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Biomedical subjects

Misa Nakamura

Publications and source records attributed to Misa Nakamura.

40 records · Page 3Linked to original sources
PubMedDate not supplied

Loss of Msh2 is not associated with FHIT deletion in breast carcinomas.

The FHIT gene is a candidate tumor suppressor gene that has been implicated in the development and progression of breast carcinoma. Recent studies have suggested that Fhit inactivation can be a consequence of defects in mismatch repair proteins, particularly Msh2. Fifty-three breast carcinomas were evaluated for Fhit and Msh2 expression by immunohistochemical staining. The same breast carcinomas were examined for allelic loss at three loci within or near FHIT by PCR-based microsatellite analysis. Seventeen of the 53 breast cancer cases were positive for Fhit protein, and 10 of the 43 informative cases showed FHIT loci deletion. Twenty-five of the 53 (47%) cases showed loss of Msh2 expression. No relationship between Msh2 protein loss and FHIT locus alteration or Fhit protein loss could be observed. Our results suggest that this mismatch repair protein may play little role in maintaining the integrity of the common fragile locus with the FHIT gene.

Acid Anhydride Hydrolases↗
PubMedDate not supplied

5-aza-2'-deoxycytidine induces retinoic acid receptor beta 2 demethylation, cell cycle arrest and growth inhibition in breast carcinoma cells.

Like all cancers, breast cancer is considered to result in part from the accumulation of multiple genetic alterations leading to oncogene overexpression and tumor suppressor loss. More recently, CpG island hypermethylation is known to be associated with gene silencing in cancer, and these silenced genes can be reactivated by 5-aza-2'-deoxycytidine (5-Aza-CdR). Retionoic acid receptor beta 2 gene is a tumor suppressor gene and the chemopreventive effects of retinoids are due to induction of RAR beta 2. In this study, the effect of 5-Aza-CdR RAR beta 2 restoration was investigated in the MRK-nu-1 human female breast cancer cell line. Changes of the RAR beta 2 methylation status were assessed by methylation-specific PCR. Reverse transcription PCR was used to evaluate RARb beta 2 restoration. Cell cycling and growth inhibition were studied using flow cytometric analysis of DNA content and CellTiter 96 AQueous non-radioactive cell proliferation assay, respectively. 5-Aza-CdR treatment resulted in complete demethylation of the RAR beta 2 gene. RAR beta 2 restoration was accompanied by cell cycle arrest (increase in the G0/G1- and decrease in the S- and G2/M-phases) and time-dependent growth inhibition. In conclusion, RAR beta 2 can be activated in vitro by 5-Aza-CdR, which may be one of the mechanisms for the tumor cell growth inhibition by 5-Aza-CdR.

Antimetabolites, Antineoplastic↗
PubMedDate not supplied

Correlation between BRCA1 expression and apoptosis-related biological parameters in sporadic breast carcinomas.

BRCA1 is a tumor suppressor gene that is responsible for hereditary breast and ovarian cancer syndrome. Increased evidence suggests that BRCA1 protein is involved in mammary carcinogenesis in sporadic and hereditary forms. Recent experimental results suggest that BRCA1 plays a role in the regulation of apoptosis. In order to test whether the analysis of human tumors would provide data supporting this hypothesis in sporadic breast carcinomas, we have investigated the relationship between BRCA1 and apoptosis-related genes. Immunohistochemical analysis was performed to determine BRCA1 and the apoptosis-related proteins bcl-2, Bax and p53 in paraffin-embedded tissues of 156 sporadic invasive ductal carcinomas. BRCA1 expression was positively-correlated with Bcl-2 expression (p = 0.0008), but no relationship between BRCA1 expression and Bax or p53 expression could be established. In addition, loss of BRCA1 expression was also related to poor tumor differentiation and lymph node metastasis. Our study shows that bcl-2 might be one of the target genes involved in the oncogenesis related to BRCA1. Loss of BRCA1 may contribute to tumor development in breast carcinomas, which may be independent of the p53 tumor suppressor.

Apoptosis↗