PubMed · 9111968
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R M Green, W J Fibison, M R Hughes. 1997. "Planned parenthood".. https://pubmed.ncbi.nlm.nih.gov/9111968/
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Gains of chromosome 7 and alterations of the 7q-arm have been frequently observed in multiple cancers using various cytogenetic and molecular genetic techniques. Using PCR analysis of microsatellite markers, we have previously reported that allelic imbalance of 7q31 is common in prostate cancer and is associated with higher tumor grade and advanced pathological stage. In an effort to better understand the chromosome 7 alterations in prostate cancer, we undertook a molecular cytogenetic study of 25 prostate specimens using fluorescence in situ hybridization (FISH) with DNA probes for the chromosome 7 centromere and for 5 loci mapped to 7q31 (D7S523, D7S486, D7S522, D7S480, and D7S490) and 1 locus at 7q11.23 (ELN). Six tumors had no apparent anomaly for any chromosome 7 probe. Nine tumors showed apparent simple gain of a whole chromosome 7, whereas one tumor had apparent simple loss of a whole chromosome 7. Four tumors had gain of the chromosome 7 centromere and additional overrepresentation of the 7q-arm. One tumor had overrepresentation of 7q31 without any apparent anomaly of the chromosome 7 centromere, and one tumor had apparent loss of the chromosome 7 centromere with no apparent anomaly of the 7q-arm. Three tumors had gain of the chromosome 7 centromere and loss of the 7q31 region. Gain of 7q31 was strongly correlated with tumor Gleason score. Multiplex PCR studies of these specimens supported these FISH observations. Mutation screening and DNA sequencing of the MET gene, which is mapped to 7q31, revealed only the presence of simple sequence polymorphisms but no apparent acquired disease-associated mutations. FISH analysis of metaphases from an aphidicolin-induced, chromosome 7 only, somatic cell hybrid demonstrated that the DNA probe for D7S522 spans the common fragile site FRA7G at 7q31. Our data indicate that the 7q-arm, particularly the 7q31 region, is genetically unstable in prostate cancer, and some of the gene dosage differences observed may be due to fragility at FRA7G.
Cytogenetic deletions of the short arm of chromosome 9, 9p, have been detected in cell lines of malignant mesothelioma as well as in tumor material. Many tumor types carry deletions of chromosome 9 or more specifically of 9p21. The tumor-suppressor genes, CDKN2A and CDKN2B, each of which encodes a structurally and functionally similar cyclin-dependent kinase inhibitor, were mapped to the commonly deleted region. The tumor-suppressive effect of these genes, or of CDKN2A alone, requires functional retinoblastoma protein, pRb. Malignant mesothelioma expresses pRb, which, together with the cytogenetic data, suggests the involvement of CDKN2A and/or CDKN2B in its tumorigenesis. We present data on the deletion status of chromosome 9 in malignant mesothelioma cell lines and tumor tissue. A deletion map of the 9p21.3-p23 region was constructed for 12 cell lines. Homozygous deletions of chromosomal regions containing CDKN2A were detected in all cell lines. The smallest region of overlap for deletion is approximately 24 kb, and does not include CDKN2B. The frequency of deletion of the centromeric region of chromosome 9 was compared with that of chromosomes 1, 6, and 10 by genomic in situ hybridization. Deletion of the centromere of chromosome 9 is the predominant event at a frequency of 73 +/- 3%. Our data show that deletions of a critical region of chromosome 9, including the CDKN2A but not the CDKN2B locus, are common among malignant mesothelioma. Such deletions may be involved in tumorigenesis of mesothelium.
The chromosomal origins and in some cases the molecular composition of 26 autosomal supernumerary marker chromosomes (SMC) were identified using combined fluorescence in situ hybridization (FISH) and polymerase chain reaction (PCR) techniques. Fifteen were de novo, 4 maternally and 2 paternally transmitted and in 5 cases the parental origin is not known. Eleven cases were non-mosaic and fifteen cases had SMC cell lines ranging from 8-87%. Ten cases were ascertained prenatally, nine postnatally with abnormal phenotypes, three with poor reproductive histories and four co-incidentally. Five SMC were small rings from chromosomes 3, 6 (2 cases), 20 and 21; 8 were bisatellited from chromosomes 13/21 (4 cases), 14 (3 cases) and 14/22 (1 case). The remaining 13 appeared to be minutes comprising centromeric material only from chromosomes 1, 4, 12, 13/21 (2 cases), 14 (3 cases), 16 (2 cases), 19; 5/19, and a centric fusion involving 13 or 21 and 14. Euchromatin was detected in 9 out of 18 SMC tested with paints and/or PCR, and abnormal phenotypes were most commonly observed in patients with small ring shaped SMCs containing euchromatic sequences. Uniparental paternal isodisomy (UPD) for chromosome 6 was detected in one patient but was the only example of UPD for the normal homologues in association with an autosomal SMC in an overall total of 30 cases examined.