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To determine the incidence of these deletions, we have analyzed a series of 50 meningiomas for the loss of alleles at four chromosome I loci. Thirteen samples displayed LOH for the markers studied; in one instance, the results were compatible with loss of the entire chromosome I, whereas in the other 12 samples deletions of the short arm were observed. Eleven of the meningiomas had previously been shown to have loss of alleles on chromosome 22, and 12 of them were characterized by increased tumor aggressiveness. These findings suggest that deletion of 1p (or the alteration of a locus located there) might represent a secondary, but nonrandom alteration in meningiomas, perhaps contributing to meningioma tumor progression. \u003Cjats:italic>Genes Chrom Cancer 9:296‐298 (1994).\u003C\u002Fjats:italic> © 1994 Wiley‐Liss. 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deletions of the short arm of chromosome 3 were found in short‐term cultures of five breast carcinomas (of 41 breast cancers with clonal aberrations analyzed by us during the same period). 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Loss of heterozygosity (LOH) was frequently observed on chromosome arms 17p (p144D6 lost in 75%, pYNZ22.1 in 55%, and \u003Cjats:italic>TP53\u003C\u002Fjats:italic> in 48% of the primary tumours), 13q (\u003Cjats:italic>RBI\u003C\u002Fjats:italic> lost in 40% of the primary tumours), and 17q (pRMU3 lost in 35%, pTHH59 in 29%, and \u003Cjats:italic>NM23HI\u003C\u002Fjats:italic> in 26% of the primary tumours). Loss of all the markers except p144D6 was observed even more frequently in the metastases. Pairwise comparisons for concordance of allele losses on 17p indicated that there might be two genes on 17p implicated in breast cancer development; the \u003Cjats:italic>TP53\u003C\u002Fjats:italic> gene and a gene located close to the p144D6 and pYNZ22.1 markers. LOH of the \u003Cjats:italic>RBI\u003C\u002Fjats:italic> gene was associated with LOH of pYNZ22.1 and p144D6, but not with LOH of \u003Cjats:italic>TP53.\u003C\u002Fjats:italic> LOH of \u003Cjats:italic>RBI\u003C\u002Fjats:italic> and \u003Cjats:italic>TP53\u003C\u002Fjats:italic> was associated with occurrence of ductal carcinomas, \u003Cjats:italic>RBI\u003C\u002Fjats:italic> and p144D6 losses with tumour size, and p144D6 losses with positive node status as well. LOH of \u003Cjats:italic>TP53\u003C\u002Fjats:italic> and the three 17q markers \u003Cjats:italic>NM23HI\u003C\u002Fjats:italic>, pTHH59, and pRMU3 was most frequently observed in tumours from postmenopausal women. p144D6 losses occurred most frequently in progesterone receptor‐negative tumours, whereas pTHH59 losses occurred most frequently in oestrogen receptor‐negative tumours. 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development of human breast cancer is characterized by a variety of genetic alterations, and cytogenetic analyses have documented the consistent involvement of both arms of chromosome I. In the present study, molecular markers detecting restriction fragment length polymorphisms were used in pairwise screening of normal and tumor DNA to determine the frequency of allelic imbalance in breast tumors. Loss of heterozygosity (LOH) in the polymorphic epithelial mucin \u003Cjats:italic>(PEM\u003C\u002Fjats:italic> or \u003Cjats:italic>MUCI\u003C\u002Fjats:italic>) gene at 1q21 was found in 16% of 89 informative (constitutionally heterozygous) cases, whereas gain in intensity of one allelic band was more frequent (37%), a total of 47% of cases manifesting either allelic loss or gain. Three additional tumors manifested a structural alteration. Allelic loss or gain in the \u003Cjats:italic>PEM\u003C\u002Fjats:italic> gene was not associated with other prognostic factors, e.g., tumor size, lymph node status, steroid receptors, DNA