658–11666.</note>
<part>
<date>2005</date>
<detail type="volume">
<caption>vol.</caption>
<number>65</number>
</detail>
<extent unit="pages">
<start>11658</start>
<end>11666</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cancer Res.</title>
</titleInfo>
<part>
<date>2005</date>
<detail type="volume">
<caption>vol.</caption>
<number>65</number>
</detail>
<extent unit="pages">
<start>11658</start>
<end>11666</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit54">
<titleInfo>
<title>Bortezomib inhibits PKR‐like endoplasmic reticulum (ER) kinase and induces apoptosis via ER stress in human pancreatic cancer cells</title>
</titleInfo>
<name type="personal">
<namePart type="given">S.T.</namePart>
<namePart type="family">Nawrocki</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Nawrocki, S.T. et al . 2005. Bortezomib inhibits PKR‐like endoplasmic reticulum (ER) kinase and induces apoptosis via ER stress in human pancreatic cancer cells. Cancer Res. 65: 11510–11519.</note>
<part>
<date>2005</date>
<detail type="volume">
<caption>vol.</caption>
<number>65</number>
</detail>
<extent unit="pages">
<start>11510</start>
<end>11519</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cancer Res.</title>
</titleInfo>
<part>
<date>2005</date>
<detail type="volume">
<caption>vol.</caption>
<number>65</number>
</detail>
<extent unit="pages">
<start>11510</start>
<end>11519</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit55">
<titleInfo>
<title>Oncogenic transformation confers a selective susceptibility to the combined suppression of the proteasome and autophagy</title>
</titleInfo>
<name type="personal">
<namePart type="given">W.X.</namePart>
<namePart type="family">Ding</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Ding, W.X. et al . 2009. Oncogenic transformation confers a selective susceptibility to the combined suppression of the proteasome and autophagy. Mol. Cancer Ther. 8: 2036–2045.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>8</number>
</detail>
<extent unit="pages">
<start>2036</start>
<end>2045</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cancer Ther.</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>8</number>
</detail>
<extent unit="pages">
<start>2036</start>
<end>2045</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit56">
<titleInfo>
<title>Proteasome inhibitors activate autophagy as a cytoprotective response in human prostate cancer cells</title>
</titleInfo>
<name type="personal">
<namePart type="given">K.</namePart>
<namePart type="family">Zhu</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">K.</namePart>
<namePart type="family">Dunner Jr.</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">D.J.</namePart>
<namePart type="family">McConkey</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Zhu, K., K. Dunner, Jr. & D.J. McConkey. 2010. Proteasome inhibitors activate autophagy as a cytoprotective response in human prostate cancer cells. Oncogene 29: 451–462.</note>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>29</number>
</detail>
<extent unit="pages">
<start>451</start>
<end>462</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Oncogene</title>
</titleInfo>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>29</number>
</detail>
<extent unit="pages">
<start>451</start>
<end>462</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit57">
<titleInfo>
<title>Autophagy suppresses tumorigenesis through elimination of p62</title>
</titleInfo>
<name type="personal">
<namePart type="given">R.</namePart>
<namePart type="family">Mathew</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Mathew, R. et al . 2009. Autophagy suppresses tumorigenesis through elimination of p62. Cell 137: 1062–1075.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>137</number>
</detail>
<extent unit="pages">
<start>1062</start>
<end>1075</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cell</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>137</number>
</detail>
<extent unit="pages">
<start>1062</start>
<end>1075</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit58">
<titleInfo>
<title>Heat shock protein 90 modulates the unfolded protein response by stabilizing IRE1alpha</title>
</titleInfo>
<name type="personal">
<namePart type="given">M.G.</namePart>
<namePart type="family">Marcu</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Marcu, M.G. et al . 2002. Heat shock protein 90 modulates the unfolded protein response by stabilizing IRE1alpha. Mol. Cell. Biol. 22: 8506–8513.</note>
<part>
<date>2002</date>
<detail type="volume">
<caption>vol.</caption>
<number>22</number>
</detail>
<extent unit="pages">
<start>8506</start>
<end>8513</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cell. Biol.</title>
</titleInfo>
