DETECTION OF CHROMOSOMAL-ABERRATIONS IN TUMOR-CELLS AND TUMOR-INFILTRATING LYMPHOCYTES BY MOLECULAR CYTOGENETICS IN PATIENTS WITH GYNECOLOGICAL CANCER

Citation
H. Engel et al., DETECTION OF CHROMOSOMAL-ABERRATIONS IN TUMOR-CELLS AND TUMOR-INFILTRATING LYMPHOCYTES BY MOLECULAR CYTOGENETICS IN PATIENTS WITH GYNECOLOGICAL CANCER, Cancer genetics and cytogenetics, 106(2), 1998, pp. 159-165
Citations number
25
Categorie Soggetti
Oncology,"Genetics & Heredity
ISSN journal
01654608
Volume
106
Issue
2
Year of publication
1998
Pages
159 - 165
Database
ISI
SICI code
0165-4608(1998)106:2<159:DOCITA>2.0.ZU;2-2
Abstract
Conventional cytogenetic studies of tumor cells from patients with bre ast or ovarian cancer have shown multiple chromosomal abnormalities in cluding chromosomes 7, 12, and 17. This study was designed to analyze the cytogenetic features of tumor cells and tumor infiltrating lymphoc ytes (TILs) by using a combination of magnetic activated cell sorting (MACS) and fluorescence in situ hybridization (FISH). Tumor cell, peri pheral blood (PB), and TIL samples from 37 patients (20 ovarian tumors , 13 breast cancers, 3 uterine sarcoma, 1 carcinoma of the filamentary tube) were analyzed for the presence of numerical aberrations of chro mosomes 7 12, and 17. All of the tumor cells showed a high frequency o f numerical aberrations of chromosomes 7, 12, and 17 especially trisom ies or tetrasomies. There was no statistically significant difference in the incidence of chromosomal abnormalities in tumor tissue and effu sions, or between primary and relapsed disease in patients with breast or ovarian tumors. However, tumor cells from patients with solid meta static disease had significantly higher numbers of aberrations of chro mosome 7 in the primary tumor than in tumors from patients without met astases (P = 0.049), suggesting that chromosome 7 is frequently involv ed in the progression of disease. Monosomies and trisomies of chromoso mes 7 and 12 also occurred at a low percentage of TILs without any sta tistically significant difference between primary and relapsed tumors. The presence of these aneuploidies might be responsible for treatment failures in the immunotherapy of gynecological cancer. (C) Elsevier S cience Inc., 1998.