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Biomedical subjects

Z Gibas

Publications and source records attributed to Z Gibas.

At least 37 records · Page 2Linked to original sources
PubMed1988

Clonal chromosome rearrangements in a uterine myoma.

A cytogenetic study of a myoma of uterus with extensive hyaline, myxoid, and cystic degeneration revealed a clonal karyotype with a complex structural rearrangement involving chromosomes #3, #12, #14, #17, and #22. The modal chromosome number of the tumor was 45 due to monosomy #22. Analysis of seven additional myomas of the uterus including five tumors with typical histology and two with degenerative changes showed no clonal abnormalities. Single metaphases with a trisomy and a translocation were detected in two tumors. We conclude that although many uterine myomas appear to have normal karyotypes, clonal chromosome abnormalities are present in some of these tumors.

Adult↗
PubMed1987

Chromosome changes associated with spontaneous phenotypic variation of transplantable melanoma.

The chromosome constitutions of black-melanotic (Ma), brown-melanotic (MI), and amelanotic (Ab) melanomas of the Syrian hamster were compared. The MI and Ab melanomas arose through a spontaneous phenotypic alteration of the Ma tumor. All three variants differ in their growth rates, with MI showing the slowest, Ab the fastest, and Ma intermediate growth rate. Cytogenetic examination revealed that each tumor line shows a distinct karyotype. The Ma tumor is near-diploid, whereas, Ab and MI tumors are hypertriploid and near-tetraploid, respectively. Each tumor line shows a unique set of marker chromosomes, though some markers are shared by two different tumor lines. No single marker chromosome was common for all three melanoma variants. We conclude that the spontaneous phenotypic variation of transplantable hamster melanomas is associated with profound changes in the chromosome constitution of the neoplastic cells. The general direction of these changes is toward increased ploidy and increased complexity of the structural abnormalities.

Animals↗
PubMed1986

Translocation (13;22) in a hemangiopericytoma.

Cytogenetic studies on primary hemangiopericytoma tumor cells from a 28 year old woman showed a single karyotypic change: t(13;22)(q22;q11). The relationship of this aberration to previously described abnormalities of chromosome #22 in other solid tumors is discussed.

Adult↗
PubMed1986

Chromosome changes in malignant mesothelioma.

Cytogenetic study was made of mesothelioma cells from 14 patients. Metaphases were obtained from 12 tumors and revealed aneuploidy and clonal abnormalities in 9 specimens. In the two remaining cases, no metaphases were obtained. The cytogenetic abnormalities were complex, and up to 12 marker chromosomes were observed in the tumors. Rearrangements of chromosomes #1, #2, #3, #6, #9, #11, #17, and #22 were most frequently observed. Chromosome markers involved diverse bands, including several that are loci of oncogenes, fragile sites, and nonrandom rearrangements in other types of cancer. This study shows that the karyotypes of malignant mesothelioma can be analyzed by standard cytogenetic techniques. Additional studies of untreated mesothelioma may help to distinguish primary cytogenetic changes from effects of prior therapy in some of our patients.

Adult↗
PubMed1986

A possible specific chromosome change in transitional cell carcinoma of the bladder.

Chromosome changes were ascertained in nine tumor samples from seven untreated patients with transitional cell carcinoma of the urinary bladder. All tumors analyzed showed abnormal karyotypes. In one tumor, a single numerical abnormality (+7) was the sole detectable change. From 1 to 19 structurally abnormal chromosomes could be identified in the remaining 8 tumors. The same abnormality, an isochromosome of the short arm of chromosome #5, was found in five tumors from four patients. We have previously described the presence of this marker chromosome in three of nine cases of transitional cell carcinoma of the bladder. We therefore conclude that i(5p) constitutes the most consistent nonrandom chromosome abnormality in this malignancy. Other chromosomes most frequently involved in structural changes in the present series of tumors were chromosomes #1, #6, #11, and #13.

Aged↗
PubMed1986

Chromosome changes in germ cell tumors of the testis.