<part>
<date>2002</date>
<detail type="volume">
<caption>vol.</caption>
<number>22</number>
</detail>
<extent unit="pages">
<start>8506</start>
<end>8513</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit59">
<titleInfo>
<title>Heat shock protein inhibition is associated with activation of the unfolded protein response pathway in myeloma plasma cells</title>
</titleInfo>
<name type="personal">
<namePart type="given">E.L.</namePart>
<namePart type="family">Davenport</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Davenport, E.L. et al . 2007. Heat shock protein inhibition is associated with activation of the unfolded protein response pathway in myeloma plasma cells. Blood 110: 2641–2649.</note>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>110</number>
</detail>
<extent unit="pages">
<start>2641</start>
<end>2649</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Blood</title>
</titleInfo>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>110</number>
</detail>
<extent unit="pages">
<start>2641</start>
<end>2649</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit60">
<titleInfo>
<title>HIV‐1 protease inhibitors nelfinavir and atazanavir induce malignant glioma death by triggering endoplasmic reticulum stress</title>
</titleInfo>
<name type="personal">
<namePart type="given">P.</namePart>
<namePart type="family">Pyrko</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Pyrko, P. et al . 2007. HIV‐1 protease inhibitors nelfinavir and atazanavir induce malignant glioma death by triggering endoplasmic reticulum stress. Cancer Res . 67: 10920–10928.</note>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>67</number>
</detail>
<extent unit="pages">
<start>10920</start>
<end>10928</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cancer Res</title>
</titleInfo>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>67</number>
</detail>
<extent unit="pages">
<start>10920</start>
<end>10928</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit61">
<titleInfo>
<title>Ritonavir induces endoplasmic reticulum stress and sensitizes sarcoma cells toward bortezomib‐induced apoptosis</title>
</titleInfo>
<name type="personal">
<namePart type="given">M.</namePart>
<namePart type="family">Kraus</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Kraus, M. et al . 2008. Ritonavir induces endoplasmic reticulum stress and sensitizes sarcoma cells toward bortezomib‐induced apoptosis. Mol. Cancer Ther. 7: 1940–1948.</note>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>7</number>
</detail>
<extent unit="pages">
<start>1940</start>
<end>1948</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cancer Ther.</title>
</titleInfo>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>7</number>
</detail>
<extent unit="pages">
<start>1940</start>
<end>1948</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit62">
<titleInfo>
<title>Brefeldin A triggers apoptosis associated with mitochondrial breach and enhances HA14‐1‐ and anti‐Fas‐mediated cell killing in follicular lymphoma cells</title>
</titleInfo>
<name type="personal">
<namePart type="given">D.</namePart>
<namePart type="family">Wlodkowic</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">J.</namePart>
<namePart type="family">Skommer</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">J.</namePart>
<namePart type="family">Pelkonen</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Wlodkowic, D., J. Skommer & J. Pelkonen. 2007. Brefeldin A triggers apoptosis associated with mitochondrial breach and enhances HA14‐1‐ and anti‐Fas‐mediated cell killing in follicular lymphoma cells. Leukemia Res. 31: 1687–1700.</note>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>31</number>
</detail>
<extent unit="pages">
<start>1687</start>
<end>1700</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Leukemia Res.</title>
</titleInfo>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>31</number>
</detail>
<extent unit="pages">
<start>1687</start>
<end>1700</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit63">
<titleInfo>
<title>Effect on tumor cells of blocking survival response to glucose deprivation</title>
</titleInfo>
<name type="personal">
<namePart type="given">H.R.</namePart>
<namePart type="family">Park</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Park, H.R. et al . 2004. Effect on tumor cells of blocking survival response to glucose deprivation. J Natl. Cancer Inst. 96: 1300–1310.</note>
<part>
<date>2004</date>
<detail type="volume">
<caption>vol.</caption>
<number>96</number>
</detail>
<extent unit="pages">
<start>1300</start>
<end>1310</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>J Natl. Cancer Inst.</title>
</titleInfo>
<part>
<date>2004</date>
<detail type="volume">
