Impact of p16 expression on surgical management of malignant melanoma and pancreatic carcinoma
Background: Recent advances in molecular oncology have provided explanations at the DNA level for the malignant transformation and metastatic potential of various cancers. Malignant melanoma and pancreatic cancer may be classified together in both these cancers exhibit mutations in, or loss of, the...
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description | Background: Recent advances in molecular oncology have provided explanations at the DNA level for the malignant transformation and metastatic potential of various cancers. Malignant melanoma and pancreatic cancer may be classified together in both these cancers exhibit mutations in, or loss of, the cell-cycle inhibitory gene,
p16. This paper reviews the current literature on
p16 expression in melanoma and pancreatic cancer, explores factors that place patients with these cancers in categories of high risk for metastases or recurrence, and addresses whether aberrant gene expressions should influence awareness of and current recommendations for the management of these aggressive cancers.
Methods: A computerized literature search was performed utilizing OVID Technology’s Medline database from 1993 to 1998.
Results: Both familial as well as sporadic cases of malignant melanoma and pancreatic carcinoma are reported in the literature. Although a low percentage of cases of either malignancy have
p16 mutations, a higher risk of their development has been reported to occur in certain families with
p16 germline mutations.
Conclusions: The increased risk determined in these families may serve to heighten awareness of the influence of positive family history of these cancers in the evaluation of patients. |
doi_str_mv | 10.1016/S0002-9610(98)00297-9 |
format | Article |
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p16. This paper reviews the current literature on
p16 expression in melanoma and pancreatic cancer, explores factors that place patients with these cancers in categories of high risk for metastases or recurrence, and addresses whether aberrant gene expressions should influence awareness of and current recommendations for the management of these aggressive cancers.
Methods: A computerized literature search was performed utilizing OVID Technology’s Medline database from 1993 to 1998.
Results: Both familial as well as sporadic cases of malignant melanoma and pancreatic carcinoma are reported in the literature. Although a low percentage of cases of either malignancy have
p16 mutations, a higher risk of their development has been reported to occur in certain families with
p16 germline mutations.
Conclusions: The increased risk determined in these families may serve to heighten awareness of the influence of positive family history of these cancers in the evaluation of patients.</description><identifier>ISSN: 0002-9610</identifier><identifier>EISSN: 1879-1883</identifier><identifier>DOI: 10.1016/S0002-9610(98)00297-9</identifier><identifier>PMID: 10037301</identifier><identifier>CODEN: AJSUAB</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Biological and medical sciences ; Cancer ; Cell cycle ; Cell growth ; Cyclin-Dependent Kinase Inhibitor p16 - genetics ; Cyclin-dependent kinases ; Deoxyribonucleic acid ; DNA ; Family medical history ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression Regulation, Neoplastic - physiology ; Genes ; Genetic engineering ; Genetic Predisposition to Disease - genetics ; Genetic testing ; Genetics ; Germ-Line Mutation - genetics ; Humans ; Kinases ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Malignancy ; Medical sciences ; Melanoma ; Melanoma - genetics ; Metastases ; Metastasis ; Mutation ; Mutation - genetics ; Pancreatic cancer ; Pancreatic carcinoma ; Pancreatic Neoplasms - genetics ; Polymorphism ; Prognosis ; Proteins ; Risk ; Signal transduction ; Skin cancer ; Skin Neoplasms - genetics ; Tomography ; Tumors</subject><ispartof>The American journal of surgery, 1999, Vol.177 (1), p.15-18</ispartof><rights>1999 Excerpta Medica Inc.</rights><rights>1999 INIST-CNRS</rights><rights>1999. Excerpta Medica Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c418t-45dcdfa357278b36a3b50bce26937f425aa03db0a329b27ea1a04307422437393</citedby><cites>FETCH-LOGICAL-c418t-45dcdfa357278b36a3b50bce26937f425aa03db0a329b27ea1a04307422437393</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0002961098002979$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,4010,27900,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1690039$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10037301$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bullock, Gloria J</creatorcontrib><creatorcontrib>Green, Judith L</creatorcontrib><creatorcontrib>Baron, Paul L</creatorcontrib><title>Impact of p16 expression on surgical management of malignant melanoma and pancreatic carcinoma</title><title>The American journal of surgery</title><addtitle>Am J Surg</addtitle><description>Background: Recent advances in molecular oncology have provided explanations at the DNA level for the malignant transformation and metastatic potential of various cancers. Malignant melanoma and pancreatic cancer may be classified together in both these cancers exhibit mutations in, or loss of, the cell-cycle inhibitory gene,
p16. This paper reviews the current literature on
p16 expression in melanoma and pancreatic cancer, explores factors that place patients with these cancers in categories of high risk for metastases or recurrence, and addresses whether aberrant gene expressions should influence awareness of and current recommendations for the management of these aggressive cancers.
