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Biomedical subjects

H E Pogosianz

Publications and source records attributed to H E Pogosianz.

14 recordsLinked to original sources
PubMed1989

Non-random karyotypic changes in Djungarian hamster tumors induced by 3-methylcholanthrene.

The karyotypes of 30 tumors (sarcomas and adenocarcinomas) induced with methylcholanthrene in Djungarian hamsters (Phodopus sungorus campbelli) have been investigated. In 23 tumors structural changes of the short arm of X-chromosome (Xp+ or Xp = type) were revealed. Non-random rearrangements of 3p, 7q and 8q were also observed. Other structural or numerical changes of the karyotype were accidential. For majority of tumors the presence of chromosome markers with long homogeneously staining regions or double minutes, structures are known as cytological manifestation of gene amplification, was typical. Induced tumors of the Djungarian hamster might serve as an interesting tool for studies of relationship of somatic cell genetic changes to different aspects of chemical carcinogenesis.

Adenocarcinoma↗
PubMed1986

Nonrandom chromosomal changes in retinoblastomas.

The analysis of the karyotype in 76 retinoblastomas (24 our cases and 52 described in the literature) has revealed nonrandom changes of Iq, 6p, 13, 16 and the sex chromosomes. Complete or partial trisomy Iq was observed in 44 out of 76 tumours. Tetra-or trisomy 6p was found in 35 and 6 cases respectively. Chromosome 13 monosomy or its long arm deletion was described in 11 tumours. Monosomy 16 and loss of the X or Y--in 18 and 12 cases. The specific feature of retinoblastoma karyotype is presence (along with two normal homologues of the pair 6) of the marker chromosome i (6p). Possible causes of unexpectedly rare abnormalities of chromosome 13 in retinoblastoma cells were discussed in the light of well known data on predisposing role of constitutional deletion 13q14, and recent molecular genetic studies showing the significance of recessive tumour genes in carcinogenesis. The cytological signs of gene amplification (HSRs, DMs) were revealed in few retinoblastomas. However, the recent data on N-myc gene amplification and its elevated expression in several retinoblastomas indicate that amplification of the oncogene(s) might be involved in the genesis of this tumour. Further studies are needed to understand the correlative role of specific chromosome rearrangements, gene(s) amplification and action of recessive rb gene, located at 13q14 in initiation and progression of retinoblastoma.

Child, Preschool↗
PubMed1983

An ovarian cancer family: clinical and cytogenetic data.

A family with five ovarian neoplasms in three subsequent generations was studied. Four women had ovarian cancer at age 38, 40, 47, and 53, and one had cystoma ovari at 24. There were other neoplasms and preneoplastic lesions in this family. Several developmental anomalies were revealed, and one of them (a tooth anomaly) may be associated with ovarian tumors. Cytogenetic studies have been carried out on six of the living relatives, including two treated for ovarian neoplasms. The incidence of spontaneous chromosome aberrations was not significantly increased in each of these cases. Polymorphism of constitutive heterochromatin regions was observed in all six individuals. The possible type of inheritance of the ovarian cancer, the significance of the tooth anomaly, and the constitutive heterochromatin polymorphism as cancer markers in this family are discussed.

Carcinoma↗
PubMed1982

Similar chromosomal abnormalities in several retinoblastomas.

The study of banded chromosomes of nine sporadic unilateral retinoblastomas revealed near diploid karyotypes with multiple numerical and (or) structural abnormalities in all tumors. An identical marker i(6p) was noted in cells of the modal class of six retinoblastomas. Extra copies of the short arm of chromosome 6 were observed in seven tumors: +i(6p) in 6 and +6q-in one. Less regular but repeated findings were a loss of one sex chromosome, and markers 1p+ and 17q+. The structure of these markers was not identical in different tumors. Abnormalities of chromosome 13 were not observed in tumor cells, nor in blood lymphocytes stimulated by PHA.

Aneuploidy↗
PubMed1981

Clastogenicity and sister chromatid exchange induction by ftorafur.

The main effect of Ftorafur at the chromosomal level is the induction of chromatid and chromosome breaks, which is some pronounced in neoplastic or transformed cells than in normal cells. Different cell lines used in the study exhibited both in vitro and in vivo varying sensitivity to Ftorafur. Ftorafur does not increase the frequency of SCE.

Animals↗
PubMed1980

Somatic cell hybrids of the Djungarian hamster: malignancy and evolution of the karyotype.

Djungarian hamster somatic cell hybrids were obtained by fusing malignant SV40-transformed fibroblasts (line DM15, HGPRT-), and normal male lymphoid cells. Tumorigenicity, growth in soft agar and karyotype changes of 10 independent hybrid clones were studied. All hybrids grew as tumors after injection of new-born hamsters with 1 x 10(6) cells. A total of 313 tumors occurred in 523 hamsters. The hybrids proliferated in soft agar as well. No correlation was noted between the ability of hybrids to grow in vivo and to form colonies in soft agar. The total chromosome number in hybrid cells was usually less than the expected sum of the parental chromosome sets. G-banding analysis showed that, in vitro, hybrids lost chromosomes of the normal parent, whereas marker chromosomes of the malignant parent were retained. In the majority of hybrid tumors the chromosome set was reduced to the diploid range. In tumors with a slightly reduced karyotype one or two homologues of chromosomes #4 and #8 were, as a rule, eliminated.

Animals↗
PubMed1975

Djungarian hamster-a suitable tool for cancer research and cytogenetic studies.

The Djungarian hamster, bred under usual laboratory conditions, developed different spontaneous neoplasms, most often mammary and skin cancers. Some mammary tumors were serially transplanted to noninbred animals. This hamster was susceptible to some chemical carcinogens and oncogenic viruses but resistant to others. It had comparatively few chromosomes (2n equal to 28), most of which could be recognized even in conventionally stained preparations. The chromosome-breaking effect of gamma-rays, chemical carcinogens, and viruses was studied with primary cultures of cells. Several transformed cell lines were developed. Karyotype abnormalities were generally not seen in primary and induced neoplasms. This hamster is a new suitable tool for cancer research and cytogenetic studies.

Animals↗