Chromosome analysis was performed on short-term cultures established from samples of six tumors of the testis. Histologically, four tumors were embryonal cell carcinomas (three primary, one metastatic) and two of mixed histology with predominance of teratoma. The modal chromosome number was hypotriploid in four tumors, triploid in one, and hypertriploid in another. All tumors contained structurally abnormal chromosomes, ranging in number from 1 to 10 in different cases. A small metacentric marker chromosome, identified as an isochromosome of the short arm of chromosome #12 [i(12p)], was present in all tumors analyzed. Unlike other marker chromosomes, this one was invariably present in at least two copies per metaphase in all cases; all other chromosome markers were present in single copy in all tumors. Together with the previous reports on the presence of i(12p) in seminoma and teratoma of the testis, our findings suggest that this karyotypic abnormality is characteristic for all histologic varieties of germ cell tumors of the testis.

Adult↗
PubMed1986

Rearrangement of chromosome 3 in renal cell carcinoma.

Rearrangements involving chromosome #3 were detected in 8 of 12 nonfamilial renal cell carcinomas. These results suggest that rearrangement of chromosome #3 is associated with the genesis and progression of a subclass of human renal cell carcinoma.

Adult↗
PubMed1986

Methodologic advances in the cytogenetic analysis of human solid tumors.

The major obstacle to successful cytogenetic analysis of human solid tumors is the acquisition of sufficient numbers of good quality metaphases for detailed cytogenetic analysis. At present, no single methodologic approach has been proven to provide successful chromosomal analysis of all human solid tumors. The technical aspects of cell culture, chromosome harvesting, and chromosome banding were the focus of considerable discussion during the First Workshop on Chromosomes in Solid Tumors. This report provides summaries of several technical protocols, emanating from several different laboratories, which have contributed to successful chromosome analysis of a variety of human solid tumors.

Cell Separation↗
PubMed1986

Chromosome abnormalities in two benign adipose tumors.

Two histologically benign adipose tumors were found to have clonal karyotypic changes. Del(4), del(6), and inv(13) were present in a fibrolipoma, and t(7;8) in a lipoblastoma. Additional studies are needed of the frequency and malignant potential of lipomas with cytogenetic abnormalities.

Child, Preschool↗
PubMed1986

Cytogenetic findings in a malignant melanoma and its derived cell line.

A cell line, MEL #26, was established from a metastatic solid tumor specimen obtained from a patient with malignant melanoma. Cytogenetic analyses were performed on both the fresh biopsy specimen (using short-term culture; 2 days) and an established cell line at three different passages. The chromosome number of the fresh biopsy specimen was in the near-triploid range and the chromosome number of the cell line was tetraploid. Three stable marker chromosomes involving #1, #6, and #7 were observed both in the original tumor and cell line. The marker chromosomes involving #1 and #7 were consistently present in all passages of this line, whereas, i(6p) was not present in every metaphase; a 15p+ marker completely disappeared after passage 20. Based on the results of the present study, we conclude that exclusive of one marker chromosome, the nonrandom chromosome changes seen in the original tumor were retained by the cell line and no particular additional clonal changes occurred during in vitro growth and establishment of this cell line. These considerations are of importance in the interpretation of results of various other studies that have been (or could be) performed with this cell line.

Cell Line↗
PubMed1986

Use of radiation induced chromosomal damage in human lymphocytes as a biological dosimeter is questionable.

Using dicentric chromosomes and acentric fragments as indicators of radiation sensitivity, a study has been performed on human lymphocyte chromosomes by irradiating peripheral blood cells at G0. Donor-to-donor variation has been noticed regarding radiation sensitivity even when metaphase spreads were scored at the first cell cycle. Thus, it appears that, at the present state, use of chromosomal damage in peripheral blood cell cultures as an effective biological dosimeter for effects of radiation is questionable.

Biological Assay↗
PubMed1986

Cytogenetic studies of tumor tissue from patients with nonfamilial renal cell carcinoma.