ploidy, S phase fraction, protooncogene amplification, histological type, or patient age. However, LOH in the \u003Cjats:italic>PEM\u003C\u002Fjats:italic> gene was significantly correlated with early disease recurrence (P = 0.006). LOH on 1p was found in 27% of 117 informative cases, using probes for either DIS57 or DIZ2 located at 1p33‐p35 and 1p36, respectively. Somatic allelic imbalance on 1p and 1q seemed to be independent events and not the effect of loss of a whole chromosome 1. LOH on 1 p was significantly correlated to the presence of lymph node metastasis, to larger tumor size, and to DNA nondiploidy, but no correlation was found to disease outcome at this limited duration of follow‐up (median 29 months). ©1992 Wiley‐Liss, Inc.\u003C\u002Fjats:p>",{"EN":1024},"Chromosome I alterations in breast cancer: Allelic loss on Ip and Iq Is related to lymphogenic metastases and poor 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fragment length polymorphism (RFLP) analysis for allelic losses on the chromosome arm 3p were performed on independent carcinomas produced in athymic nude mice after transformation in vitro of a pseudodiploid clonal SV40‐immortalized human uroepithelial cell line (SV‐HUC). We analyzed ten primary carcinomas with heterogeneous phenotypes for deletions on 3p by using three informative probes, D3S30, D3S2, and D3F15S2, which map to the 3p11‐p14, 3p21.1, and 3p21 regions, respectively. Five of the ten primary cancers showed reduction to homozygosity with at least one of the probes, and all five cancers were high‐grade and poorly differentiated. We also analyzed six carcinomas that arose after progression of low‐grade cancers, either spontaneously or after exposure to a human bladder carcinogen, to higher grades (progressed carcinomas). Four of the six exhibited 3p allelic loss. No preferential loss of a specific 3p allele was observed in any of the carcinomas. In addition, whereas most of the carcinomas showed allelic loss for all three of the probes, indicating a large‐scale deletion, several of the carcinomas exhibited losses for only one or two of the probes, thus making it possible, along with the cytogenetic data, to define the least common region of deletion to 3p13→p14.2. These results support the hypothesis that nonrandom loss of a gene or genes on 3p leads to the development of cancer. 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44",{},{"id":24,"text":2375,"url":24,"identifiers":2376},"10.1016\u002F0165-4608(88)90090-8",{"doi":2375},{"id":24,"text":2378,"url":24,"identifiers":2379},"10.1126\u002Fscience.2565047",{"doi":2378},{"id":24,"text":2381,"url":24,"identifiers":2382},"10.1073\u002Fpnas.86.13.5099",{"doi":2381},{"id":24,"text":690,"url":24,"identifiers":2384},{"doi":690},{"id":24,"text":2386,"url":24,"identifiers":2387},"10.1016\u002F0165-4608(88)90077-5",{"doi":2386},{"id":24,"text":2389,"url":24,"identifiers":2390},"Wu S‐Q, 1991, Nonrandom chromosome losses in stepwise neoplastic transformation in vitro of human uroepithelial cells, Cancer Res, 51, 3323",{},{"id":24,"text":2392,"url":24,"identifiers":2393},"Yokota J, 1989, Loss of heterozygosity on the short arm of chromosome 3 in carcinoma of the uterine cervix, Cancer Res, 49, 3598",{},{"id":24,"text":2395,"url":24,"identifiers":2396},"Yoshida MA, 1986, Cytogenetic studies of tumor tissue from patients with nonfamilial renal cell carcinoma, Cancer Res, 46, 