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Biomedical subjects

M Yadav

Publications and source records attributed to M Yadav.

93 records · Page 6Linked to original sources

Non-random primary and secondary chromosomal abnormalities in human gastric cancers.

By using Giemsa-banding and fluorescence in situ hybridization techniques, we have been able to identify primary and secondary cytogenetic abnormalities in four gastric tumors at different stages of development. Structural and numerical abnormalities were present in all four gastric tumors in chromosomes 3, 7, 11, and X. Other abnormalities involving chromosomes 1, 5, 6, 8, 13, 15, 17, 18, 19 and 22 were observed, but only in three advanced gastric tumors, suggesting that these were secondary/tertiary genetic defects. Based on these results it was possible for us to decipher primary and secondary genetic abnormalities in these four gastric tumors.

Biopsy↗

Paclitaxel and water-soluble poly (L-glutamic acid)-paclitaxel, induce direct chromosomal abnormalities and cell death in a murine metastatic melanoma cell line.

The purpose of this study was to demonstrate the effects of paclitaxel and water-soluble poly (L-glutamic acid)-paclitaxel (PG-TXL), on chromosome morphology, telomeric associations, and induction of cell death in a murine melanoma cell line (K-1735 clone X-21). Murine melanoma cells were treated with various concentrations (0.1 microgram, 1.0 microgram, 4.0 micrograms, and 8.0 micrograms/ml) of paclitaxel alone, PG alone, or PG-TXL for 2 hr and 4 hr and harvested immediately without recovery. We found that: (1) the frequency of metaphases with telomeric associations increased, (2) metaphases had clumped and distorted chromosome morphology, (3) cells accumulated in metaphase (mitotic arrest), and (4) cell death had been induced. Cells treated with PG-TXL showed more such abnormalities than did cells treated with either paclitaxel or PG alone. Our preliminary results indicate that PG-TXL may be superior to paclitaxel alone in inducing cytotoxic effects, and these effects could be mediated by various chromosomal abnormalities in cancer cells.

Animals↗

Immunohistochemical analysis of p53 expression in primary breast carcinomas.

Expression of p53 protein was investigated by immunohistochemical techniques in archival cases of 134 primary breast carcinomas comprising 13 comedo ductal carcinoma in situ (DCIS), 105 invasive ductal carcinomas, 7 contained the comedo DCIS component adjacent to the invasive ductal component, 5 invasive lobular carcinomas, three colloid carcinomas and one medullary carcinoma. Overexpression of p53 gene product was studied to determine the association with clinico-pathological parameters and also its relationship to c-erbB2. Overexpression of p53 protein was observed in 31% (4/13) of comedo DCIS, 37% (39/105) of invasive ductal carcinomas, 57% (4/7) of carcinomas containing both the in situ and invasive lesions and all medullary carcinomas. A significant relationship (p < 0.05) was observed between strong immunoreactivity of p53 protein and absence of estrogen receptor, histological grade and c-erbB2 but not with lymph node metastases or age of patient. These observations suggest that overexpression of p53 protein may play an important role in tumor progression from noninvasive to invasive in some breast carcinomas and may have potential as an indicator for poorer prognosis.

Adult↗