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Molecular Mechanisms Underlying Autophagy-Mediated Treatment Resistance in Cancer

Identifieur interne : 000570 ( Pmc/Checkpoint ); précédent : 000569; suivant : 000571

Molecular Mechanisms Underlying Autophagy-Mediated Treatment Resistance in Cancer

Auteurs : Cally J. Ho [Canada] ; Sharon M. Gorski [Canada]

Source :

RBID : PMC:6896088

Abstract

Despite advances in diagnostic tools and therapeutic options, treatment resistance remains a challenge for many cancer patients. Recent studies have found evidence that autophagy, a cellular pathway that delivers cytoplasmic components to lysosomes for degradation and recycling, contributes to treatment resistance in different cancer types. A role for autophagy in resistance to chemotherapies and targeted therapies has been described based largely on associations with various signaling pathways, including MAPK and PI3K/AKT signaling. However, our current understanding of the molecular mechanisms underlying the role of autophagy in facilitating treatment resistance remains limited. Here we provide a comprehensive summary of the evidence linking autophagy to major signaling pathways in the context of treatment resistance and tumor progression, and then highlight recently emerged molecular mechanisms underlying autophagy and the p62/KEAP1/NRF2 and FOXO3A/PUMA axes in chemoresistance.


Url:
DOI: 10.3390/cancers11111775
PubMed: 31717997
PubMed Central: 6896088


Affiliations:


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PMC:6896088

Le document en format XML

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</TEI>
<pmc article-type="review-article">
<pmc-dir>properties open_access</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">Cancers (Basel)</journal-id>
<journal-id journal-id-type="iso-abbrev">Cancers (Basel)</journal-id>
<journal-id journal-id-type="publisher-id">cancers</journal-id>
<journal-title-group>
<journal-title>Cancers</journal-title>
</journal-title-group>
<issn pub-type="epub">2072-6694</issn>
<publisher>
<publisher-name>MDPI</publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">31717997</article-id>
<article-id pub-id-type="pmc">6896088</article-id>
<article-id pub-id-type="doi">10.3390/cancers11111775</article-id>
<article-id pub-id-type="publisher-id">cancers-11-01775</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Review</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Molecular Mechanisms Underlying Autophagy-Mediated Treatment Resistance in Cancer</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Ho</surname>
<given-names>Cally J.</given-names>
</name>
<xref ref-type="aff" rid="af1-cancers-11-01775">1</xref>
<xref ref-type="aff" rid="af2-cancers-11-01775">2</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Gorski</surname>
<given-names>Sharon M.</given-names>
</name>
<xref ref-type="aff" rid="af1-cancers-11-01775">1</xref>
<xref ref-type="aff" rid="af2-cancers-11-01775">2</xref>
<xref ref-type="aff" rid="af3-cancers-11-01775">3</xref>
<xref rid="c1-cancers-11-01775" ref-type="corresp">*</xref>
</contrib>
</contrib-group>
<aff id="af1-cancers-11-01775">
<label>1</label>
Canada’s Michael Smith Genome Sciences Centre, BC Cancer, Vancouver, BC V5Z 1L3, Canada;
<email>caho@bcgsc.ca</email>
</aff>
<aff id="af2-cancers-11-01775">
<label>2</label>
Department of Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, BC V5A 1S6, Canada</aff>
<aff id="af3-cancers-11-01775">
<label>3</label>
Centre for Cell Biology, Development, and Disease, Simon Fraser University, Burnaby, BC V5A 1S6, Canada</aff>
<author-notes>
<corresp id="c1-cancers-11-01775">
<label>*</label>
Correspondence:
<email>sgorski@bcgsc.ca</email>
</corresp>
</author-notes>
<pub-date pub-type="epub">
<day>11</day>
<month>11</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="collection">
<month>11</month>
<year>2019</year>
</pub-date>
<volume>11</volume>
<issue>11</issue>
<elocation-id>1775</elocation-id>
<history>
<date date-type="received">
<day>01</day>
<month>10</month>
<year>2019</year>
</date>
<date date-type="accepted">
<day>31</day>
<month>10</month>
<year>2019</year>
</date>
</history>
<permissions>
<copyright-statement>© 2019 by the authors.</copyright-statement>
<copyright-year>2019</copyright-year>
<license license-type="open-access">
<license-p>Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (
<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>
).</license-p>
</license>
</permissions>
<abstract>
