Chromosome 3p and breast cancer.
Solid tumors in humans are now believed to develop through a multistep process that activates oncogenes and inactivates tumor suppressor genes. Loss of heterozygosity at chromosomes 3p25, 3p22-24, 3p21.3, 3p21.2-21.3, 3p14.2, 3p14.3, and 3p12 has been reported in breast cancers. Retinoid acid receptor beta2 (3p24), thyroid hormone receptor beta1 (3p24.3), Ras association domain family 1A (3p21.3), and the fragile histidine triad gene (3p14.2) have been considered as tumor suppressor genes (TSGs) for breast cancers. Epigenetic change may play an important role for the inactivation of these TSGs. Screens for promoter hypermethylation may be able to identify other TSGs in chromosome 3p. Alternatively, use of an "epigenetic modifier" may enhance the response to another type of agent for breast cancer.
Second Department of Pathology, Wakayama Medical University School of Medicine, 811-1 Kimiidera, Wakayama 641-8509, Japan. yang-qf@mail.wakayama-med.ac.jp
Qifeng
Q
Yang
Goro
G
Yoshimura
Ichiro
I
Mori
Takeo
T
Sakurai
Kennichi
K
Kakudo
D001943:Breast Neoplasms / Q000235:genetics* / Q000473:pathology; D002893:Chromosomes, Human, Pair 3 / Q000235:genetics*; D019175:DNA Methylation; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D020868:Gene Silencing; D016147:Genes, Tumor Suppressor; D006801:Humans; D019656:Loss of Heterozygosity; D009857:Oncogenes; D011401:Promoter Regions, Genetic