Methods: A computerized literature search was performed utilizing OVID Technology’s Medline database from 1993 to 1998.
Results: Both familial as well as sporadic cases of malignant melanoma and pancreatic carcinoma are reported in the literature. Although a low percentage of cases of either malignancy have
p16 mutations, a higher risk of their development has been reported to occur in certain families with
p16 germline mutations.
Conclusions: The increased risk determined in these families may serve to heighten awareness of the influence of positive family history of these cancers in the evaluation of patients.</description><subject>Biological and medical sciences</subject><subject>Cancer</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - genetics</subject><subject>Cyclin-dependent kinases</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Family medical history</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression Regulation, Neoplastic - physiology</subject><subject>Genes</subject><subject>Genetic engineering</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genetic testing</subject><subject>Genetics</subject><subject>Germ-Line Mutation - genetics</subject><subject>Humans</subject><subject>Kinases</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Malignancy</subject><subject>Medical sciences</subject><subject>Melanoma</subject><subject>Melanoma - genetics</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mutation</subject><subject>Mutation - genetics</subject><subject>Pancreatic cancer</subject><subject>Pancreatic carcinoma</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Polymorphism</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Risk</subject><subject>Signal transduction</subject><subject>Skin cancer</subject><subject>Skin Neoplasms - genetics</subject><subject>Tomography</subject><subject>Tumors</subject><issn>0002-9610</issn><issn>1879-1883</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkE2L1TAUhoMozp3Rn6AUFNFFNV9tktUgw6gDAy7UreE0Pb1kaNKatKL_3vTei4obIZAc8uTlzUPIE0ZfM8raN58opbw2LaMvjX5VzkbV5h7ZMa1MzbQW98nuN3JGznO-KyNjUjwkZ4xSoQRlO_L1Jszglmoaqpm1Ff6YE-bsp1iVlde09w7GKkCEPQaMBzDA6PcRyhBwhDgFqCD21QzRJYTFu8pBcn67eEQeDDBmfHzaL8iXd9efrz7Utx_f31y9va2dZHqpZdO7fgDRKK50J1oQXUM7h7w1Qg2SNwBU9B0FwU3HFQIDKgVVknNZPmLEBXlxzJ3T9G3FvNjgs8Ox1MNpzbY1jWkY0wV89g94N60plm6Wa6lkQ5mihWqOlEtTzgkHOycfIP20jNpNvz3ot5tba7Q96Ldbjaen9LUL2P_16ui7AM9PAOQidkjFmc9_uNYUcsu5PGJYnH33mGx2HqPD3id0i-0n_58mvwAxNZ_a</recordid><startdate>1999</startdate><enddate>1999</enddate><creator>Bullock, Gloria J</creator><creator>Green, Judith L</creator><creator>Baron, Paul L</creator><general>Elsevier Inc</general><general>Elsevier</general><general>Elsevier Limited</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>1999</creationdate><title>Impact of p16 expression on surgical management of malignant melanoma and pancreatic carcinoma</title><author>Bullock, Gloria J ; Green, Judith L ; Baron, Paul L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c418t-45dcdfa357278b36a3b50bce26937f425aa03db0a329b27ea1a04307422437393</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Biological and medical sciences</topic><topic>Cancer</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - genetics</topic><topic>Cyclin-dependent kinases</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Family medical history</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Expression Regulation, Neoplastic - physiology</topic><topic>Genes</topic><topic>Genetic engineering</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Genetic testing</topic><topic>Genetics</topic><topic>Germ-Line Mutation - genetics</topic><topic>Humans</topic><topic>Kinases</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Malignancy</topic><topic>Medical