<p>Despite advances in diagnostic tools and therapeutic options, treatment resistance remains a challenge for many cancer patients. Recent studies have found evidence that autophagy, a cellular pathway that delivers cytoplasmic components to lysosomes for degradation and recycling, contributes to treatment resistance in different cancer types. A role for autophagy in resistance to chemotherapies and targeted therapies has been described based largely on associations with various signaling pathways, including MAPK and PI3K/AKT signaling. However, our current understanding of the molecular mechanisms underlying the role of autophagy in facilitating treatment resistance remains limited. Here we provide a comprehensive summary of the evidence linking autophagy to major signaling pathways in the context of treatment resistance and tumor progression, and then highlight recently emerged molecular mechanisms underlying autophagy and the p62/KEAP1/NRF2 and FOXO3A/PUMA axes in chemoresistance.</p>
</abstract>
<kwd-group>
<kwd>autophagy</kwd>
<kwd>cancer</kwd>
<kwd>treatment resistance</kwd>
<kwd>targeted agents</kwd>
<kwd>chemotherapy</kwd>
<kwd>molecular mechanisms</kwd>
<kwd>chemoresistance</kwd>
</kwd-group>
</article-meta>
</front>
<floats-group>
<fig id="cancers-11-01775-f001" orientation="portrait" position="float">
<label>Figure 1</label>
<caption>
<p>Reactivation of ERK signaling via AKT-ETS-1-mediated positive feedback loop contributes to resistance to the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), Gefitinib, in non-small cell lung cancers (NSCLCs). Gefitinib treatment inhibits EGFR-mediated activation of AKT and ERK1/2 signaling in NSCLCs. Reduced AKT signaling inhibits the activation of the E26 transformation-specific (ETS) transcription factor, Ets-1. Ets-1 is responsible for the transcriptional upregulation of dual specificity phosphatase 6 (DUSP6), a negative regulator of ERK1/2 activity. Reduced DUSP6 levels therefore result in a gradual reactivation of ERK1/2 activity, which promotes the turnover of the pro-apoptotic protein, BIM, and consequently supports tumor cell survival. Reduced Ets-1 activity also leads to a decrease in the transcriptional upregulation of cell cycle regulatory proteins, like cyclins D1, D3, and E3, and this consequently leads to tumor cell dormancy [
<xref rid="B321-cancers-11-01775" ref-type="bibr">321</xref>
].</p>
</caption>
<graphic xlink:href="cancers-11-01775-g001"></graphic>
</fig>
<fig id="cancers-11-01775-f002" orientation="portrait" position="float">
<label>Figure 2</label>
<caption>
<p>The stress-activated p38 MAPK pathway contributes to tumor resistance against targeted therapies and chemotherapies in cancers. (
<bold>a</bold>
) Overexpression of the human epidermal growth factor receptor 2 (HER2) protein has been observed in cancers, like breast, and has been associated with the aberrant activation of growth and survival pathways, like AKT signaling and ERK signaling. The HER2-targeted antibody trastuzumab binds to the extracellular domain of HER2 and inhibits HER2 dimerization and HER2-mediated signaling events, consequently mitigating tumorigenesis. Ectopic activation of the p38 MAPK pathway in HER2-overexpressing (HER2+) breast cancers can confer resistance to trastuzumab by promoting cell growth and survival independent of HER2 activity [
<xref rid="B331-cancers-11-01775" ref-type="bibr">331</xref>
]. To date, the mechanisms underlying the relationship between HER2 signaling and p38 MAPK remain unknown. (
<bold>b</bold>
) Resistance to chemotherapies, like cisplatin and dacarbazine, have also been associated with p38 MAPK activity in melanoma cells. Chemotherapy-induced cellular stress activates the p38 MAPK pathway, and this results in the activation of cellular repair mechanisms that promote tumor cell growth and survival. Activation of p38 MAPK is further sustained by the immune checkpoint molecule, CD276/B7-H3, which inhibits the p38 MAPK-negative regulator dual specificity protein phosphatase 10 (DUSP10) [
<xref rid="B335-cancers-11-01775" ref-type="bibr">335</xref>
]. To date, the mechanistic relationship between CD276/B7-H3 activity and DUSP10 inhibition remains unknown.</p>
</caption>
<graphic xlink:href="cancers-11-01775-g002"></graphic>
</fig>
<fig id="cancers-11-01775-f003" orientation="portrait" position="float">
<label>Figure 3</label>
<caption>
<p>Associations between the autophagy pathway and MAPK signaling in to tumor tolerance against targeted therapies and chemotherapies. (
<bold>a</bold>
