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001-es BibID:	BIBFORM033279
035-os BibID:	PMID:7600900 WOS:A1995QV46400009
Első szerző:	Balázs Margit (sejtbiológus, molekuláris genetikus)
Cím:	Karyotypic heterogeneity and its relation to labeling index in interphase breast tumor cells / Margit Balázs, Kouji Matsumura, Dan Moore, Daniel Pinkel, Joe W. Gray, Frederic M. Waldman
Dátum:	1995
Megjegyzések:	We have used fluorescence in situ hybridization (FISH) with chromosome-specific probes and immunofluorescent detection of in vivo bromodeoxyuridine (BrdUrd) incorporation to evaluate simultaneously numerical chromosome aberrations and proliferative activity of breast cancers. The number of distinct hybridization domains specific for repetitive pericentromeric sequences on chromosomes 1, 7, 11, 15, 17, and X was used as an indicator of copy number of these chromosomes in interphase tumor cells from 23 human breast cancers. Every tumor analyzed showed a heterogeneous distribution of copy number for at least one chromosome type. The copy number distribution for different chromosomes within a tumor frequently showed differing patterns. Major cell populations showing monosomy were relatively rare, occurring only in five cases for chromosome 17, once for chromosome 1, and once for chromosome 15. Flow cytometric analysis of DNA ploidy correlated well with FISH analysis, although flow cytometry failed to detect aneuploidy when only a few chromosomes were affected. To determine whether cell populations with different chromosomal copy numbers have identical proliferation characteristics in vivo, BrdUrd incorporation and centromeric copy number were detected simultaneously. Comparison of the chromosome copy number distribution in BrdUrd-positive cells vs. the distribution of the entire cell population showed different distributions in seven of the 20 cases analyzed. This study demonstrates the common occurrence of chromosome copy number heterogeneity and suggests that a cell phenotype (proliferation) may be associated with genotypic subpopulations.
Tárgyszavak:	Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban Breast neoplasms cell cycle nucleic acid hybridization brornodeoxyuridine chromosome aberration külföldön készült közlemény
Megjelenés:	Cytometry. - 20 : 1 (1995), p. 62-73. -
További szerzők:	Matsumura, Kouji Moore, Dan Pinkel, Daniel Gray, Joe W. Waldman, Frederick
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM033281
035-os BibID:	WOS:A1991FK18400070
Első szerző:	Chen, Ling-Chun
Cím:	Loss of heterozygosity on the short arm of chromosome 17 is associated with high proliferative capacity and DNA aneuploidy in primary human breast cancer / Ling-Chun Chen, Andreas Neubauer, Wayne Kurisu, Frederic M. Waldman, Britt-Marie Ljung, William Goodson, Eric S. Goldman, Dan Moore, Margit Balázs, Edison Liu, Brian H. Mayall, Helene S. Smith
Dátum:	1991
Megjegyzések:	Loss of heterozygosity (LOH) on the short arm of chromosome 17 (17p) was found in 27 of 52 (52%) previously untreated primary breast cancers. There was a significant correlation between this 17p allelic loss and two parameters associated with aggressive tumor behavior: high cellular proliferative fraction and DNA aneuploidy. These correlations with high cellular proliferative fraction and DNA aneuploidy were not found in tumors with LOH at nine other chromosome locations. The p53 gene, a putative tumor suppressor gene located at 17p13, was examined for aberrations to determine whether it is the target for the 17p LOH in breast cancer. Unlike other types of human cancer, there were no homozygous deletions or rearrangements of the p53 gene, and only 2 of 13 (15%) were mutated in the conserved region where mutational "hot spots" have been previously located. Therefore, we hypothesize that, in breast cancer, either loss or inactivation of gene(s) on chromosome 17p other than the p53 gene or a different mechanism of p53 gene inactivation may be responsible for the observed high labeling index and DNA aneuploidy associated with LOH at 17p.
Tárgyszavak:	Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban külföldön készült közlemény
Megjelenés:	Proceedings of the National Academy of Sciences of the United States of America. - 88 : 9 (1991), p. 3847-3851. -
További szerzők:	Neubauer, Andreas Kurisu, Wayne Waldman, Frederick Ljung, Britt-Marie Goodson, William Goldman, Eric S. Moore, Dan Balázs Margit (1952-) (sejtbiológus, molekuláris genetikus) Liu, Edison Mayall, Brian H. Smith, Helene S.
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM033275
035-os BibID:	WOS:000075481800016 PMID:9721860
Első szerző:	Hovey, Regina M.
Cím:	Genetic alterations in primary bladder cancers and their metastases / Regina M. Hovey, Lisa Chu, Margit Balazs, Sandy DeVries, Dan Moore, Guido Sauter, Peter R. Carroll, Frederic M. Waldman
Dátum:	1998
Megjegyzések:	Bladder cancer progression is thought to be associated with sequential genetic events. To search for the specific genetic changes associated with the metastatic process, comparative genomic hybridization was performed on 22 primary tumors and 24 metastases (10 distant and 14 nodal metastases) from 17 patients with stage pT2-4 bladder cancer. There was a striking similarity between the genetic alterations present in the primary and metastatic tumor samples from the same patient. The mean number of genetic changes/tumor was 12.2 for primary tumors and 11.7 for metastases. There was a strong concordance in the specific aberrations present in each patient's primary and metastatic lesions (mean, 75%). Concordance was also high among multiple sites from an individual primary tumor (mean, 96%) and multiple metastases from the same patient (mean, 75%). There were no specific genetic changes overrepresented in the metastases compared with their primary tumors. Genetic alterations present in more than 40% of tumors included gains on 6p, 8q, 10q, and 17q and losses involving 8p, 10q, and Y. Two regions of high-level amplification were common: (a) 10q22.1-q23.1 (32.6%); and (b) 17q11-21.3 (23.9%; the locus of erbB-2). A summary statistic was developed to quantitate the degree of clonal relationships between biopsies from the same patient. These data support a model in which minimal clonal evolution occurs in the metastatic tumor cell population after the metastatic event. When comparing primary cancers from patients with and without metastases, however, several unique genetic changes were identified in those cancers with metastases, suggesting that these loci may harbor genes important to the metastatic process.
Tárgyszavak:	Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban külföldön készült közlemény
Megjelenés:	Cancer Research. - 58 : 16 (1998), p. 3555-3560. -
További szerzők:	Chu, Lisa DeVries, Sandy Moore, Dan Sauter, Guido Carroll, Peter Waldman, Frederick Balázs Margit (1952-) (sejtbiológus, molekuláris genetikus)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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