A method combining an enzymatic technique and short term culture was applied to 27 tumor tissues from 22 patients with nonfamilial renal cell carcinoma in order to establish the chromosome changes in these tumors. Chromosome analyses were successfully carried out in quinacrine mustard-Hoechst 33258 and G-banded preparations of 14 tumors from 12 patients, including 2 cases in which established cell lines were obtained after 43 and 64 days in culture and maintained for 25 and 30 passages in an in vitro system, respectively. The modal chromosome numbers ranged from 38-46 in 11 samples, involving chromosomes in structural and numerical changes and 72 chromosomes in one case, with the remaining 2 samples showing a variety of chromosome numbers. Banding analysis revealed 45 clonal aberrations in 11 tumor samples from 10 patients and nonclonal aberrations in the remaining 3 samples from 2 of the patients. Rearrangements of chromosome 3 were observed in 12 tumors, with the breakpoints on this chromosome almost totally clustered from p11 to p21. In one case both primary and metastatic tumors were studied, and an isochromosome for the long arm of chromosome 1 was observed as clonal in origin in the metastatic tissue. Two cases showed nonclonal changes. The remaining case had one clonal abnormality, i.e., deletion of 6q. Of the remaining 33 clones, chromosomes 1, 2, 6, 11, and 17 were frequently involved. These results suggest that renal cell carcinoma may be cytogenetically classified into 3 categories: (a) tumors with changes of chromosome 3: (b) tumors with other clonal aberrations; and (c) tumors without clonal changes. Rearrangements of chromosome 3 may be possibly associated with the genesis and/or progression of renal cell carcinoma.

Adult↗
PubMed1985

Chromosome rearrangements in a metastatic adenocarcinoma of the prostate.

Cytogenetic analysis of a metastatic tumor derived from an adenocarcinoma of the prostate revealed a hypodiploid karyotype with the presence of six marker chromosomes. The findings are discussed in relation to cytogenetic findings in other cancers, including those in prostatic cancer.

Adenocarcinoma↗
PubMed1985

Induction of superoxide dismutase, chromosomal aberrations and sister-chromatid exchanges by paraquat in Chinese hamster fibroblasts.

We have recently shown that Bloom syndrome fibroblasts have elevated levels of superoxide dismutase activity compared to those of normal fibroblasts. Based on this observation we decided to test whether an increased rate of superoxide radical production could be responsible for the induction of superoxide dismutase and of chromosomal aberrations and sister-chromatid exchanges characteristic of Bloom syndrome. Utilizing the superoxide-generating herbicide paraquat in Chinese hamster fibroblasts, we assayed the cells for dismutase activity, chromosomal aberrations and sister-chromatid exchanges. All 3 parameters investigated demonstrated a dose-dependent increase with paraquat and, consequently, with the superoxide produced. Since the induction of the enzyme is mediated by its substrate, the superoxide anion radical, we concluded that the increased dismutase activity (in Bloom syndrome and paraquat-treated cells) may be a secondary manifestation of an overall imbalance in oxygen metabolism and that this elevated enzymatic activity is insufficient to detoxify the high superoxide levels, which results in elevated levels of chromosomal damage.

Animals↗
PubMed1985

Cytogenic analysis of transplantable mouse B16 melanomas.

The cytogenetic analysis of transplantable in vivo melanotic and amelanotic lines of mouse B16 melanoma was performed. The second line arose by spontaneous alteration of the first one and these lines are the same in the rate of malignant growth during passages in vivo. The melanotic line shows stable near-diploid karyotype with modal chromosome number 41. The amelanotic line is mostly hypotetraploid karyotype with modal chromosome number 76. The balance of the diploids in the melanotic line is disturbed by the fact that chromosome 15 is partially trisomic, chromosome 6 trisomic, and chromosome 13 and X monosomic. Four marker chromosomes were common to both lines: M1-rob(12;12), M2-rob(5;15), M3-minute, M4-inv(1), M5-del-(14q-), but in the amelanotic line in most cases their number was doubled. Additionally, in the amelanotic line other specific aberrations rob(6;6) and rob(16;16) were observed. Both lines had comparable SCE frequencies. Constitutive heterochromatin in amelanotic line revealed the nonrandom deletion of the heterochromatic segments in chromosome 11 and, occasionally in chromosome 19.

Animals↗