) Chemotherapeutic agents, like 5-fluorouracil, activate the p38 MAPK pathway in response to cellular stress, and thus promote cell survival in colorectal cancers. Pharmacological or genetic inhibition of p38 MAPK induces the autophagy pathway, and autophagy inhibition in p38 MAPK-deficient colorectal cancer cells potentiates the cytotoxic effects of chemotherapy [
<xref rid="B344-cancers-11-01775" ref-type="bibr">344</xref>
]. To date, the relationship between autophagy regulation and the p38 MAPK remains poorly understood. (
<bold>b</bold>
) Crosstalk between the autophagy pathway and the ERK signaling arm of the MAPK pathway has been associated with resistance to B-RAF inhibitors (BRAFi) or MEK inhibitors (MEKi) in melanomas. BRAFi or MEKi-mediated inhibition of ERK1/2 signaling has been associated with the nuclear translocation of ERK2, and stabilization of the transcription factor, Activating Transcription Factor 4 (ATF4). This promotes the transcriptional upregulation of ATF4 target genes, like autophagy-related genes (ATGs) ATG5 and ATG7, and ER stress response genes, Asparagine synthetase 3 (ASN3), Cyclic AMP-dependent transcription factor (ATF3), and C/EBP-Homologous Protein (CHOP) [
<xref rid="B345-cancers-11-01775" ref-type="bibr">345</xref>
].</p>
</caption>
<graphic xlink:href="cancers-11-01775-g003"></graphic>
</fig>
<fig id="cancers-11-01775-f004" orientation="portrait" position="float">
<label>Figure 4</label>
<caption>
<p>The AKT signaling pathway contributes to treatment resistance against targeted therapies and chemotherapies in cancers. (
<bold>a</bold>
) BRAF inhibition (BRAFi) upregulates AKT activity in melanomas with concurrent PTEN loss and activating BRAFv600E mutations. This result in AKT-mediated inhibition of the transcription factor Forkhead Box O3A (FOXO3A), and reduces the transcriptional upregulation of its pro-apoptotic target gene, BIM. Combined pharmacological inhibition of BRAF activity and AKT activity, by PI3K inhibition, increases BIM expression and potentiates apoptosis, suggesting that AKT activity contributes to the resistance of BRAFV600E mutation-bearing melanomas to BRAFi [
<xref rid="B352-cancers-11-01775" ref-type="bibr">352</xref>
]. (
<bold>b</bold>
) Activating mutations in the catalytic subunit of PI3K (PI3KCA) also contribute to resistance against chemotherapies in colorectal cancers through suppression of pro-apoptotic responses, and inhibition of PI3K can potentiate the cytotoxic effects of chemotherapy [
<xref rid="B353-cancers-11-01775" ref-type="bibr">353</xref>
].</p>
</caption>
<graphic xlink:href="cancers-11-01775-g004"></graphic>
</fig>
<fig id="cancers-11-01775-f005" orientation="portrait" position="float">
<label>Figure 5</label>
<caption>
<p>Associations between AKT signaling and autophagy in tumor tolerance against targeted therapies and chemotherapies. (
<bold>a</bold>
) The pan-PI3K inhibitor, pictilisib, inhibits PI3K-mediated AKT activation, and results in cytoprotective autophagy. Pharmacological and genetic inhibition of autophagy potentiates the pro-apoptotic and growth inhibitory effects of pictilisib in breast cancers [
<xref rid="B262-cancers-11-01775" ref-type="bibr">262</xref>
]. (
<bold>b</bold>
) Chemotherapy-induced cellular stress results in the activation of autophagy and the cytoprotective enzyme, heme oxygenase-1 (HO-1). HO-1 is transcriptionally upregulated by NRF2, a downstream target of AKT. Pharmacological inhibition of AKT signaling, by PI3K inhibition, potentiates the cytotoxic effects of anthracyclines, like pharmorubicin, and is associated with a reduction of autophagy and HO-1 levels [
<xref rid="B362-cancers-11-01775" ref-type="bibr">362</xref>
].</p>
</caption>
<graphic xlink:href="cancers-11-01775-g005"></graphic>
</fig>
<fig id="cancers-11-01775-f006" orientation="portrait" position="float">
<label>Figure 6</label>
<caption>
<p>Autophagy mediates the clearance of p62-bound cytotoxic cellular aggregates generated by chemotherapy-induced oxidative stresses. Chemotherapy-induced oxidative stress results in the oxidation of the ubiquitin ligase complex adaptor protein, KEAP1. This inhibits the interaction between KEAP1 and the oxidative stress response transcription factor NRF2, and stabilizes cellular levels of NRF2. NRF2 transcriptionally upregulates various target genes involved in cellular anti-oxidation and stress response, like p62. The autophagy cargo receptor, p62, binds to cellular aggregates generated by chemotherapy-induced oxidative stress, and targets these cytotoxic aggregates for degradation and recycling through the process of autophagy [