2139",{},{"id":24,"text":2398,"url":24,"identifiers":2399},"10.1038\u002F327721a0",{"doi":2398},{"id":24,"text":2401,"url":24,"identifiers":2402},"10.1007\u002F978-1-4471-1362-1",{"doi":2401},{"id":2404,"createTime":2405,"updateTime":2405,"relativeEntities":2406,"slug":2407,"properties":2408,"entityType":117,"verifyStatus":118,"verifyTime":2421,"verifyNote":120,"languages":2422,"translateLanguages":24,"viewCount":25,"primaryUrl":2423,"fullTextUrl":24,"authors":2424,"publicationType":254,"publisherRelationship":2561,"citationCount":2610,"citationInfo":2611,"publishDate":2614,"publishYear":2612,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":2615,"openAccess":24,"references":2616,"isForceReanalyzing":389},"786c3389-d3f7-4827-aba5-7bf05247b6bd","2024-11-25T22:55:47.105+00:00",[],"Identification-of-gains-and-losses-of-DNA-sequences-in-primary-bladder-cancer-by-comparative-genomic-hybridization",{"openalex":2409,"mag":2411,"abstract":2413,"title":2415,"pm":2417,"doi":2419},{"VOID":2410},"W2033345513",{"VOID":2412},"2033345513",{"EN":2414},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Comparative genomic hybridization (CGH) makes it possible to detect losses and gains of DNA sequences along all chromosomes in a tumor specimen based on the hybridization of differentially labeled tumor and normal DNA to normal human metaphase chromosomes. In this study, CGH analysis was applied to the identification of genomic imbalances in 26 bladder cancers in order to gain information on the genetic events underlying the development and progression of this malignancy. Losses affecting 11p, 11q, 8p, 9, 17p, 3p, and 12q were all seen in more than 20% of the tumors. The minimal common region of loss in each chromosome was identified based on the analysis of overlapping deletions in different tumors. Gains of DNA sequences were most often found at chromosomal regions distinct from the locations of currently known oncogenes. The bands involved in more than 10% of the tumors were 8q21, 13q21‐q34, 1q31, 3q24‐q26, and 1p22. In conclusion, these CGH data highlight several previously unreported genetic alterations in bladder cancer. Further detailed studies of these regions with specific molecular genetic techniques may lead to the identification of tumor suppressor genes and oncogenes that play an important role in bladder tumorigenesis.\u003C\u002Fjats:p>",{"EN":2416},"Identification of gains and losses of DNA sequences in primary bladder cancer by comparative genomic hybridization",{"VOID":2418},"7536461",{"VOID":2420},"10.1002\u002Fgcc.2870120309","2024-11-25T22:55:47.104+00:00",[122],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fgcc.2870120309",[2425,2444,2461,2478,2497,2512,2531,2546],{"id":2426,"sortIndex":25,"researcher":24,"roles":2427,"affiliations":2428,"properties":2437,"displayName":2441,"givenName":24,"familyName":24},"b2af939e-ce84-4aab-8e50-c12df240f9f9",[],[2429],{"id":2430,"sortIndex":25,"affiliation":2431,"properties":24},"f1563a20-cfae-417d-ba47-e3b872f1cfad",{"id":2430,"createTime":24,"updateTime":24,"relativeEntities":2432,"slug":24,"properties":2433,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2436,"statistic":24},[],{"title":2434},{"EN":2435},"Laboratory of Cancer Genetics, Department of Laboratory Medicine, Tampere University Hospital, Tampere, 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Cytometry (in press).",{},{"id":24,"text":2673,"url":24,"identifiers":2674},"Sakamoto M, 1993, Comparative genomic hybridization and loss of heterozygosity studies in ovarian cancer, Am J Hum Genet, 53, 356",{},{"id":24,"text":2676,"url":24,"identifiers":2677},"Sano T, 1991, Frequent loss of heterozygosity on chromosomes 1q, 5q, and 17p in human gastric carcinomas, Cancer Res, 51, 2926",{},{"id":24,"text":2679,"url":24,"identifiers":2680},"Sato T, 1991, Allelotype of human ovarian cancer, Cancer Res, 51, 5118",{},{"id":24,"text":2682,"url":24,"identifiers":2683},"Sauter G, 1993, Heterogeneity of erbB‐2 amplification in bladder cancer, Cancer Res, 53, 2199",{},{"id":24,"text":2685,"url":24,"identifiers":2686},"Sauter G, 1994, Physical deletion of the p53 gene in bladder cancer: Detection by fluorescence in situ hybridization, Am J Pathol, 144, 756",{},{"id":24,"text":2688,"url":24,"identifiers":2689},"SauterG MochH CarrollP KerschmannR MihatschM