<caption>vol.</caption>
<number>96</number>
</detail>
<extent unit="pages">
<start>1300</start>
<end>1310</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit64">
<titleInfo>
<title>Temsirolimus downregulates p21 without altering cyclin D1 expression and induces autophagy and synergizes with vorinostat in mantle cell lymphoma</title>
</titleInfo>
<name type="personal">
<namePart type="given">V.Y.</namePart>
<namePart type="family">Yazbeck</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Yazbeck, V.Y. et al . 2008. Temsirolimus downregulates p21 without altering cyclin D1 expression and induces autophagy and synergizes with vorinostat in mantle cell lymphoma. Exp. Hematol. 36: 443–450.</note>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>36</number>
</detail>
<extent unit="pages">
<start>443</start>
<end>450</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Exp. Hematol.</title>
</titleInfo>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>36</number>
</detail>
<extent unit="pages">
<start>443</start>
<end>450</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit65">
<titleInfo>
<title>RAD001 (Everolimus) induces autophagy in acute lymphoblastic leukemia</title>
</titleInfo>
<name type="personal">
<namePart type="given">R.</namePart>
<namePart type="family">Crazzolara</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">K.F.</namePart>
<namePart type="family">Bradstock</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">L.J.</namePart>
<namePart type="family">Bendall</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Crazzolara, R., K.F. Bradstock & L.J. Bendall. 2009. RAD001 (Everolimus) induces autophagy in acute lymphoblastic leukemia. Autophagy 5: 727–728.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>5</number>
</detail>
<extent unit="pages">
<start>727</start>
<end>728</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Autophagy</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>5</number>
</detail>
<extent unit="pages">
<start>727</start>
<end>728</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit66">
<titleInfo>
<title>Potentiating effects of RAD001 (Everolimus) on vincristine therapy in childhood acute lymphoblastic leukemia</title>
</titleInfo>
<name type="personal">
<namePart type="given">R.</namePart>
<namePart type="family">Crazzolara</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Crazzolara, R. et al . 2009. Potentiating effects of RAD001 (Everolimus) on vincristine therapy in childhood acute lymphoblastic leukemia. Blood 113: 3297–3306.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>113</number>
</detail>
<extent unit="pages">
<start>3297</start>
<end>3306</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Blood</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>113</number>
</detail>
<extent unit="pages">
<start>3297</start>
<end>3306</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit67">
<titleInfo>
<title>Autophagy for cancer therapy through inhibition of pro‐apoptotic proteins and mammalian target of rapamycin signaling</title>
</titleInfo>
<name type="personal">
<namePart type="given">K.W.</namePart>
<namePart type="family">Kim</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Kim, K.W. et al . 2006. Autophagy for cancer therapy through inhibition of pro‐apoptotic proteins and mammalian target of rapamycin signaling. J. Biol. Chem. 281: 36883–36890.</note>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>281</number>
</detail>
<extent unit="pages">
<start>36883</start>
<end>36890</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>J. Biol. Chem.</title>
</titleInfo>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>281</number>
</detail>
<extent unit="pages">
<start>36883</start>
<end>36890</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit68">
<titleInfo>
<title>Inhibition of mammalian target of rapamycin or apoptotic pathway induces autophagy and radiosensitizes PTEN null prostate cancer cells</title>
</titleInfo>
<name type="personal">
<namePart type="given">C.</namePart>
<namePart type="family">Cao</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Cao, C. et al . 2006. Inhibition of mammalian target of rapamycin or apoptotic pathway induces autophagy and radiosensitizes PTEN null prostate cancer cells. Cancer Res. 66: 10040–10047.</note>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>66</number>
</detail>
<extent unit="pages">
<start>10040</start>
<end>10047</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cancer Res.</title>
</titleInfo>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>66</number>
</detail>
<extent unit="pages">
<start>10040</start>
<end>10047</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit69">
<titleInfo>