<xref rid="B377-cancers-11-01775" ref-type="bibr">377</xref>
].</p>
</caption>
<graphic xlink:href="cancers-11-01775-g006"></graphic>
</fig>
<fig id="cancers-11-01775-f007" orientation="portrait" position="float">
<label>Figure 7</label>
<caption>
<p>Autophagic degradation of the transcription factor FOXO3A confers tumor tolerance to pro-apoptotic signals. FOXO3A is a transcription factor involved in the transcriptional upregulation of pro-apoptotic genes, like PUMA, and genes involved in cellular stress responses, like autophagy-related genes (ATG). Autophagy is upregulated in response to chemotherapy-induced cellular stresses as a pro-survival response. Stress-induced autophagy mediates the degradation and turnover of FOXO3A, thereby greatly mitigating the transcription of genes encoding pro-apoptotic proteins, like PUMA, and reducing sensitivity to apoptosis [
<xref rid="B189-cancers-11-01775" ref-type="bibr">189</xref>
].</p>
</caption>
<graphic xlink:href="cancers-11-01775-g007"></graphic>
</fig>
<table-wrap id="cancers-11-01775-t003" orientation="portrait" position="float">
<object-id pub-id-type="pii">cancers-11-01775-t003_Table 3</object-id>
<label>Table 3</label>
<caption>
<p>Examples of pre-clinical studies demonstrating that autophagy and autophagy-related (ATG) genes contribute to cancer resistance to different targeted therapies.</p>
</caption>
<table frame="hsides" rules="groups">
<thead>
<tr>
<th rowspan="2" align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" colspan="1">Targeted Agent</th>
<th rowspan="2" align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" colspan="1">Cancer Types</th>
<th colspan="2" align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1">Mode of Autophagy Inhibition</th>
<th rowspan="2" align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" colspan="1">Ref.</th>
</tr>
<tr>
<th align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Pharmacological</th>
<th align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Genetic</th>
</tr>
</thead>
<tbody>
<tr>
<td colspan="5" align="left" valign="middle" style="border-bottom:solid thin" rowspan="1">Monoclonal antibodies</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Bevacizumab
<break></break>
(VEGF (vascular endothelial growth factor) inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Gliomas,
<break></break>
Colorectal cancers,
<break></break>
Liver cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CQ, HCQ</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">BECN1 siRNA (small interfering Ribonucleic Acid),
<break></break>
ATG7 shRNA (short hairpin Ribonucleic Acid)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B113-cancers-11-01775" ref-type="bibr">113</xref>
,
<xref rid="B192-cancers-11-01775" ref-type="bibr">192</xref>
,
<xref rid="B193-cancers-11-01775" ref-type="bibr">193</xref>
,
<xref rid="B194-cancers-11-01775" ref-type="bibr">194</xref>
,
<xref rid="B195-cancers-11-01775" ref-type="bibr">195</xref>
,
<xref rid="B196-cancers-11-01775" ref-type="bibr">196</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Trastuzumab
<break></break>
(HER2 (human epidermal growth factor receptor 2) inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Breast cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">3-MA, Baf A1</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">LC3B siRNA,
<break></break>
ATG4B siRNA,
<break></break>
ATG12 shRNA,
<break></break>
ATG4B siRNA </td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B197-cancers-11-01775" ref-type="bibr">197</xref>
,
<xref rid="B198-cancers-11-01775" ref-type="bibr">198</xref>
,
<xref rid="B199-cancers-11-01775" ref-type="bibr">199</xref>
,
<xref rid="B200-cancers-11-01775" ref-type="bibr">200</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Cetuximab
<break></break>
(EGFR (epidermal growth factor receptor) inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Vulvar cancers,
<break></break>
Lung cancers,
<break></break>
Head and neck cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CQ, 3-MA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">BECN1 siRNA,
<break></break>
ATG7 siRNA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B201-cancers-11-01775" ref-type="bibr">201</xref>
,
<xref rid="B202-cancers-11-01775" ref-type="bibr">202</xref>
,
<xref rid="B203-cancers-11-01775" ref-type="bibr">203</xref>
]</td>
</tr>
<tr>
<td colspan="5" align="left" valign="middle" style="border-bottom:solid thin" rowspan="1">Small molecule inhibitors</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Sorafenib
