{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T00:47:52Z","timestamp":1791161272593,"version":"4.1.0"},"reference-count":25,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2011,4,18]],"date-time":"2011-04-18T00:00:00Z","timestamp":1303084800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["BioEssays"],"published-print":{"date-parts":[[2011,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>According to the somatic mutation theory (SMT), cancer begins with a genetic change in a single cell that passes it on to its progeny, thereby generating a clone of malignant cells. It is strongly supported by observations of leukemias that bear specific chromosome translocations, such as Burkitt's lymphoma, in which a translocation activates the <jats:italic>c\u2010myc<\/jats:italic> gene, and chronic myeloid leukemia (CML), in which the Philadelphia chromosome causes production of the BCR\u2010ABL oncoprotein. Although the SMT has been modified and extended to encompass tumor suppressor genes, epigenetic inheritance, and tumor progression through accumulation of further mutations, perhaps the strongest validation comes from the successful treatment of certain malignancies with drugs that directly target the product of the mutant gene.<\/jats:p><jats:p><jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/jpeg\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/mgra001.jpg\"><jats:alt-text>magnified image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text><\/jats:p><jats:p><jats:bold>David Vaux<\/jats:bold> is at the Walter and Eliza Hall Institute and La Trobe Institute for Molecular Science, Melbourne, Australia<\/jats:p>","DOI":"10.1002\/bies.201100022","type":"journal-article","created":{"date-parts":[[2011,4,18]],"date-time":"2011-04-18T16:08:29Z","timestamp":1303142909000},"page":"341-343","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":74,"title":["In defense of the somatic mutation theory of cancer"],"prefix":"10.1002","volume":"33","author":[{"given":"David L.","family":"Vaux","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2011,4,18]]},"reference":[{"key":"e_1_2_4_2_2","first-page":"64","volume-title":"Zur Frage der Entstehung maligner Tumoren","author":"Boveri 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