<title>Apoptotic and autophagic cell death induced by histone deacetylase inhibitors</title>
</titleInfo>
<name type="personal">
<namePart type="given">Y.</namePart>
<namePart type="family">Shao</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Shao, Y. et al . 2004. Apoptotic and autophagic cell death induced by histone deacetylase inhibitors. Proc. Natl. Acad. Sci. USA 101: 18030–18035.</note>
<part>
<date>2004</date>
<detail type="volume">
<caption>vol.</caption>
<number>101</number>
</detail>
<extent unit="pages">
<start>18030</start>
<end>18035</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Proc. Natl. Acad. Sci. USA</title>
</titleInfo>
<part>
<date>2004</date>
<detail type="volume">
<caption>vol.</caption>
<number>101</number>
</detail>
<extent unit="pages">
<start>18030</start>
<end>18035</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit70">
<titleInfo>
<title>The histone deacetylase inhibitors LAQ824 and LBH589 do not require death receptor signaling or a functional apoptosome to mediate tumor cell death or therapeutic efficacy</title>
</titleInfo>
<name type="personal">
<namePart type="given">L.</namePart>
<namePart type="family">Ellis</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Ellis, L. et al . 2009. The histone deacetylase inhibitors LAQ824 and LBH589 do not require death receptor signaling or a functional apoptosome to mediate tumor cell death or therapeutic efficacy. Blood 114: 380–393.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>114</number>
</detail>
<extent unit="pages">
<start>380</start>
<end>393</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Blood</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>114</number>
</detail>
<extent unit="pages">
<start>380</start>
<end>393</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit71">
<titleInfo>
<title>Role of autophagy in histone deacetylase inhibitor‐induced apoptotic and nonapoptotic cell death</title>
</titleInfo>
<name type="personal">
<namePart type="given">N.</namePart>
<namePart type="family">Gammoh</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Gammoh, N. et al . 2012. Role of autophagy in histone deacetylase inhibitor‐induced apoptotic and nonapoptotic cell death. Proc. Natl. Acad. Sci. USA 109: 6561–6565.</note>
<part>
<date>2012</date>
<detail type="volume">
<caption>vol.</caption>
<number>109</number>
</detail>
<extent unit="pages">
<start>6561</start>
<end>6565</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Proc. Natl. Acad. Sci. USA</title>
</titleInfo>
<part>
<date>2012</date>
<detail type="volume">
<caption>vol.</caption>
<number>109</number>
</detail>
<extent unit="pages">
<start>6561</start>
<end>6565</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit72">
<titleInfo>
<title>Cell growth inhibition, G2/M cell cycle arrest, and apoptosis induced by chloroquine in human breast cancer cell line Bcap‐37</title>
</titleInfo>
<name type="personal">
<namePart type="given">P.D.</namePart>
<namePart type="family">Jiang</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Jiang, P.D. et al . 2008. Cell growth inhibition, G2/M cell cycle arrest, and apoptosis induced by chloroquine in human breast cancer cell line Bcap‐37. Cell Physiol. Biochem. 22: 431–440.</note>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>22</number>
</detail>
<extent unit="pages">
<start>431</start>
<end>440</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cell Physiol. Biochem.</title>
</titleInfo>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>22</number>
</detail>
<extent unit="pages">
<start>431</start>
<end>440</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit73">
<titleInfo>
<title>Chloroquine inhibits colon cancer cell growth in vitro and tumor growth in vivo via induction of apoptosis</title>
</titleInfo>
<name type="personal">
<namePart type="given">Y.</namePart>
<namePart type="family">Zheng</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Zheng, Y. et al . 2009. Chloroquine inhibits colon cancer cell growth in vitro and tumor growth in vivo via induction of apoptosis. Cancer Invest. 27: 286–292.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>27</number>
</detail>
<extent unit="pages">
<start>286</start>
<end>292</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cancer Invest.</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>27</number>
</detail>
<extent unit="pages">
<start>286</start>
<end>292</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit74">
<titleInfo>
<title>Adding chloroquine to conventional treatment for glioblastoma multiforme: a randomized, double‐blind, placebo‐controlled trial</title>
</titleInfo>
<name type="personal">
<namePart type="given">J.</namePart>
<namePart type="family">Sotelo</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">E.</namePart>