WaldmanF(1994b)Chromosome 9 loss detected by fluorescence in situ hybridization in bladder cancer. Am J Pathol (in press).",{"doi":2690},"10.1002\u002Fijc.2910640205",{"id":24,"text":2366,"url":24,"identifiers":2692},{"doi":2366},{"id":24,"text":2694,"url":24,"identifiers":2695},"Tsuchiya E, 1992, Allelotype of non‐small cell lung carcinoma—Comparison between loss of heterozygosity in squamous cell carcinoma and adenocarcinoma, Cancer Res, 52, 2478",{},{"id":24,"text":2375,"url":24,"identifiers":2697},{"doi":2375},{"id":24,"text":2699,"url":24,"identifiers":2700},"10.1016\u002FS0022-5347(17)37212-9",{"doi":2699},{"id":2702,"createTime":2703,"updateTime":2703,"relativeEntities":2704,"slug":2705,"properties":2706,"entityType":117,"verifyStatus":118,"verifyTime":2703,"verifyNote":120,"languages":2719,"translateLanguages":24,"viewCount":25,"primaryUrl":2720,"fullTextUrl":24,"authors":2721,"publicationType":254,"publisherRelationship":2756,"citationCount":2806,"citationInfo":2807,"publishDate":2809,"publishYear":2612,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":2810,"openAccess":24,"references":2811,"isForceReanalyzing":389},"2274250d-08ba-48bf-a05d-121c6d2d2eb9","2024-11-25T22:55:32.267+00:00",[],"Deletion-mapping-of-chromosome-II-in-carcinoma-of-the-bladder",{"openalex":2707,"mag":2709,"abstract":2711,"title":2713,"pm":2715,"doi":2717},{"VOID":2708},"W1973693817",{"VOID":2710},"1973693817",{"EN":2712},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Deletions of the short arm of chromosome II have been identified by both cytogenetic and molecular criteria in bladder and other types of solid tumor, indicating the presence of one or more suppressor loci in this region. To localize the II p deletion target(s) more precisely and to screen for loss of heterozygosity (LOH) on the long arm of the chromosome, I00 bladder tumors were analyzed for LOH on chromosome II using restriction fragment length polymorphism (RFLPs) and microsatellite markers mapped to both II p and II q. Thirty‐four tumors were found to have LOH at I or more loci. Of these, I7 had LOH restricted to II p, I3 had LOH of both II p and II q, and 4 had LOH of II q only. Eight tumors showed LOH at all informative loci indicating probable loss of an entire copy of chromosome II. A common region of deletion was defined on II p between DIIS922(IIpI5.5) and DlIS569 (IIpI5.I‐I5.2). This region does not include the \u003Cjats:italic>HRAS\u003C\u002Fjats:italic> or \u003Cjats:italic>WTI\u003C\u002Fjats:italic> loci (at IIpI5.5and IIp13, respectively). Seventeen tumors had LOH on II q, 4 of which had LOH on II q only. The common region of deletion on II q was between \u003Cjats:italic>FGF3\u003C\u002Fjats:italic> and DI IS490 (IIq I3‐q23.2). Two tumors showed LOH on both II p and II q with a clear region of retention of heterozygosity between, indicatinn the existence of two deletion targets on chromosome II. © 1995 Wiley‐Liss, Inc.\u003C\u002Fjats:p>",{"EN":2714},"Deletion mapping of chromosome II in carcinoma of the bladder",{"VOID":2716},"7541638",{"VOID":2718},"10.1002\u002Fgcc.2870130102",[122],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fgcc.2870130102",[2722,2739],{"id":2723,"sortIndex":25,"researcher":24,"roles":2724,"affiliations":2725,"properties":2734,"displayName":2736,"givenName":24,"familyName":24},"7d99f1f0-5087-4a01-a43e-1c74759f77ac",[],[2726],{"id":2727,"sortIndex":25,"affiliation":2728,"properties":24},"c37a9244-3493-46b8-852c-efa17248b9bd",{"id":2727,"createTime":24,"updateTime":24,"relativeEntities":2729,"slug":24,"properties":2730,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2733,"statistic":24},[],{"title":2731},{"EN":2732},"Molecular Genetics Laboratory, Marie Curie Research Institute, Oxted, Surrey, United Kingdom",[],{"title":2735,"openalex":2737},{"EN":2736},"Margaret E. 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