Abstract:
:The frequent loss of the INK4a/ARF locus, encoding for both p16(INK4a)and p19(ARF)in human melanoma, raises the question as to which INK4a/ARF gene product functions to suppress melanoma-genesis in vivo. Studies in the mouse have shown that activated RAS mutation can cooperate with INK4a(Delta 2/3)deficiency (null for both p16(INK4a)and p19(ARF)) to promote development of melanoma, and these melanomas retain wild-type p53. Given the functional link between p19(ARF)and p53, we have now shown that activated RAS can also cooperate with p53 deficiency to produce melanoma in the mouse. Moreover, genome-wide analysis of RAS-induced p53 mutant melanomas reveals alterations of key components governing RB-regulated G1/S transition, such as c-Myc. These experimental findings suggest that both RB and p53 pathways function to suppress melanocyte transformation in vivo in the mouse.
journal_name
Semin Cancer Bioljournal_title
Seminars in cancer biologyauthors
Yang FC,Merlino G,Chin Ldoi
10.1006/scbi.2000.0376keywords:
subject
Has Abstractpub_date
2001-06-01 00:00:00pages
261-8issue
3eissn
1044-579Xissn
1096-3650pii
S1044579X00903766journal_volume
11pub_type
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journal_title:Seminars in cancer biology
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journal_title:Seminars in cancer biology
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