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Blood, 1 March 2001, Vol. 97, No. 5, pp. 1442-1450
NEOPLASIA
Interleukin 3 and granulocyte-macrophage colony-stimulating
factor are not required for induction of chronic myeloid leukemia-like
myeloproliferative disease in mice by BCR/ABL
Shaoguang Li,
Silke Gillessen,
Michael H. Tomasson,
Glenn Dranoff,
D. Gary Gilliland, and
Richard A. Van Etten
From The Center for Blood Research, Dana-Farber Cancer
Institute, and Harvard Institutes of Medicine and Howard Hughes Medical
Institute, Harvard Medical School, Boston, MA.
Primitive hematopoietic progenitors from some patients with
Philadelphia chromosome (Ph)-positive chronic myeloid leukemia (CML)
express aberrant transcripts for interleukin 3 (IL-3) and granulocyte
colony-stimulating factor (G-CSF), and exhibit autonomous proliferation
in serum-free cultures that is inhibited by anti-IL-3 and anti-IL-3
receptor antibodies. Expression of the product of the Ph chromosome,
the BCR/ABL oncogene, in mice by retroviral bone marrow
transduction and transplantation induces CML-like leukemia, and some
leukemic mice have increased circulating IL-3, and perhaps
granulocyte-macrophage colony-stimulating factor (GM-CSF). These
observations raise the possibility of autocrine or paracrine cytokine
production in the pathogenesis of human CML. Mice with homozygous
inactivation of the Il-3 gene, the Gm-csf gene,
or both, were used to test the requirement for these cytokines for induction of CML-like disease by BCR/ABL. Neither IL-3 nor
GM-CSF was required in donor, recipient, or both for induction of
CML-like leukemia by p210 BCR/ABL. Use of novel mice
deficient in both IL-3 and GM-CSF demonstrated that the lack of effect
on leukemogenesis was not due to redundancy between these hematopoietic
growth factors. Analysis of cytokine levels in leukemic mice where
either donor or recipient was Il-3 /
indicated that the increased IL-3 originated from the recipient, suggestive of a host reaction to the disease. These results demonstrate that IL-3 and GM-CSF are not required for BCR/ABL-induced
CML-like leukemia in mice and suggest that autocrine production of IL-3 does not play a role in established chronic phase CML in humans.
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