PMID- 8909313
OWN - NLM
STAT- MEDLINE
DCOM- 19961205
LR  - 20190620
IS  - 0008-543X (Print)
IS  - 0008-543X (Linking)
VI  - 78
IP  - 9
DP  - 1996 Nov 1
TI  - Two distinct commonly deleted regions on chromosome 13q suggest involvement of 
      BRCA2 and retinoblastoma genes in sporadic breast carcinomas.
PG  - 1929-34
AB  - BACKGROUND: Frequent allelic losses on the long arm of chromosome 13 in sporadic 
      breast carcinomas suggest that a tumor suppressor gene(s) on 13q is involved in 
      this type of carcinoma. The presence of a familial breast carcinoma 
      susceptibility gene, BRCA2, and the retinoblastoma susceptibility gene (RB) on 
      the same chromosomal arm implies that one or the other, or both, of these genes 
      may be critically affected by those allelic losses. METHODS: To investigate the 
      possible involvement of BRCA2 and RB in sporadic breast carcinomas, the authors 
      examined allelic losses in 246 breast carcinomas with 14 polymorphic 
      microsatellite markers on 13q12.q14. RESULTS: Allelic loss was observed in 95 of 
      the 246 sporadic breast carcinomas (39%). Detailed deletion mapping identified 
      two commonly deleted regions. The more proximal of these two segments was located 
      in a 6-cM interval flanked by marker loci D13S289 and D13S267 and containing the 
      BRCA2 gene; the more distal region was located in a 9-cM interval flanked by 
      marker loci D13S328 and D13S172 and containing the RB gene. Allelic loss on 13q 
      was found more frequently in tumors of the solid tubular histologic type (36 of 
      66; 55%) than in other types (52 of 146; 36%) (P = 0.0096). Furthermore, a 
      significant association was observed between allelic loss on 13q and the absence 
      of progesterone receptor (P = 0.0001). CONCLUSIONS: The results indicate that 
      BRCA2 and RB are independent targets of allelic loss and that inactivation of 
      either of these genes may play a role in the development of some sporadic breast 
      carcinomas, particularly those of the solid tubular type.
FAU - Tsukamoto, K
AU  - Tsukamoto K
AD  - Department of Molecular Biology, Nippon Medical School, Kawasaki, Japan.
FAU - Ito, N
AU  - Ito N
FAU - Yoshimoto, M
AU  - Yoshimoto M
FAU - Iwase, T
AU  - Iwase T
FAU - Tada, T
AU  - Tada T
FAU - Kasumi, F
AU  - Kasumi F
FAU - Nakamura, Y
AU  - Nakamura Y
FAU - Emi, M
AU  - Emi M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cancer
JT  - Cancer
JID - 0374236
SB  - IM
MH  - Chromosome Mapping
MH  - Chromosomes, Human, Pair 13/*genetics
MH  - Female
MH  - *Gene Deletion
MH  - Genes, Retinoblastoma/*genetics
MH  - Genes, Tumor Suppressor/*genetics
MH  - Humans
EDAT- 1996/11/01 00:00
MHDA- 2000/06/20 09:00
CRDT- 1996/11/01 00:00
PHST- 1996/11/01 00:00 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1996/11/01 00:00 [entrez]
AID - 10.1002/(SICI)1097-0142(19961101)78:9<1929::AID-CNCR13>3.0.CO;2-# [pii]
AID - 10.1002/(sici)1097-0142(19961101)78:9<1929::aid-cncr13>3.0.co;2-# [doi]
PST - ppublish
SO  - Cancer. 1996 Nov 1;78(9):1929-34. doi: 
      10.1002/(sici)1097-0142(19961101)78:9<1929::aid-cncr13>3.0.co;2-#.