<namePart type="family">Briceno</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">M.A.</namePart>
<namePart type="family">Lopez‐Gonzalez</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Sotelo, J., E. Briceno & M.A. Lopez‐Gonzalez. 2006. Adding chloroquine to conventional treatment for glioblastoma multiforme: a randomized, double‐blind, placebo‐controlled trial. Ann. Inter. Med. 144: 337–343.</note>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>144</number>
</detail>
<extent unit="pages">
<start>337</start>
<end>343</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Ann. Inter. Med.</title>
</titleInfo>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>144</number>
</detail>
<extent unit="pages">
<start>337</start>
<end>343</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit75">
<titleInfo>
<title>Autophagy inhibition enhances vorinostat‐induced apoptosis via ubiquitinated protein accumulation</title>
</titleInfo>
<name type="personal">
<namePart type="given">J.S.</namePart>
<namePart type="family">Carew</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Carew, J.S. et al . 2010. Autophagy inhibition enhances vorinostat‐induced apoptosis via ubiquitinated protein accumulation. J. Cell. Mol. Med. 14: 2448–2459.</note>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>14</number>
</detail>
<extent unit="pages">
<start>2448</start>
<end>2459</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>J. Cell. Mol. Med.</title>
</titleInfo>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>14</number>
</detail>
<extent unit="pages">
<start>2448</start>
<end>2459</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit76">
<titleInfo>
<title>PHYTOALEXINS: what have we learned after 60 years</title>
</titleInfo>
<name type="personal">
<namePart type="given">R.</namePart>
<namePart type="family">Hammerschmidt</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Hammerschmidt, R. 1999. PHYTOALEXINS: what have we learned after 60 years Annu. Rev. Phytopathol. 37: 285–306.</note>
<part>
<date>1999</date>
<detail type="volume">
<caption>vol.</caption>
<number>37</number>
</detail>
<extent unit="pages">
<start>285</start>
<end>306</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Annu. Rev. Phytopathol.</title>
</titleInfo>
<part>
<date>1999</date>
<detail type="volume">
<caption>vol.</caption>
<number>37</number>
</detail>
<extent unit="pages">
<start>285</start>
<end>306</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit77">
<titleInfo>
<title>Resveratrol‐induced cytotoxicity in human Burkitt's lymphoma cells is coupled to the unfolded protein response</title>
</titleInfo>
<name type="personal">
<namePart type="given">Y.</namePart>
<namePart type="family">Yan</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Yan, Y. et al . 2010. Resveratrol‐induced cytotoxicity in human Burkitt's lymphoma cells is coupled to the unfolded protein response. BMC Cancer 10: 445.</note>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>10</number>
</detail>
<extent unit="pages">
<start>445</start>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>BMC Cancer</title>
</titleInfo>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>10</number>
</detail>
<extent unit="pages">
<start>445</start>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit78">
<titleInfo>
<title>Natural dietary anti‐cancer chemopreventive compounds: redox‐mediated differential signaling mechanisms in cytoprotection of normal cells versus cytotoxicity in tumor cells</title>
</titleInfo>
<name type="personal">
<namePart type="given">S.</namePart>
<namePart type="family">Nair</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">W.</namePart>
<namePart type="family">Li</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">A.N.</namePart>
<namePart type="family">Kong</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Nair, S., W. Li & A.N. Kong. 2007. Natural dietary anti‐cancer chemopreventive compounds: redox‐mediated differential signaling mechanisms in cytoprotection of normal cells versus cytotoxicity in tumor cells. Acta Pharmacol. Sinica 28: 459–472.</note>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>28</number>
</detail>
<extent unit="pages">
<start>459</start>
<end>472</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Acta Pharmacol. Sinica</title>
</titleInfo>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>28</number>
</detail>
<extent unit="pages">
<start>459</start>
<end>472</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit79">
<titleInfo>
<title>Curcumin induces pro‐apoptotic endoplasmic reticulum stress in human leukemia HL‐60 cells</title>
</titleInfo>
<name type="personal">
<namePart type="given">H.O.</namePart>
