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A novel retrovirus provides the cooperating oncogenic event(s) required to demonstrate the tumor suppressor activity of p15(Ink4b) in myeloid cells in vivo

  1. Author:
    Wolff, L.
    Garin, M. T.
    Koller, R.
    Bies, J.
    Tessarollo, L.
    Anver, M. R.
    Powell, D.
    Perella, C.

  2. Author Address

    Wolff, L, NCI, Ctr Canc Res, NIH, Bldg 37,Room 4124,37 Convent Dr,MSC4255, Bethesda, MD 20892 USA NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. NCI, SAIC Frederick, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, Data Management Serv, Frederick, MD 21702 USA.
    1. Year: 2004
    2. Date: JAN-FEB
  2. Journal: Blood Cells Molecules and Diseases
    1. 32
    2. 1
    3. Pages: 226-231
  4. Type of Article: Article
  1. Abstract:

    Cancer is a multistep process resulting from an accumulation of several genetic changes. The determination of cooperating events in experimental models can help scientists decipher specific neoplastic pathways and place genes with similar functions in complementation groups. In leukemia models, retrovirus tagging is a powerful approach to determine genes that cooperate with oncogenic transgenes or tumor suppressors that have undergone targeted deletion. Experimental models for B and T cell leukemias involving transgenic c-myc were the first to show the utility of retroviral tagging. Here we review these experiments and present examples of new models of myeloid leukemia where retroviruses have collaborated with a transgene [Cbfbeta-MYH111 from Inv(16)] and with loss of a tumor suppressor (Ink4b) mice to induce disease. (C) 2003 Elsevier Inc. All rights reserved

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