sciences</topic><topic>Melanoma</topic><topic>Melanoma - genetics</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mutation</topic><topic>Mutation - genetics</topic><topic>Pancreatic cancer</topic><topic>Pancreatic carcinoma</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Polymorphism</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>Risk</topic><topic>Signal transduction</topic><topic>Skin cancer</topic><topic>Skin Neoplasms - genetics</topic><topic>Tomography</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bullock, Gloria J</creatorcontrib><creatorcontrib>Green, Judith L</creatorcontrib><creatorcontrib>Baron, Paul L</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Biotechnology Research Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>The American journal of surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bullock, Gloria J</au><au>Green, Judith L</au><au>Baron, Paul L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impact of p16 expression on surgical management of malignant melanoma and pancreatic carcinoma</atitle><jtitle>The American journal of surgery</jtitle><addtitle>Am J Surg</addtitle><date>1999</date><risdate>1999</risdate><volume>177</volume><issue>1</issue><spage>15</spage><epage>18</epage><pages>15-18</pages><issn>0002-9610</issn><eissn>1879-1883</eissn><coden>AJSUAB</coden><abstract>Background: Recent advances in molecular oncology have provided explanations at the DNA level for the malignant transformation and metastatic potential of various cancers. Malignant melanoma and pancreatic cancer may be classified together in both these cancers exhibit mutations in, or loss of, the cell-cycle inhibitory gene,
p16. This paper reviews the current literature on
p16 expression in melanoma and pancreatic cancer, explores factors that place patients with these cancers in categories of high risk for metastases or recurrence, and addresses whether aberrant gene expressions should influence awareness of and current recommendations for the management of these aggressive cancers.
Methods: A computerized literature search was performed utilizing OVID Technology’s Medline database from 1993 to 1998.
Results: Both familial as well as sporadic cases of malignant melanoma and pancreatic carcinoma are reported in the literature. Although a low percentage of cases of either malignancy have
p16 mutations, a higher risk of their development has been reported to occur in certain families with
p16 germline mutations.
Conclusions: The increased risk determined in these families may serve to heighten awareness of the influence of positive family history of these cancers in the evaluation of patients.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>10037301</pmid><doi>10.1016/S0002-9610(98)00297-9</doi><tpages>4</tpages></addata></record> |
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subjects | Biological and medical sciences Cancer Cell cycle Cell growth Cyclin-Dependent Kinase Inhibitor p16 - genetics Cyclin-dependent kinases Deoxyribonucleic acid DNA Family medical history Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Regulation, Neoplastic - physiology Genes Genetic engineering Genetic Predisposition to Disease - genetics Genetic testing Genetics Germ-Line Mutation - genetics Humans Kinases Liver. Biliary tract. Portal circulation. Exocrine pancreas Malignancy Medical sciences Melanoma Melanoma - genetics Metastases Metastasis Mutation Mutation - genetics Pancreatic cancer Pancreatic carcinoma Pancreatic Neoplasms - genetics Polymorphism Prognosis Proteins Risk Signal transduction Skin cancer Skin Neoplasms - genetics Tomography Tumors |
title | Impact of p16 expression on surgical management of malignant melanoma and pancreatic carcinoma |
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