<namePart type="family">Pae</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Pae, H.O. et al . 2007. Curcumin induces pro‐apoptotic endoplasmic reticulum stress in human leukemia HL‐60 cells. Biochem. Biophys. Res. Commun. 353: 1040–1045.</note>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>353</number>
</detail>
<extent unit="pages">
<start>1040</start>
<end>1045</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Biochem. Biophys. Res. Commun.</title>
</titleInfo>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>353</number>
</detail>
<extent unit="pages">
<start>1040</start>
<end>1045</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit80">
<titleInfo>
<title>Resveratrol induces growth inhibition and apoptosis in metastatic breast cancer cells via de novo ceramide signaling</title>
</titleInfo>
<name type="personal">
<namePart type="given">F.</namePart>
<namePart type="family">Scarlatti</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Scarlatti, F. et al . 2003. Resveratrol induces growth inhibition and apoptosis in metastatic breast cancer cells via de novo ceramide signaling. FASEB J. 17: 2339–2341.</note>
<part>
<date>2003</date>
<detail type="volume">
<caption>vol.</caption>
<number>17</number>
</detail>
<extent unit="pages">
<start>2339</start>
<end>2341</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>FASEB J.</title>
</titleInfo>
<part>
<date>2003</date>
<detail type="volume">
<caption>vol.</caption>
<number>17</number>
</detail>
<extent unit="pages">
<start>2339</start>
<end>2341</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit81">
<titleInfo>
<title>The SERCA pump as a therapeutic target: making a “smart bomb” for prostate cancer</title>
</titleInfo>
<name type="personal">
<namePart type="given">S.R.</namePart>
<namePart type="family">Denmeade</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">J.T.</namePart>
<namePart type="family">Isaacs</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Denmeade, S.R. & J.T. Isaacs. 2005. The SERCA pump as a therapeutic target: making a “smart bomb” for prostate cancer. Cancer Biol. Therapy 4: 14–22.</note>
<part>
<date>2005</date>
<detail type="volume">
<caption>vol.</caption>
<number>4</number>
</detail>
<extent unit="pages">
<start>14</start>
<end>22</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cancer Biol. Therapy</title>
</titleInfo>
<part>
<date>2005</date>
<detail type="volume">
<caption>vol.</caption>
<number>4</number>
</detail>
<extent unit="pages">
<start>14</start>
<end>22</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit82">
<titleInfo>
<title>The anticancer drug imatinib induces cellular autophagy</title>
</titleInfo>
<name type="personal">
<namePart type="given">A.</namePart>
<namePart type="family">Ertmer</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Ertmer, A. et al . 2007. The anticancer drug imatinib induces cellular autophagy. Leukemia 21: 936–942.</note>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>21</number>
</detail>
<extent unit="pages">
<start>936</start>
<end>942</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Leukemia</title>
</titleInfo>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>21</number>
</detail>
<extent unit="pages">
<start>936</start>
<end>942</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit83">
<titleInfo>
<title>Dasatinib‐induced autophagy is enhanced in combination with temozolomide in glioma</title>
</titleInfo>
<name type="personal">
<namePart type="given">V.</namePart>
<namePart type="family">Milano</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Milano, V. et al . 2009. Dasatinib‐induced autophagy is enhanced in combination with temozolomide in glioma. Mol. Cancer Ther. 8: 394–406.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>8</number>
</detail>
<extent unit="pages">
<start>394</start>
<end>406</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cancer Ther.</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>8</number>
</detail>
<extent unit="pages">
<start>394</start>
<end>406</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit84">
<titleInfo>
<title>NV‐128, a novel isoflavone derivative, induces caspase‐independent cell death through the Akt/mammalian target of rapamycin pathway</title>
</titleInfo>
<name type="personal">
<namePart type="given">A.B.</namePart>
<namePart type="family">Alvero</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Alvero, A.B. et al . 2009. NV‐128, a novel isoflavone derivative, induces caspase‐independent cell death through the Akt/mammalian target of rapamycin pathway. Cancer 115: 3204–3216.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>115</number>
</detail>
<extent unit="pages">
<start>3204</start>
<end>3216</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cancer</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>115</number>
