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10.1038/ncomms15770

http://scihub22266oqcxt.onion/10.1038/ncomms15770
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C5472759!5472759!28593993
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suck abstract from ncbi


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pmid28593993      Nat+Commun 2017 ; 8 (ä): ä
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  • MYC activation cooperates with Vhl and Ink4a/Arf loss to induce clear cell renal cell carcinoma #MMPMID28593993
  • Bailey ST; Smith AM; Kardos J; Wobker SE; Wilson HL; Krishnan B; Saito R; Lee HJ; Zhang J; Eaton SC; Williams LA; Manocha U; Peters DJ; Pan X; Carroll TJ; Felsher DW; Walter V; Zhang Q; Parker JS; Yeh JJ; Moffitt RA; Leung JY; Kim WY
  • Nat Commun 2017[]; 8 (ä): ä PMID28593993show ga
  • Renal carcinoma is a common and aggressive malignancy whose histopathogenesis is incompletely understood and that is largely resistant to cytotoxic chemotherapy. We present two mouse models of kidney cancer that recapitulate the genomic alterations found in human papillary (pRCC) and clear cell RCC (ccRCC), the most common RCC subtypes. MYC activation results in highly penetrant pRCC tumours (MYC), while MYC activation, when combined with Vhl and Cdkn2a (Ink4a/Arf) deletion (VIM), produce kidney tumours that approximate human ccRCC. RNAseq of the mouse tumours demonstrate that MYC tumours resemble Type 2 pRCC, which are known to harbour MYC activation. Furthermore, VIM tumours more closely simulate human ccRCC. Based on their high penetrance, short latency, and histologic fidelity, these models of papillary and clear cell RCC should be significant contributions to the field of kidney cancer research.
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