Absence of p53 allows direct immortalization of hematopoietic cells by the myc and raf oncogenes

T Metz, AW Harris, JM Adams - Cell, 1995 - cell.com
T Metz, AW Harris, JM Adams
Cell, 1995cell.com
The~ 53 tumor suppressor is implicated here as a crucial barrier to unlimited cell
proliferation. Its role In transformation of hematopoietic cells was studied by infecting fetal
liver cells from wild-type or p53-'-mice with oncogenic retroviruses. Transformed colonies
arose with a raf and a myc-raf virus. Absence of~ 53 did not affect their frequency but proved
crltlcal for their continued propagation. Colonies of p53-'-cells bearing both myc and raf
readily yielded continuous cell lines without apparent requirement for genetic alteration. The …
Summary
The~ 53 tumor suppressor is implicated here as a crucial barrier to unlimited cell proliferation. Its role In transformation of hematopoietic cells was studied by infecting fetal liver cells from wild-type or p53-‘-mice with oncogenic retroviruses. Transformed colonies arose with a raf and a myc-raf virus. Absence of~ 53 did not affect their frequency but proved crltlcal for their continued propagation. Colonies of p53-‘-cells bearing both myc and raf readily yielded continuous cell lines without apparent requirement for genetic alteration. The lines, mainly of erythroid or myelomonocytic origin, were diploid but highly tumorlgenic from their inception. These findings imply that~ 53 losscontributes directly to immortalization and tumorlgenesls, probably by abrogating an intrinsic senescence program.
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