Growth Factor Mediated Signaling in Pancreatic Pathogenesis
Identifieur interne : 005F13 ( Ncbi/Merge ); précédent : 005F12; suivant : 005F14Growth Factor Mediated Signaling in Pancreatic Pathogenesis
Auteurs : Debashis Nandy ; Debabrata MukhopadhyaySource :
- Cancers [ 2072-6694 ] ; 2011.
Abstract
Functionally, the pancreas consists of two types of tissues: exocrine and endocrine. Exocrine pancreatic disorders mainly involve acute and chronic pancreatitis. Acute pancreatitis typically is benign, while chronic pancreatitis is considered a risk factor for developing pancreatic cancer. Pancreatic carcinoma is the fourth leading cause of cancer related deaths worldwide. Most pancreatic cancers develop in the exocrine tissues. Endocrine pancreatic tumors are more uncommon, and typically are less aggressive than exocrine tumors. However, the endocrine pancreatic disorder, diabetes, is a dominant cause of morbidity and mortality. Importantly, different growth factors and their receptors play critical roles in pancreatic pathogenesis. Hence, an improved understanding of how various growth factors affect pancreatitis and pancreatic carcinoma is necessary to determine appropriate treatment. This chapter describes the role of different growth factors such as vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF), platelet derived growth factor (PDGF), fibroblast growth factor (FGF), epidermal growth factor (EGF), and transforming growth factor (TGF) in various pancreatic pathophysiologies. Finally, the crosstalk between different growth factor axes and their respective signaling mechanisms, which are involved in pancreatitis and pancreatic carcinoma, are also discussed.
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DOI: 10.3390/cancers3010841
PubMed: 24212642
PubMed Central: 3756392
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Growth Factor Mediated Signaling in Pancreatic Pathogenesis</title><author><name sortKey="Nandy, Debashis" sort="Nandy, Debashis" uniqKey="Nandy D" first="Debashis" last="Nandy">Debashis Nandy</name></author><author><name sortKey="Mukhopadhyay, Debabrata" sort="Mukhopadhyay, Debabrata" uniqKey="Mukhopadhyay D" first="Debabrata" last="Mukhopadhyay">Debabrata Mukhopadhyay</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">24212642</idno><idno type="pmc">3756392</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3756392</idno><idno type="RBID">PMC:3756392</idno><idno type="doi">10.3390/cancers3010841</idno><date when="2011">2011</date><idno type="wicri:Area/Pmc/Corpus">004936</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">004936</idno><idno type="wicri:Area/Pmc/Curation">004935</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">004935</idno><idno type="wicri:Area/Pmc/Checkpoint">002F50</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">002F50</idno><idno type="wicri:Area/Ncbi/Merge">005F13</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Growth Factor Mediated Signaling in Pancreatic Pathogenesis</title><author><name sortKey="Nandy, Debashis" sort="Nandy, Debashis" uniqKey="Nandy D" first="Debashis" last="Nandy">Debashis Nandy</name></author><author><name sortKey="Mukhopadhyay, Debabrata" sort="Mukhopadhyay, Debabrata" uniqKey="Mukhopadhyay D" first="Debabrata" last="Mukhopadhyay">Debabrata Mukhopadhyay</name></author></analytic><series><title level="j">Cancers</title><idno type="eISSN">2072-6694</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Functionally, the pancreas consists of two types of tissues: exocrine and endocrine. Exocrine pancreatic disorders mainly involve acute and chronic pancreatitis. Acute pancreatitis typically is benign, while chronic pancreatitis is considered a risk factor for developing pancreatic cancer. Pancreatic carcinoma is the fourth leading cause of cancer related deaths worldwide. Most pancreatic cancers develop in the exocrine tissues. Endocrine pancreatic tumors are more uncommon, and typically are less aggressive than exocrine tumors. However, the endocrine