</detail>
<extent unit="pages">
<start>3204</start>
<end>3216</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit85">
<titleInfo>
<title>Active cell death induced by the anti‐estrogens tamoxifen and ICI 164 384 in human mammary carcinoma cells (MCF‐7) in culture: the role of autophagy</title>
</titleInfo>
<name type="personal">
<namePart type="given">W.</namePart>
<namePart type="family">Bursch</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Bursch, W. et al . 1996. Active cell death induced by the anti‐estrogens tamoxifen and ICI 164 384 in human mammary carcinoma cells (MCF‐7) in culture: the role of autophagy. Carcinogenesis 17: 1595–1607.</note>
<part>
<date>1996</date>
<detail type="volume">
<caption>vol.</caption>
<number>17</number>
</detail>
<extent unit="pages">
<start>1595</start>
<end>1607</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Carcinogenesis</title>
</titleInfo>
<part>
<date>1996</date>
<detail type="volume">
<caption>vol.</caption>
<number>17</number>
</detail>
<extent unit="pages">
<start>1595</start>
<end>1607</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit86">
<titleInfo>
<title>Autophagy induced by farnesyltransferase inhibitors in cancer cells</title>
</titleInfo>
<name type="personal">
<namePart type="given">J.</namePart>
<namePart type="family">Pan</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Pan, J. et al . 2008. Autophagy induced by farnesyltransferase inhibitors in cancer cells. Cancer Biol. Therapy 7: 1679–1684.</note>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>7</number>
</detail>
<extent unit="pages">
<start>1679</start>
<end>1684</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Cancer Biol. Therapy</title>
</titleInfo>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>7</number>
</detail>
<extent unit="pages">
<start>1679</start>
<end>1684</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit87">
<titleInfo>
<title>Inhibition of poly(ADP‐ribose) polymerase enhances cell death and improves tumor growth delay in irradiated lung cancer models</title>
</titleInfo>
<name type="personal">
<namePart type="given">J.M.</namePart>
<namePart type="family">Albert</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Albert, J.M. et al . 2007. Inhibition of poly(ADP‐ribose) polymerase enhances cell death and improves tumor growth delay in irradiated lung cancer models. Clin. Cancer Res. 13: 3033–3042.</note>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>13</number>
</detail>
<extent unit="pages">
<start>3033</start>
<end>3042</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Clin. Cancer Res.</title>
</titleInfo>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>13</number>
</detail>
<extent unit="pages">
<start>3033</start>
<end>3042</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit88">
<titleInfo>
<title>Potentiation of radiation sensitivity in breast tumor cells by the vitamin D3 analogue, EB 1089, through promotion of autophagy and interference with proliferative recovery</title>
</titleInfo>
<name type="personal">
<namePart type="given">G.</namePart>
<namePart type="family">Demasters</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Demasters, G. et al . 2006. Potentiation of radiation sensitivity in breast tumor cells by the vitamin D3 analogue, EB 1089, through promotion of autophagy and interference with proliferative recovery. Mol. Cancer Ther. 5: 2786–2797.</note>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>5</number>
</detail>
<extent unit="pages">
<start>2786</start>
<end>2797</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Cancer Ther.</title>
</titleInfo>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>5</number>
</detail>
<extent unit="pages">
<start>2786</start>
<end>2797</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit89">
<titleInfo>
<title>BCL‐2 family inhibitors enhance histone deacetylase inhibitor and sorafenib lethality via autophagy and overcome blockade of the extrinsic pathway to facilitate killing</title>
</titleInfo>
<name type="personal">
<namePart type="given">A.P.</namePart>
<namePart type="family">Martin</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Martin, A.P. et al . 2009. BCL‐2 family inhibitors enhance histone deacetylase inhibitor and sorafenib lethality via autophagy and overcome blockade of the extrinsic pathway to facilitate killing. Mol. Pharmacol. 76: 327–341.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>76</number>
</detail>
<extent unit="pages">
<start>327</start>
<end>341</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Mol. Pharmacol.</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>76</number>
</detail>
<extent unit="pages">
