B-cell leukemia Bcr-Abl1
Skin tumors ErbB2
Lung hyperplasias Fgf7
T-cell lymphomas, AML Myc
T-cell lymphomas Myc
Melanomas Hrasv12G + Cdkn2a
Lung adenocarcinomas KrasG12D + Cdkn2a~'~ or KrasG12D + Trp53~'~
*Combinations with conventional tumor suppressor gene knockouts (for example, Cdkn2a~f~ or Trp53~/~) are included. Apc, adenomatous polyposis coli; Bcr-Abl1, breakpoint cluster region Abelson 1; Brcal, breast cancer gene 1; Brca2, breast cancer gene 2; Cdk4, cyclin-dependent kinase 4; Cdkn2a, cyclin-dependent kinase inhibitor 2a (which encodes the Ink4a and Arf tumor suppressors); ErbB2, avian erythroblastic leukemia viral oncogene homologue 2 (which encodes an epidermal growth factor receptor homologue); Fgf7, fibroblast growth factor 7; Hras, Harvey rat sarcoma viral oncogene homologue; Kras, Kirsten rat sarcoma viral oncogene homologue; Myc, avian myelocytomatosis viral oncogene homologue; Nf 2, neuro-fibromatosis type 2; Fdgf, platelet-derived growth factor; Fyv-mT, polyomavirus middle T antigen; Rb, retinoblastoma; SV40 TAg, simian virus 40 large T antigen; Trp53, transformation-related protein 53; Vhl, Von Hippel-Landau. (From Jonkers and Berns,92 reprinted by permission from Macmillan Publishers Ltd.)
systems, regulatable oncogene expression, and retroviral gene transfer in transgenic mice that express an avian retroviral receptor (reviewed in Reference 92). These models provide for the induction of somatic mutations in tissue-specific and time-sequenced way. These models more closely mimic human cancer development, which involves the activation of oncogenes and inacti-vation of tumor suppressor genes over time. They enable investigators to determine the contribution that individual mutations make to the various stages of tumor development. These models also provide a way to validate various targets for anticancer drug development.
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