pancreatic disorder, diabetes, is a dominant cause of morbidity and mortality. Importantly, different growth factors and their receptors play critical roles in pancreatic pathogenesis. Hence, an improved understanding of how various growth factors affect pancreatitis and pancreatic carcinoma is necessary to determine appropriate treatment. This chapter describes the role of different growth factors such as vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF), platelet derived growth factor (PDGF), fibroblast growth factor (FGF), epidermal growth factor (EGF), and transforming growth factor (TGF) in various pancreatic pathophysiologies. Finally, the crosstalk between different growth factor axes and their respective signaling mechanisms, which are involved in pancreatitis and pancreatic carcinoma, are also discussed.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Suckale, J" uniqKey="Suckale J">J. Suckale</name></author><author><name sortKey="Solimena, M" uniqKey="Solimena M">M. Solimena</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Le Bras, S" uniqKey="Le Bras S">S. Le Bras</name></author><author><name sortKey="Miralles, F" uniqKey="Miralles F">F. 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<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>Molecular Diversity Preservation International (MDPI)</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">24212642</article-id><article-id pub-id-type="pmc">3756392</article-id><article-id pub-id-type="doi">10.3390/cancers3010841</article-id><article-id pub-id-type="publisher-id">cancers-03-00841</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Growth Factor Mediated Signaling in Pancreatic Pathogenesis</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Nandy</surname><given-names>Debashis</given-names></name></contrib><contrib contrib-type="author"><name><surname>Mukhopadhyay</surname><given-names>Debabrata</given-names></name><xref ref-type="corresp" rid="c1-cancers-03-00841"><sup>*</sup></xref></contrib><aff id="af1-cancers-03-00841">Department of Biochemistry and Molecular Biology, College of Medicine, Mayo Clinic, 200 First Street SW, Guggenheim 1321C, Rochester, MN 55905, USA; E-Mail:<email>nandy.debashis@mayo.edu</email></aff></contrib-group><author-notes><corresp id="c1-cancers-03-00841"><label>*</label> Author to whom correspondence should be addressed; E-Mail: <email>mukhopadhyay.debabrata@mayo.edu</email>; Tel.: +1-507-538-3581; Fax: +1-507-284-1767.</corresp></author-notes><pub-date pub-type="collection"><month>3</month><year>2011</year></pub-date><pub-date pub-type="epub"><day>24</day><month>2</month><year>2011</year></pub-date><volume>3</volume><issue>1</issue><fpage>841</fpage><lpage>871</lpage><history><date date-type="received"><day>26</day><month>1</month><year>2011</year></date><date date-type="rev-recd"><day>12</day><month>2</month><year>2011</year></date><date date-type="accepted"><day>16</day><month>2</month><year>2011</year></date></history><permissions><copyright-statement>© 2011 by the authors; licensee MDPI, Basel, Switzerland.</copyright-statement><copyright-year>2011</copyright-year><license><license-p><pmc-comment>CREATIVE COMMONS</pmc-comment>This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/3.0/">http://creativecommons.org/licenses/by/3.0/</ext-link>).</license-p></license></permissions><abstract><p>Functionally, the pancreas consists of two types of tissues: exocrine and endocrine. Exocrine pancreatic disorders mainly involve acute and chronic pancreatitis. Acute pancreatitis typically is benign, while chronic pancreatitis is considered a risk factor for developing pancreatic cancer. Pancreatic carcinoma is the fourth leading cause of cancer related deaths worldwide. Most pancreatic cancers develop in the exocrine tissues. Endocrine pancreatic tumors are more uncommon, and typically are less aggressive than exocrine tumors. However, the endocrine pancreatic disorder, diabetes, is a dominant cause of morbidity and mortality. Importantly, different