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Blood, 1 January 2002, Vol. 99, No. 1, pp. 372-374
BRIEF REPORT
Genomic structure of the PIK3CG gene on
chromosome band 7q22 and evaluation as a candidate myeloid tumor
suppressor
Christian P. Kratz,
Brooke
M. Emerling,
Jeannette Bonifas,
Winfred Wang,
Eric D. Green,
Michelle M. Le Beau, and
Kevin M. Shannon
From the Department of Pediatrics, University of
California, San Francisco; Department of Hematology/Oncology, St Jude
Children's Research Hospital, Memphis, TN; Genome Technology Branch,
National Human Genome Research Institute, Bethesda, MD; and Section of
Hematology/Oncology, Department of Medicine, and The Cancer Research
Center, University of Chicago, IL.
PIK3CG, which encodes the catalytic subunit
p110 of phosphoinositide 3-OH-kinase- (PI3K),
has been assigned to chromosome band 7q22, a region that is frequently
deleted in myeloid malignancies. PI3K-mutant mice have
hematologic defects and are predisposed to colon cancer. On the basis
of these data, PIK3CG was evaluated as a candidate myeloid
tumor suppressor gene (TSG). PIK3CG was mapped by
fluorescence in situ hybridization adjacent and telomeric to a commonly
deleted segment defined previously in myeloid leukemias with
breakpoints within 7q22. PIK3CG contains 10 exons and spans approximately 37 kilobases of genomic DNA. Forty leukemias with monosomy 7 or a del(7q) were screened for PIK3CG mutations.
Two patients had missense variations affecting residue 859 in the N-terminal catalytic domain of the protein. This allele was also detected in unaffected parents and in 1 of 60 control alleles; it
probably represents a polymorphism. PIK3CG is unlikely to
act as a recessive TSG in myeloid leukemias with monosomy 7.
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