Growth Suppression by Members of the Retinoblastoma Protein Family

  1. L. Zhu*,
  2. G.H. Enders*,,
  3. C.-L. Wu*,
  4. M.A. Starz,
  5. K.H. Moberg,
  6. J.A. Lees,
  7. N. Dyson*, and
  8. E. Harlow*
  1. *Massachusetts General Hospital Cancer Center, Charlestown, Massachusetts 02129; Gastrointestinal Unit, Massachusetts General Hospital, Boston, Massachusetts 02114; Center for Cancer Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139

This extract was created in the absence of an abstract.

Excerpt

Cellular changes induced by oncogenes of small DNA tumor viruses have provided unique insights into the mechanisms of cell transformation and growth regulation. Studies of adenovirus E1A, SV40 large T antigen, and E7 proteins of human papillomaviruses suggest that these viral oncoproteins use similar mechanisms to transform cells. An important feature of these oncoproteins is that they physically interact with key regulators of cellular proliferation. One such cellular target is the retinoblastoma protein (pRB). pRB is the product of the prototype tumor suppressor gene, which is mutated or deleted in all retinoblastomas and a wide variety of other tumors (for review, see Weinberg 1991, 1992). Overexpression of wild-type pRB in tumor cell lines that lack functional pRB causes a growth arrest in the G1 phase of the cell cycle in some cells and often reduces their tumorigenic potential (Huang et al. 1988; Bookstein et al. 1990; Goodrich et al. 1991;...

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