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1.
001-es BibID:
BIBFORM033277
035-os BibID:
PMID:9171998
Első szerző:
Balázs Margit (sejtbiológus, molekuláris genetikus)
Cím:
Frequent homozygous deletion of cyclin-dependent kinase inhibitor 2 (MTS1, p16) in superficial bladder cancer detected by fluorescence in situ hybridization / Margit Balázs, Peter Carroll, Russell Kerschmann, Guido Sauter, Frederic M. Waldman
Dátum:
1997
Megjegyzések:
Deletion of all or part of chromosome 9 is a well-described genetic alteration in bladder tumors. It has been proposed that inactivation of a tumor-suppressor gene on chromosome 9 is an important event in tumor development. Recent reports have supported cyclin-dependent kinase inhibitor 2 (CDKN2, also known as MTS1, INK4, p16) at 9p21 as a candidate tumor-suppressor gene in solid tumors. However, the prevalence of CDKN2 mutations in primary bladder tumors has been controversial. Therefore, we applied gene-specific probes for CDKN2 and the interferon alpha gene (IFNA), also located at 9p21, to characterize further the genomic deletions at this locus in bladder cancer. Seventeen superficial (pTa or pT1) bladder tumor specimens were examined for gene deletion by fluorescence in situ hybridization. Dual-labeling hybridization with a repetitive pericentromeric probe for chromosome 9 and a gene-specific probe for CDKN2 was performed to characterize the gene copy number in relation to the chromosome 9 copy number on a cell-by-cell basis. Homozygous deletion for CDKN2 without homozygous IFNA deletion was found in 5 of 17 tumors tested. Both genes were deleted in one additional case, and one tumor showed deletion of IFNA without deletion of CDKN2. Homozygous deletion at the 9p21 locus was found only in tumors having monosomy for the chromosome 9 centromeric signal. These results indicate that the homozygous deletion of the CDKN2 gene is a frequent and early event in superficial bladder cancer.
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Egészségtudományok
idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:
Genes, chromosomes & cancer. - 19 : 2 (1997), p. 84-89. -
További szerzők:
Carroll, Peter
Kerschmann, Russell
Sauter, Guido
Waldman, Frederick
Internet cím:
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:
2.
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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