<start>327</start>
<end>341</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit90">
<titleInfo>
<title>Targeting tumor metabolism with 2‐deoxyglucose in patients with castrate‐resistant prostate cancer and advanced malignancies</title>
</titleInfo>
<name type="personal">
<namePart type="given">M.</namePart>
<namePart type="family">Stein</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Stein, M. et al . 2010. Targeting tumor metabolism with 2‐deoxyglucose in patients with castrate‐resistant prostate cancer and advanced malignancies. Prostate 70: 1388–1394.</note>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>70</number>
</detail>
<extent unit="pages">
<start>1388</start>
<end>1394</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Prostate</title>
</titleInfo>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>70</number>
</detail>
<extent unit="pages">
<start>1388</start>
<end>1394</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit91">
<titleInfo>
<title>Autophagy inhibition and antimalarials promote cell death in gastrointestinal stromal tumor (GIST)</title>
</titleInfo>
<name type="personal">
<namePart type="given">A.</namePart>
<namePart type="family">Gupta</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Gupta, A. et al . 2010. Autophagy inhibition and antimalarials promote cell death in gastrointestinal stromal tumor (GIST). Proc. Natl. Acad. Sci. USA 107: 14333–14338.</note>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>107</number>
</detail>
<extent unit="pages">
<start>14333</start>
<end>14338</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Proc. Natl. Acad. Sci. USA</title>
</titleInfo>
<part>
<date>2010</date>
<detail type="volume">
<caption>vol.</caption>
<number>107</number>
</detail>
<extent unit="pages">
<start>14333</start>
<end>14338</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit92">
<titleInfo>
<title>Involvement of macroautophagy in the caspase‐independent killing of Burkitt lymphoma cell lines by rituximab</title>
</titleInfo>
<name type="personal">
<namePart type="given">J.</namePart>
<namePart type="family">Turzanski</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">I.</namePart>
<namePart type="family">Daniels</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">A.P.</namePart>
<namePart type="family">Haynes</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Turzanski, J., I. Daniels & A.P. Haynes. 2009. Involvement of macroautophagy in the caspase‐independent killing of Burkitt lymphoma cell lines by rituximab. Br. J. Haematol. 145: 137–140.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>145</number>
</detail>
<extent unit="pages">
<start>137</start>
<end>140</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Br. J. Haematol.</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>145</number>
</detail>
<extent unit="pages">
<start>137</start>
<end>140</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit93">
<titleInfo>
<title>Autophagy: novel action of panitumumab in colon cancer</title>
</titleInfo>
<name type="personal">
<namePart type="given">E.</namePart>
<namePart type="family">Giannopoulou</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Giannopoulou, E. et al . 2009. Autophagy: novel action of panitumumab in colon cancer. Anticancer Res . 29: 5077–5082.</note>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>29</number>
</detail>
<extent unit="pages">
<start>5077</start>
<end>5082</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>Anticancer Res</title>
</titleInfo>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>29</number>
</detail>
<extent unit="pages">
<start>5077</start>
<end>5082</end>
</extent>
</part>
</relatedItem>
</relatedItem>
<relatedItem type="references" displayLabel="cit94">
<titleInfo>
<title>Autophagy inhibition enhances therapy‐induced apoptosis in a Myc‐induced model of lymphoma</title>
</titleInfo>
<name type="personal">
<namePart type="given">R.K.</namePart>
<namePart type="family">Amaravadi</namePart>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<genre>journal-article</genre>
<note type="citation/reference">Amaravadi, R.K. et al . 2007. Autophagy inhibition enhances therapy‐induced apoptosis in a Myc‐induced model of lymphoma. J. Clin. Invest. 117: 326–336.</note>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>117</number>
</detail>
<extent unit="pages">
<start>326</start>
<end>336</end>
</extent>
</part>
<relatedItem type="host">
<titleInfo>
<title>J. Clin. Invest.</title>
</titleInfo>
<part>
<date>2007</date>
<detail type="volume">
<caption>vol.</caption>
<number>117</number>
</detail>
<extent unit="pages">
<start>326</start>
<end>336</end>
</extent>
</part>
</relatedItem>
</relatedItem>
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