<break></break>
(multi-kinase inhibitor—VEGFRs, PDGFRs (platelet-derived growth factor receptor), RAF (Rapidly Accelerated Fibrosarcoma) kinases)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Endometrial cancers,
<break></break>
Liver cancers,
<break></break>
Kidney cancers,
<break></break>
Gliomas,
<break></break>
Desmoid tumors</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CQ, 3-MA, Baf A1</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">BECN1 siRNA,
<break></break>
BECN1 shRNA,
<break></break>
ATG5 siRNA,
<break></break>
ATG5 shRNA,
<break></break>
miR (microRNA)-375 (ATG7 knockdown)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B204-cancers-11-01775" ref-type="bibr">204</xref>
,
<xref rid="B205-cancers-11-01775" ref-type="bibr">205</xref>
,
<xref rid="B206-cancers-11-01775" ref-type="bibr">206</xref>
,
<xref rid="B207-cancers-11-01775" ref-type="bibr">207</xref>
,
<xref rid="B208-cancers-11-01775" ref-type="bibr">208</xref>
,
<xref rid="B209-cancers-11-01775" ref-type="bibr">209</xref>
,
<xref rid="B210-cancers-11-01775" ref-type="bibr">210</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Linifanib
<break></break>
(multi-kinase inhibitor—VEGFRs and PDFRs)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Liver cancers </td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CQ, 3-MA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ATG7 siRNA,
<break></break>
ATG5 siRNA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B211-cancers-11-01775" ref-type="bibr">211</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Sunitinib
<break></break>
(Multi-kinase inhibitor—PDGFRs, VEGFRs, KIRs (Killer cell immunoglobulin like receptors), FLT-3 (fms like tyrosine kinase-3), CSF-1R (Colony stimulating factor 1 receptor), RET (rearranged during transfection) kinases)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Ovarian cancers,
<break></break>
Kidney cancers,
<break></break>
Prostate cancers,
<break></break>
Pancreatic cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Lys05, CQ, 3-MA, Baf A1</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ATG7 siRNA,
<break></break>
ATG5 siRNA,
<break></break>
ATG5 shRNA,
<break></break>
LAMP2 shRNA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B212-cancers-11-01775" ref-type="bibr">212</xref>
,
<xref rid="B213-cancers-11-01775" ref-type="bibr">213</xref>
,
<xref rid="B214-cancers-11-01775" ref-type="bibr">214</xref>
,
<xref rid="B215-cancers-11-01775" ref-type="bibr">215</xref>
,
<xref rid="B216-cancers-11-01775" ref-type="bibr">216</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Gefitinib
<break></break>
(EGFR inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Breast cancers,
<break></break>
Bladder cancers,
<break></break>
Skin cancers,
<break></break>
Lung cancers,
<break></break>
Liver cancers,
<break></break>
Pancreatic cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">3-MA, Baf A1, CQ, HCQ</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ATG12 siRNA,
<break></break>
BECN1 siRNA,
<break></break>
ATG7 siRNA,
<break></break>
ATG5 siRNA,
<break></break>
VPS34 siRNA,
<break></break>
miR-153-3p (ATG5 knockdown)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B217-cancers-11-01775" ref-type="bibr">217</xref>
,
<xref rid="B218-cancers-11-01775" ref-type="bibr">218</xref>
,
<xref rid="B219-cancers-11-01775" ref-type="bibr">219</xref>
,
<xref rid="B220-cancers-11-01775" ref-type="bibr">220</xref>
,
<xref rid="B221-cancers-11-01775" ref-type="bibr">221</xref>
,
<xref rid="B222-cancers-11-01775" ref-type="bibr">222</xref>
,
<xref rid="B223-cancers-11-01775" ref-type="bibr">223</xref>
,
<xref rid="B224-cancers-11-01775" ref-type="bibr">224</xref>
,
<xref rid="B225-cancers-11-01775" ref-type="bibr">225</xref>
,
<xref rid="B226-cancers-11-01775" ref-type="bibr">226</xref>
,
<xref rid="B227-cancers-11-01775" ref-type="bibr">227</xref>
,
<xref rid="B228-cancers-11-01775" ref-type="bibr">228</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Osimertinib
<break></break>
(EGFR inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Lung cancers,
<break></break>
Breast cancers,
<break></break>
Colorectal cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Spautin-1, CQ, 3-MA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">BECN1 siRNA,
<break></break>
ATG5 siRNA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B229-cancers-11-01775" ref-type="bibr">229</xref>
,
<xref rid="B230-cancers-11-01775" ref-type="bibr">230</xref>
