Welcome to the new version of CaltechAUTHORS. Login is currently restricted to library staff. If you notice any issues, please email coda@library.caltech.edu
Published December 1, 1988 | Published
Journal Article Open

Transformation of an Interleukin 3-Dependent Hematopoietic Cell Line by the Chronic Myelogenous Leukemia-Specific P210bcr/abl Protein

Abstract

The P210bcr/abl protein is associated with virtually every case of human chronic myelogenous leukemia. Unlike the related P160gag/v-abl oncogene product of Abelson murine leukemia virus, P210bcr/abl does not transform NIH 3T3 fibroblasts. To assess whether P210bcr/abl might transform hematopoietic cell types, retroviral constructs encoding P210bcr/abl were used to infect the bone marrow-derived interleukin 3-dependent Ba/F3 cell line. As for P160gag/v-abl, cell lines expressing P210bcr/abl were growth factor independent and tumorigenic in nude mice. No evidence for autocrine production of interleukin 3 by factor-independent cell lines was found. These experiments establish that P210bcr/abl can transform hematopoietic cell types to tumorigenicity.

Additional Information

© 1988 by the National Academy of Sciences Contributed by David Baltimore, September 6, 1988 We thank David Schatz, Matiorie Oettinger, Stephen Smale, and Rick Van Etten for critical comments on the manuscript. This work was supported by a program project grant (CA38497) from the National Cancer Institute. G.Q.D. was supported by Public Health Service National Research Service Award 2T 32 GM07753-07 from the National Institute of General Medical Sciences. The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

Attached Files

Published - DALpnas88.pdf

Files

DALpnas88.pdf
Files (1.3 MB)
Name Size Download all
md5:15085d57d055203441a6143b651e9d4a
1.3 MB Preview Download

Additional details

Created:
August 22, 2023
Modified:
October 16, 2023