TY - JOUR
T1 - The BAX gene maps to the glioma candidate region at 19q13.3, but is not altered in human gliomas
AU - Chou, Dean
AU - Miyashita, Toshiyuki
AU - Mohrenweiser, Harvey W.
AU - Ueki, Keisuke
AU - Kastury, Kumar
AU - Druck, Teresa
AU - Von Deimling, Andreas
AU - Huebner, Kay
AU - Reed, John C.
AU - Louis, David N.
N1 - Funding Information:
This work was funded by NIH CA 57683, CA 60181, and CA 51083, and by grant #IRG-173F from the American Cancer Society. Work performed by the L,awrence Livermore National Laboratory is under the auspices of the U.S. Department of Energy, contract W-7405-Eng-48. D.C. was supported by a Howard Hughes Research Training Fellowship for Medical Students. J.C.R. is a Scholar of the Leukemia Society of America.
PY - 1996/6
Y1 - 1996/6
N2 - The bax protein regulates apoptosis in a cellular pathway that involves both bcl-2 and p53, two molecules associated with human glioma tumorigenesis. We therefore evaluated the possibility that BAX functions as a glioma tumor suppressor gene. Somatic cell hybrid panels, fluorescence in situ hybridization and cosmid mapping localized the BAX gene to 19q13.3, approximately 300 kb centromeric to HRC. Thus BAX maps to the region of chromosome 19 most frequently deleted in gliomas. Routine and pulsed-field gel electrophoresis/Southern blotting studies, however, failed to reveal large-scale deletions or rearrangements of the BAX gene in gliomas. In addition, single strand conformation polymorphism analysis of all six BAX exons and flanking intronic sequences did not disclose mutations in 20 gliomas with allelic loss of the other copy of 19q. A C/T polymorphism was detected in intron 3 and was common in the general population. Therefore, although BAX maps to the glioma candidate region on the long arm of chromosome 19, BAX is probably not the 19q glioma tumor suppressor gene.
AB - The bax protein regulates apoptosis in a cellular pathway that involves both bcl-2 and p53, two molecules associated with human glioma tumorigenesis. We therefore evaluated the possibility that BAX functions as a glioma tumor suppressor gene. Somatic cell hybrid panels, fluorescence in situ hybridization and cosmid mapping localized the BAX gene to 19q13.3, approximately 300 kb centromeric to HRC. Thus BAX maps to the region of chromosome 19 most frequently deleted in gliomas. Routine and pulsed-field gel electrophoresis/Southern blotting studies, however, failed to reveal large-scale deletions or rearrangements of the BAX gene in gliomas. In addition, single strand conformation polymorphism analysis of all six BAX exons and flanking intronic sequences did not disclose mutations in 20 gliomas with allelic loss of the other copy of 19q. A C/T polymorphism was detected in intron 3 and was common in the general population. Therefore, although BAX maps to the glioma candidate region on the long arm of chromosome 19, BAX is probably not the 19q glioma tumor suppressor gene.
UR - https://www.scopus.com/pages/publications/0029902618
U2 - 10.1016/0165-4608(95)00341-X
DO - 10.1016/0165-4608(95)00341-X
M3 - Article
C2 - 8640722
AN - SCOPUS:0029902618
SN - 0165-4608
VL - 88
SP - 136
EP - 140
JO - Cancer Genetics and Cytogenetics
JF - Cancer Genetics and Cytogenetics
IS - 2
ER -