,
<xref rid="B231-cancers-11-01775" ref-type="bibr">231</xref>
,
<xref rid="B232-cancers-11-01775" ref-type="bibr">232</xref>
,
<xref rid="B233-cancers-11-01775" ref-type="bibr">233</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Erlotinib
<break></break>
(EGFR inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Lung cancers,
<break></break>
Glioblastomas,
<break></break>
Head and neck cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">l
<break></break>
CQ, 3-MA, Quinacrine</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ATG5 siRNA,
<break></break>
ATG7 siRNA,
<break></break>
BECN1 siRNA,
<break></break>
LC3 siRNA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B228-cancers-11-01775" ref-type="bibr">228</xref>
,
<xref rid="B234-cancers-11-01775" ref-type="bibr">234</xref>
,
<xref rid="B235-cancers-11-01775" ref-type="bibr">235</xref>
,
<xref rid="B236-cancers-11-01775" ref-type="bibr">236</xref>
,
<xref rid="B237-cancers-11-01775" ref-type="bibr">237</xref>
,
<xref rid="B238-cancers-11-01775" ref-type="bibr">238</xref>
,
<xref rid="B239-cancers-11-01775" ref-type="bibr">239</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Everolimus
<break></break>
(mTORC1 (mammalian target of rapamycin complex 1) inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Blood cancers,
<break></break>
Kidney cancers,
<break></break>
Bladder cancers,
<break></break>
Breast cancer,
<break></break>
Neuroendocrine tumors</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">HCQ, CQ, Baf A1, 3-MA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">-</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B240-cancers-11-01775" ref-type="bibr">240</xref>
,
<xref rid="B241-cancers-11-01775" ref-type="bibr">241</xref>
,
<xref rid="B242-cancers-11-01775" ref-type="bibr">242</xref>
,
<xref rid="B243-cancers-11-01775" ref-type="bibr">243</xref>
,
<xref rid="B244-cancers-11-01775" ref-type="bibr">244</xref>
,
<xref rid="B245-cancers-11-01775" ref-type="bibr">245</xref>
,
<xref rid="B246-cancers-11-01775" ref-type="bibr">246</xref>
,
<xref rid="B247-cancers-11-01775" ref-type="bibr">247</xref>
] </td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Temsirolimus
<break></break>
(mTORC1 inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Colorectal cancers,
<break></break>
Skin cancers,
<break></break>
Kidney cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CQ, HCQ</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ATG7 shRNA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B248-cancers-11-01775" ref-type="bibr">248</xref>
,
<xref rid="B249-cancers-11-01775" ref-type="bibr">249</xref>
,
<xref rid="B250-cancers-11-01775" ref-type="bibr">250</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Dactolisib/NVP-BEZ235
<break></break>
(Dual mTOR/Class I PI3K (phosphoinositide 3-kinase) inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Kidney cancers,
<break></break>
Liver cancers,
<break></break>
Blood cancers,
<break></break>
Colorectal cancers,
<break></break>
Head and neck cancers,
<break></break>
Gliomas,
<break></break>
Mesotheliomas,
<break></break>
Gastric cancers,
<break></break>
Rhabdomyosarcomas,
<break></break>
Neuroblastomas,
<break></break>
Lung cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">3-MA, CQ, Baf A1,
<break></break>
VPS34 inhibitor (VPS34-IN1)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ATG5 siRNA,
<break></break>
BECN1 siRNA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B251-cancers-11-01775" ref-type="bibr">251</xref>
,
<xref rid="B252-cancers-11-01775" ref-type="bibr">252</xref>
,
<xref rid="B253-cancers-11-01775" ref-type="bibr">253</xref>
,
<xref rid="B254-cancers-11-01775" ref-type="bibr">254</xref>
,
<xref rid="B255-cancers-11-01775" ref-type="bibr">255</xref>
,
<xref rid="B256-cancers-11-01775" ref-type="bibr">256</xref>
,
<xref rid="B257-cancers-11-01775" ref-type="bibr">257</xref>
,
<xref rid="B258-cancers-11-01775" ref-type="bibr">258</xref>
,
<xref rid="B259-cancers-11-01775" ref-type="bibr">259</xref>
,
<xref rid="B260-cancers-11-01775" ref-type="bibr">260</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Buparlisib/BKM120
<break></break>
(Pan-Class I PI3K inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Lung cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CQ</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">-</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B261-cancers-11-01775" ref-type="bibr">261</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Pictilisib/GDC-0941
