Quantitative Analysis of BRCA1 and BRCA2 mRNA Expression in Sporadic Breast Carcinomas and Its Relationship with Clinicopathological Characteristics

BRCA1 and BRCA2 mRNA expression in sporadic breast cancers was quantified by a real‐time reverse transcriptase‐polymerase chain reaction (RT‐PCR), and the relationship of their expression with various Clinicopathological factors was studied. BRCA2 mRNA levels (0.993±1.395, mean±SD (BRCA2/β‐glucuroni...

Full description

Saved in:
Bibliographic Details
Published inCancer science Vol. 92; no. 6; pp. 624 - 630
Main Authors Egawa, Chiyomi, Miyoshi, Yasuo, Taguchi, Tetsuya, Tamaki, Yasuhiro, Noguchi, Shinzaburo
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.06.2001
Japanese Cancer Association
John Wiley & Sons, Inc
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:BRCA1 and BRCA2 mRNA expression in sporadic breast cancers was quantified by a real‐time reverse transcriptase‐polymerase chain reaction (RT‐PCR), and the relationship of their expression with various Clinicopathological factors was studied. BRCA2 mRNA levels (0.993±1.395, mean±SD (BRCA2/β‐glucuronidase mRNA ratios)) were significantly (P<0.01) higher than BRCA1 mRNA levels (0.519±0.570 (BRCAl/p‐glucuronidase mRNA ratios)), and a weak but significant (r=0.390, P<0.01) correlation was observed between BRCA1 and BRCA2 mRNA expression levels. There was no significant association between BRCA1 mRNA expression and Clinicopathological factors such as menstrual status, tumor size, lymph node status, estrogen and progesterone receptor status, and histological grade. On the other hand, there was a significant association between higher BRCA2 mRNA expression and estrogen receptor (ER) negativity (P<0.01) or progesterone receptor (PR) negativity (P<0.01) or high histological grade (P<0.01). These results suggest a differential contribution of BRCA1 and BRCA2 in the pathogenesis of sporadic breast cancers. BRCA2 mRNA is speculated to be up‐regulated in response to proliferation and genomic instability in high histological grade tumors.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ObjectType-Article-1
ObjectType-Feature-2
ISSN:0910-5050
1347-9032
1349-7006
1876-4673
DOI:10.1111/j.1349-7006.2001.tb01140.x