growth factors and their receptors play critical roles in pancreatic pathogenesis. Hence, an improved understanding of how various growth factors affect pancreatitis and pancreatic carcinoma is necessary to determine appropriate treatment. This chapter describes the role of different growth factors such as vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF), platelet derived growth factor (PDGF), fibroblast growth factor (FGF), epidermal growth factor (EGF), and transforming growth factor (TGF) in various pancreatic pathophysiologies. Finally, the crosstalk between different growth factor axes and their respective signaling mechanisms, which are involved in pancreatitis and pancreatic carcinoma, are also discussed.</p></abstract><kwd-group><kwd>growth factors</kwd><kwd>signaling</kwd><kwd>pancreatitis</kwd><kwd>pancreatic carcinoma</kwd></kwd-group></article-meta></front><floats-group><fig id="f1-cancers-03-00841" position="float"><label>Figure 1.</label><caption><p>The pancreas is developed from fusion of ventral and dorsal bud.</p></caption><graphic xlink:href="cancers-03-00841f1"></graphic></fig><fig id="f2-cancers-03-00841" position="float"><label>Figure 2.</label><caption><p>VEGF signaling in pancreatic cancer. Binding of ligands with VEGFRs stimulates malignant transformation of the pancreas. EC = endothelial cell.</p></caption><graphic xlink:href="cancers-03-00841f2"></graphic></fig><fig id="f3-cancers-03-00841" position="float"><label>Figure 3.</label><caption><p>Variable expression of VEGF and VEGFRs in normal pancreas, pancreatitis and pancreatic carcinoma.</p></caption><graphic xlink:href="cancers-03-00841f3"></graphic></fig><fig id="f4-cancers-03-00841" position="float"><label>Figure 4.</label><caption><p>The role of IGF-1 in promoting a strong desmoplastic reaction leading to pancreatitis and, thus, promoting pancreatic carcinoma.</p></caption><graphic xlink:href="cancers-03-00841f4"></graphic></fig><fig id="f5-cancers-03-00841" position="float"><label>Figure 5.</label><caption><p>Role of PDGF in formation of pancreatitis, pancreatic carcinoma and progression of cancer.</p></caption><graphic xlink:href="cancers-03-00841f5"></graphic></fig><fig id="f6-cancers-03-00841" position="float"><label>Figure 6.</label><caption><p>FGF-dependent regulation in transformation from pancreatitis to pancreatic intraepithelial neoplasia to invasive cancer.</p></caption><graphic xlink:href="cancers-03-00841f6"></graphic></fig><fig id="f7-cancers-03-00841" position="float"><label>Figure 7.</label><caption><p>Role of EGF and EGFRs family members in pancreatic diseases.</p></caption><graphic xlink:href="cancers-03-00841f7"></graphic></fig><fig id="f8-cancers-03-00841" position="float"><label>Figure 8.</label><caption><p>TGF-β-mediated upregulation of desmoplasia in pancreatitis and pancreatic carcinoma development.</p></caption><graphic xlink:href="cancers-03-00841f8"></graphic></fig><fig id="f9-cancers-03-00841" position="float"><label>Figure 9.</label><caption><p>Major growth factor-dependent exocrine pancreatic diseases</p></caption><graphic xlink:href="cancers-03-00841f9"></graphic></fig><table-wrap id="t1-cancers-03-00841" position="float"><label>Table 1.</label><caption><p>Histological classification of exocrine pancreatic epithelial tumors [<xref ref-type="bibr" rid="b143-cancers-03-00841">143</xref>].</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left" valign="middle" rowspan="1" colspan="1"><bold>Benign</bold></th><th align="left" valign="middle" rowspan="1" colspan="1"><bold>Borderline (Uncertain Malignant Potential)</bold></th><th align="left" valign="middle" rowspan="1" colspan="1"><bold>Malignant</bold></th></tr></thead><tbody><tr><td align="left" valign="top" rowspan="1" colspan="1"><list list-type="bullet"><list-item><p>Serous cystadenoma</p></list-item><list-item><p>Mucinous cystadenoma</p></list-item><list-item><p>Intraductal papillary-mucinous adenoma</p></list-item><list-item><p>Mature teratoma</p></list-item></list></td><td