Cancer genetics
Cancer is a genetic disease of somatic cells. Tumor karyotypes are rarely normal, and most show multiple abnormalities of both number and structure. The first direct evidence for this concept of cancer came from studies of tumor‐specific translocations in leukemias and lymphomas, revealing the impor...
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| Veröffentlicht in: | American journal of medical genetics 2002-07, Vol.111 (1), p.96-102 |
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| container_title | American journal of medical genetics |
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| creator | Knudson, Alfred G. |
| description | Cancer is a genetic disease of somatic cells. Tumor karyotypes are rarely normal, and most show multiple abnormalities of both number and structure. The first direct evidence for this concept of cancer came from studies of tumor‐specific translocations in leukemias and lymphomas, revealing the importance of oncogenes and the regulation of gene transcription in cancer. A second major source of information about human cancer genes is hereditary cancer. Genetic predisposition of the autosomal dominant type imposes a high relative risk for one or more kinds of cancer. In the past decade or so, more than 30 mutant genes for such hereditary cancers have been cloned. Penetrance depends upon additional, somatic, mutations. A few of the genes are oncogenes or DNA repair genes, but most are tumor suppressor genes. Some tumor suppressors regulate transcription, while others operate in signal transduction pathways that are involved in regulating processes of cell birth, differentiation, and death. The knowledge gained is stimulating new approaches to the treatment and prevention of cancer. © 2002 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/ajmg.10320 |
| format | Article |
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J. Med. Genet</addtitle><description>Cancer is a genetic disease of somatic cells. Tumor karyotypes are rarely normal, and most show multiple abnormalities of both number and structure. The first direct evidence for this concept of cancer came from studies of tumor‐specific translocations in leukemias and lymphomas, revealing the importance of oncogenes and the regulation of gene transcription in cancer. A second major source of information about human cancer genes is hereditary cancer. Genetic predisposition of the autosomal dominant type imposes a high relative risk for one or more kinds of cancer. In the past decade or so, more than 30 mutant genes for such hereditary cancers have been cloned. Penetrance depends upon additional, somatic, mutations. A few of the genes are oncogenes or DNA repair genes, but most are tumor suppressor genes. 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Genetic counseling</subject><subject>Genes, Tumor Suppressor</subject><subject>Genetic Predisposition to Disease</subject><subject>Humans</subject><subject>Male</subject><subject>Medical genetics</subject><subject>Medical sciences</subject><subject>Mutation</subject><subject>mutational equilibrium</subject><subject>Neoplasms - epidemiology</subject><subject>Neoplasms - genetics</subject><subject>Neoplastic Syndromes, Hereditary - genetics</subject><subject>Neurocutaneous Syndromes - genetics</subject><subject>Oncogenes</subject><subject>penetrance</subject><subject>phakomatoses</subject><subject>Retinoblastoma Protein - physiology</subject><subject>Selection, Genetic</subject><subject>signal transduction</subject><subject>somatic mutation</subject><subject>transcription factors</subject><subject>tumor suppressor genes</subject><subject>Tumor Suppressor Protein p53 - physiology</subject><issn>0148-7299</issn><issn>1096-8628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9j8FOwkAQhjdGI4jGxAcwXvRgUt2Z3e62RwKKEkQPJHrbbLdbUmwBdyHK21tslZunmUy-_598hJwBvQFK8VbPymm1MaR7pA00FkEkMNonbQo8CiTGcYsceT-jFKoDHpIWICCXnLfJaU_PjXUXUzu3q9z4Y3KQ6cLbk2Z2yOT-btJ7CEbPg8dedxQYHsY0AJtKSVO0oA1LWRyZNJOYSJsJJrI0pDpkEmmchCgihsgja0LOIJEMBALrkKu6dukWH2vrV6rMvbFFoed2sfZKQozAq2iHXNegcQvvnc3U0uWldhsFVG3t1dZe_dhX8HnTuk5Km-7QRrcCLhtAe6OLzFXyud9xTMZAJVYc1NxnXtjNPy9Vd_g0-H0e1Jncr-zXX0a7dyUkk6F6HQ-U6L-99OV4qCj7BgGzfOc</recordid><startdate>20020722</startdate><enddate>20020722</enddate><creator>Knudson, Alfred G.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><scope>BSCLL</scope><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>7X8</scope></search><sort><creationdate>20020722</creationdate><title>Cancer genetics</title><author>Knudson, Alfred G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4590-1ed770d2e1ac3d398cdf72b7ef636fd50a537209b526832248ec5431b7316213</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Biological and medical sciences</topic><topic>cell cycle</topic><topic>Cell Cycle - genetics</topic><topic>chromosomal translocation</topic><topic>Cloning, Molecular</topic><topic>DNA Repair - genetics</topic><topic>DNA repair genes</topic><topic>Female</topic><topic>General aspects. Genetic counseling</topic><topic>Genes, Tumor Suppressor</topic><topic>Genetic Predisposition to Disease</topic><topic>Humans</topic><topic>Male</topic><topic>Medical genetics</topic><topic>Medical sciences</topic><topic>Mutation</topic><topic>mutational equilibrium</topic><topic>Neoplasms - epidemiology</topic><topic>Neoplasms - genetics</topic><topic>Neoplastic Syndromes, Hereditary - genetics</topic><topic>Neurocutaneous Syndromes - genetics</topic><topic>Oncogenes</topic><topic>penetrance</topic><topic>phakomatoses</topic><topic>Retinoblastoma Protein - physiology</topic><topic>Selection, Genetic</topic><topic>signal transduction</topic><topic>somatic mutation</topic><topic>transcription factors</topic><topic>tumor suppressor genes</topic><topic>Tumor Suppressor Protein p53 - physiology</topic><toplevel>online_resources</toplevel><creatorcontrib>Knudson, Alfred G.</creatorcontrib><collection>Istex</collection><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>MEDLINE - Academic</collection><jtitle>American journal of medical genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Knudson, Alfred G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cancer genetics</atitle><jtitle>American journal of medical genetics</jtitle><addtitle>Am. 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A few of the genes are oncogenes or DNA repair genes, but most are tumor suppressor genes. Some tumor suppressors regulate transcription, while others operate in signal transduction pathways that are involved in regulating processes of cell birth, differentiation, and death. The knowledge gained is stimulating new approaches to the treatment and prevention of cancer. © 2002 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>12124744</pmid><doi>10.1002/ajmg.10320</doi><tpages>7</tpages></addata></record> |
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| subjects | Adolescent Adult apoptosis Apoptosis - genetics Biological and medical sciences cell cycle Cell Cycle - genetics chromosomal translocation Cloning, Molecular DNA Repair - genetics DNA repair genes Female General aspects. Genetic counseling Genes, Tumor Suppressor Genetic Predisposition to Disease Humans Male Medical genetics Medical sciences Mutation mutational equilibrium Neoplasms - epidemiology Neoplasms - genetics Neoplastic Syndromes, Hereditary - genetics Neurocutaneous Syndromes - genetics Oncogenes penetrance phakomatoses Retinoblastoma Protein - physiology Selection, Genetic signal transduction somatic mutation transcription factors tumor suppressor genes Tumor Suppressor Protein p53 - physiology |
| title | Cancer genetics |
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