<break></break>
(Pan-Class I PI3K inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Breast cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CQ</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ATG5 siRNA,
<break></break>
ATG7 siRNA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B262-cancers-11-01775" ref-type="bibr">262</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Lapatinib
<break></break>
(Dual EGFR/HER2 inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Breast cancers,
<break></break>
Esophageal cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CQ, 3-MA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ATG12 shRNA,
<break></break>
ATG5 siRNA,
<break></break>
BECN1 siRNA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B200-cancers-11-01775" ref-type="bibr">200</xref>
,
<xref rid="B263-cancers-11-01775" ref-type="bibr">263</xref>
,
<xref rid="B264-cancers-11-01775" ref-type="bibr">264</xref>
,
<xref rid="B265-cancers-11-01775" ref-type="bibr">265</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Afatinib
<break></break>
(EGFR/HER2/HER4 inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Lung cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">HCQ, 3-MA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">-</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B266-cancers-11-01775" ref-type="bibr">266</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Bortezomib
<break></break>
(Proteasome inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Breast cancers,
<break></break>
Blood cancers,
<break></break>
Pancreatic cancers,
<break></break>
Cervical cancers,
<break></break>
Prostate cancers,
<break></break>
Neuroblastomas</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">3-MA, HCQ, CQ, Baf A1</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">LC3B siRNA,
<break></break>
ATG5 siRNA,
<break></break>
P62 shRNA,
<break></break>
GABARAPL1 shRNA,
<break></break>
BECN1 siRNA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B267-cancers-11-01775" ref-type="bibr">267</xref>
,
<xref rid="B268-cancers-11-01775" ref-type="bibr">268</xref>
,
<xref rid="B269-cancers-11-01775" ref-type="bibr">269</xref>
,
<xref rid="B270-cancers-11-01775" ref-type="bibr">270</xref>
,
<xref rid="B271-cancers-11-01775" ref-type="bibr">271</xref>
,
<xref rid="B272-cancers-11-01775" ref-type="bibr">272</xref>
,
<xref rid="B273-cancers-11-01775" ref-type="bibr">273</xref>
,
<xref rid="B274-cancers-11-01775" ref-type="bibr">274</xref>
,
<xref rid="B275-cancers-11-01775" ref-type="bibr">275</xref>
,
<xref rid="B276-cancers-11-01775" ref-type="bibr">276</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Carfilzomib
<break></break>
(Proteasome inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Blood cancers,
<break></break>
Neuroblastomas</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CQ, HCQ</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">-</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B277-cancers-11-01775" ref-type="bibr">277</xref>
,
<xref rid="B278-cancers-11-01775" ref-type="bibr">278</xref>
,
<xref rid="B279-cancers-11-01775" ref-type="bibr">279</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Vemurafenib
<break></break>
(B-RAF inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Brain cancers,
<break></break>
Skin cancers,
<break></break>
Thyroid cancers,
<break></break>
Colorectal cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CQ, HCQ, Baf A1, Lys05</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ATG5 siRNA,
<break></break>
ATG5 shRNA,
<break></break>
ATG7 siRNA,
<break></break>
ATG13 siRNA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B280-cancers-11-01775" ref-type="bibr">280</xref>
,
<xref rid="B281-cancers-11-01775" ref-type="bibr">281</xref>
,
<xref rid="B282-cancers-11-01775" ref-type="bibr">282</xref>
,
<xref rid="B283-cancers-11-01775" ref-type="bibr">283</xref>
,
<xref rid="B284-cancers-11-01775" ref-type="bibr">284</xref>
,
<xref rid="B285-cancers-11-01775" ref-type="bibr">285</xref>
,
<xref rid="B286-cancers-11-01775" ref-type="bibr">286</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Trametinib
<break></break>
(MEK1/2 (mitogen-activated protein kinase kinase 1/ 2) inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Skin cancers,
<break></break>
Pancreatic cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CQ, HCQ, PIK-III</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Inactive dominant-negative ATG4B
<sup>C74A</sup>
