Biomedical subjects

V V Murty

Publications and source records attributed to V V Murty.

76 records · Page 5Linked to original sources

PubMed1985

Spontaneous chromosomal aberrations in patients with precancerous and cancerous lesions of the cervix uteri.

Chromosomal aberrations were studied in metaphases from peripheral blood cultures of 52 women with cancer of the cervix uteri, 89 cases of various grades of cervical precancerous lesions, and 47 age-matched normal (control) women. The frequency of metaphases with chromosome and chromatid aberrations was 17.24% in cancer patients, 10.41% in those with precancerous lesions, and 6.39% in control women. There was a significant (p less than 0.001) increase in the frequency of chromosome aberrations in patients with cervical precancerous and cancerous lesions, compared with controls. After the exclusion of the treated cases, cancer patients also revealed a highly significant (p less than 0.001) increase in the frequency of chromosome aberrations, compared with controls. The results of the present study indicate the existence of chromosomal instability in the majority of cervical cancer patients and in some cases of precancerous lesions. The increased frequency of spontaneous chromosome aberrations in patients with precancerous lesions may be of importance for the understanding of their biological behavior.

Adult↗

PubMed1985

Friend murine leukemia virus-immortalized myeloid cells are converted into tumorigenic cell lines by Abelson leukemia virus.

Friend murine leukemia virus (Fr-MuLV) is a replication-competent murine retrovirus that induces acute nonlymphocytic leukemias in NFS/n mice. Fr-MuLV disease is divided into two stages based on the ability of the leukemia cells to grow in culture and transplant into syngeneic mice. Hematopoietic cells taken from the early stage of disease after Fr-MuLV infection grow as immortal myeloid cell lines in the presence of WEHI-3 cell-conditioned medium (CM) or interleukin 3. These growth factor-dependent cell lines do not grow in culture in the absence of CM and do not form tumors in syngeneic animals. If these Fr-MuLV-infected cells are superinfected with Abelson murine leukemia virus (Ab-MuLV), they lose their dependence on WEHI-3 CM and proliferate in culture in the absence of exogenous growth factors. Concomitant with the loss of growth factor dependence in culture, the Ab-MuLV-infected cell lines become tumorigenic in syngeneic mice. This secondary level of transformation is Ab-MuLV specific. Fr-MuLV-immortalized myeloid cell lines superinfected with Harvey murine sarcoma virus (Ha-MuSV) or amphotropic virus remain dependent on WEHI-3 CM for growth in vitro and are not tumorigenic in vivo. Neither Ab-MuLV- nor Ha-MuSV-infected normal mouse myeloid cell cultures produce growth factor-independent or tumorigenic cell lines. We conclude that at least two genetic events are needed to convert a murine myeloid precursor into a tumorigenic cell line. The first event occurs in Fr-MuLV-infected mice, generating cells that are growth factor dependent but immortal in vitro. The second event, which can be accomplished by Ab-MuLV infection, converts these immortal myeloid precursors into growth factor-independent and tumorigenic cells.

Abelson murine leukemia virus↗

PubMed1983

Double-minute chromosomes in the leukocytes of a patient with a previous history of cervical carcinoma.

Double-minute chromosomes (DMs) were observed in repeated samples in the leukocytes of a patient with a previous history of cervical carcinoma. The most interesting cytogenetic finding was the coexistence of DMs and a dicentric chromosome along with chromosome- and chromatid-type breaks and gaps. This observation suggests that DMs might originate through the breakage of existing chromosomes. The presence of DMs in leukocytes may also indicate the possibility that certain common agents cause DMs in tumor cells as well as in normal cells.

Chromosome Aberrations↗

PubMed1982

Sister chromatid exchanges in leukocytes of patients with cancer of cervix uteri.

The frequency of sister chromatid exchange (SCE) was investigated in 13 women with cervical cancer together with 11 control women. The SCE frequencies were found to be 10.05 +/- 2.35 and 6.95 +/- 1.53 in cancer cases and controls, respectively. The SCE values of cancer cases deviate significantly from that of controls. The SCE in chromosome groups E, F, and G was found to be more in comparison to controls (P less than 0.001). This preliminary study indicates the possibility of using SCE as a preclinical marker.

Carcinoma↗