align="left" valign="top" rowspan="1" colspan="1"><list list-type="bullet"><list-item><p>Mucinous cystic tumor with moderate dysplasia</p></list-item><list-item><p>Intraductal papillary-mucinous tumor with moderate dysplasia</p></list-item><list-item><p>Solid-pseudopapillary tumor</p></list-item></list></td><td align="left" valign="top" rowspan="1" colspan="1"><list list-type="bullet"><list-item><p>Severe ductal dysplasia-carcinoma in situ</p></list-item><list-item><p>Ductal adenocarcinoma</p></list-item><list-item><p>Mucinous noncystic carcinoma</p></list-item><list-item><p>Signet-ring-cell carcinoma</p></list-item><list-item><p>Adenosquamous carcinoma</p></list-item><list-item><p>Undifferentiated (anaplastic) carcinoma</p></list-item><list-item><p>Mixed ductal endocrine carcinoma</p></list-item><list-item><p>Osteoclast-like giant-cell tumor</p></list-item><list-item><p>Serous cyst adenocarcinoma</p></list-item><list-item><p>Mucinous cyst adenocarcinoma</p></list-item><list-item><p>Noninvasive</p></list-item><list-item><p>Invasive</p></list-item><list-item><p>Intraductal papillary-mucinous carcinoma</p></list-item><list-item><p>Noninvasive</p></list-item><list-item><p>Invasive (papillary-mucinous carcinoma)</p></list-item><list-item><p>Acinar cell carcinoma</p></list-item><list-item><p>Acinar-cell cystadenocarcinoma</p></list-item><list-item><p>Mixed acinar- endocrine carcinoma</p></list-item><list-item><p>Pancreatoblastoma</p></list-item><list-item><p>Solid pseudopapillary carcinoma</p></list-item><list-item><p>Miscellaneous carcinomas</p></list-item></list></td></tr></tbody></table></table-wrap><table-wrap id="t2-cancers-03-00841" position="float"><label>Table 2.</label><caption><p>Variability of growth factor expression in pancreatitis <italic>versus</italic> pancreatic carcinoma.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left" valign="top" rowspan="1" colspan="1"><bold>Growth Factors</bold></th><th align="left" valign="top" rowspan="1" colspan="1"><bold>Pancreatitis</bold></th><th align="left" valign="top" rowspan="1" colspan="1"><bold>Pancreatic Carcinoma</bold></th></tr></thead><tbody><tr><td align="left" valign="top" rowspan="1" colspan="1">FGF</td><td align="left" valign="top" rowspan="1" colspan="1">↑FGF, ↑FGF BP</td><td align="left" valign="top" rowspan="1" colspan="1">↑FGF, ↑FGF protein</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">EGF</td><td align="left" valign="top" rowspan="1" colspan="1">↑EGFR, ↑TGFα, ↑PLCγ 1, ↑cerB2, ↑c-erB3</td><td align="left" valign="top" rowspan="1" colspan="1">↑EGFR</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">TGF</td><td align="left" valign="top" rowspan="1" colspan="1">↑TGF</td><td align="left" valign="top" rowspan="1" colspan="1">↑TGF, ↑↑TβRII</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">VEGF</td><td align="left" valign="top" rowspan="1" colspan="1">No VEGFR expression</td><td align="left" valign="top" rowspan="1" colspan="1">↑VEGFR, ↑t-VEGF, ↑plasma VEGF</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">PDGF</td><td align="left" valign="top" rowspan="1" colspan="1">PDGF needed for early fibrogenesis</td><td align="left" valign="top" rowspan="1" colspan="1">PDGF overexpression related to migration and invasion(<italic>in vitro</italic>)</td></tr><tr><td align="left" valign="top" rowspan="1" colspan="1">IGF</td><td align="left" valign="top" rowspan="1" colspan="1">Participate in tissue regeneration</td><td align="left" valign="top" rowspan="1" colspan="1">↑IGF1R in patholgical tumor progression</td></tr></tbody></table></table-wrap></floats-group></pmc><affiliations><list></list><tree><noCountry><name sortKey="Mukhopadhyay, Debabrata" sort="Mukhopadhyay, Debabrata" uniqKey="Mukhopadhyay D" first="Debabrata" last="Mukhopadhyay">Debabrata Mukhopadhyay</name><name sortKey="Nandy, Debashis" sort="Nandy, Debashis" uniqKey="Nandy D" first="Debashis" last="Nandy">Debashis Nandy</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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