</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B287-cancers-11-01775" ref-type="bibr">287</xref>
,
<xref rid="B288-cancers-11-01775" ref-type="bibr">288</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">AKTi-1/2
<break></break>
(Dual AKT 1/2 (Protein kinase B 1/ 2) inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Ovarian cancers,
<break></break>
Liver cancers,
<break></break>
Prostate cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CQ, Spautin-1, 3-MA, Baf A1</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ATG7 siRNA,
<break></break>
ATG5 siRNA,
<break></break>
BECN1 siRNA, BECN1 shRNA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B289-cancers-11-01775" ref-type="bibr">289</xref>
,
<xref rid="B290-cancers-11-01775" ref-type="bibr">290</xref>
,
<xref rid="B291-cancers-11-01775" ref-type="bibr">291</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">AZD5363
<break></break>
(AKT 1/2/3 inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Prostate cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CQ, 3-MA, Baf A1</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ATG3 siRNA,
<break></break>
ATG7 siRNA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B292-cancers-11-01775" ref-type="bibr">292</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Tamoxifen
<break></break>
(ER (estrogen receptor) inhibitor; anti-estrogenic analog)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Breast cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">HCQ, Baf A1, 3-MA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ATG7 siRNA,
<break></break>
BECN1 siRNA,
<break></break>
LAMP3 shRNA,
<break></break>
LC3B siRNA,
<break></break>
ATG5 siRNA,
<break></break>
BECN1 siRNA</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B293-cancers-11-01775" ref-type="bibr">293</xref>
,
<xref rid="B294-cancers-11-01775" ref-type="bibr">294</xref>
,
<xref rid="B295-cancers-11-01775" ref-type="bibr">295</xref>
,
<xref rid="B296-cancers-11-01775" ref-type="bibr">296</xref>
,
<xref rid="B297-cancers-11-01775" ref-type="bibr">297</xref>
,
<xref rid="B298-cancers-11-01775" ref-type="bibr">298</xref>
,
<xref rid="B299-cancers-11-01775" ref-type="bibr">299</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Imatinib
<break></break>
(BCR-ABL (breakpoint cluster region-abelson murine leukemia viral oncogene homolog 1) inhibitor)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Blood cancers,
<break></break>
Gastrointestinal cancers,
<break></break>
Colorectal cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Spautin-1, CQ, HCQ,
<break></break>
Quinacrine, Vincristine</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ATG7 siRNA,
<break></break>
ATG12 siRNA,
<break></break>
ATG4B shRNA,
<break></break>
BECN1 shRNA,
<break></break>
ATG5 shRNA,
<break></break>
miR-30a (BECN1 and ATG5 knockdown)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B73-cancers-11-01775" ref-type="bibr">73</xref>
,
<xref rid="B300-cancers-11-01775" ref-type="bibr">300</xref>
,
<xref rid="B301-cancers-11-01775" ref-type="bibr">301</xref>
,
<xref rid="B302-cancers-11-01775" ref-type="bibr">302</xref>
,
<xref rid="B303-cancers-11-01775" ref-type="bibr">303</xref>
,
<xref rid="B304-cancers-11-01775" ref-type="bibr">304</xref>
,
<xref rid="B305-cancers-11-01775" ref-type="bibr">305</xref>
,
<xref rid="B306-cancers-11-01775" ref-type="bibr">306</xref>
]</td>
</tr>
<tr>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">HDIL-2
<break></break>
(high-dose interleukin-2 immunotherapy)</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Liver cancers</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CQ</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">-</td>
<td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[
<xref rid="B307-cancers-11-01775" ref-type="bibr">307</xref>
,
<xref rid="B308-cancers-11-01775" ref-type="bibr">308</xref>
]</td>
</tr>
</tbody>
</table>
</table-wrap>
</floats-group>
</pmc>
<affiliations>
<list>
<country>
<li>Canada</li>
</country>
</list>
<tree>
<country name="Canada">
<noRegion>
<name sortKey="Ho, Cally J" sort="Ho, Cally J" uniqKey="Ho C" first="Cally J." last="Ho">Cally J. Ho</name>
</noRegion>
<name sortKey="Gorski, Sharon M" sort="Gorski, Sharon M" uniqKey="Gorski S" first="Sharon M." last="Gorski">Sharon M. Gorski</name>
<name sortKey="Gorski, Sharon M" sort="Gorski, Sharon M" uniqKey="Gorski S" first="Sharon M." last="Gorski">Sharon M. Gorski</name>
</country>
</tree>
</affiliations>
</record>

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