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Chromosome 21

About: Chromosome 21 is a research topic. Over the lifetime, 4736 publications have been published within this topic receiving 206655 citations. The topic is also known as: chr21 & Homo sapiens chromosome 21.


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Journal ArticleDOI
TL;DR: The chromosome banding patterns of all seven extant species of the horse family, Equidae, are presented.
Abstract: The chromosome banding patterns of all seven extant species of the horse family, Equidae, are presented. This mammalian family is composed of a single genus, Equus, notable for its rapid karyotypic ev

120 citations

Journal ArticleDOI
TL;DR: Earlier chromosome studies and the present cases suggest that regions near the centromere and q21 are vulnerable points on human chromosome No. 1, and that region q21–32 is important for development of certain tumour types.
Abstract: Marker chromosomes involving chromosome No. 1 were studied with banding techniques in 10 primary solid tumours. Structural or numerical aberrations of chromosome No. 1 were found in nine of these. Two major types of rearrangement of chromosome No. 1 were observed: translocation of the long arm (partial trisomy) and an isochromosome of of 1q. Earlier chromosome studies and the present cases suggest that regions near the centromere and q21 are vulnerable points on human chromosome No. 1, and that region q21-32 is important for development of certain tumour types.

119 citations

Journal ArticleDOI
TL;DR: The findings suggest that the AML1 gene is a target gene in the 21q22 amplicon in childhood ALL, and to understand the role, if any, of the AMl1 amplification in leukemogenesis, further studies are needed.
Abstract: BACKGROUND AND OBJECTIVE: We previously found a high-level amplification in chromosomal region 21q22 in two children with acute lymphoblastic leukemia (ALL) using comparative genomic hybridization. The same region harbors the AML1 gene. The aim of the present study was to investigate whether AML1 is a target gene in these amplifications. DESIGN AND METHODS: Bone marrow samples were obtained from 112 childhood ALL patients. The copy number of AML1 was studied using fluorescent in situ hybridization with a dual color DNA probe specific for the AML1 and TEL genes. RESULTS: Three of the patients had 3-to-8 fold amplification of AML1 and showed a high-level amplification of 21q22 by comparative genomic hybridization. In two of them the extra copies were shown to be located tandemly in a derivative of chromosome 21. Thirty-seven of the patients (33%) had 1-to-2 extra copies of AML1, most probably reflecting the incidence of trisomy 21 and tetrasomy 21. The TEL-AML1 fusion was less frequent in the patients with extra copies of AML1 (7/40; 18%) than in the patients with no extra copy (24/72; 33%). None of the three patients with 3-to-8 fold amplification of AML1 showed the fusion or loss of TEL. INTERPRETATION AND CONCLUSIONS: Our findings suggest that the AML1 gene is a target gene in the 21q22 amplicon in childhood ALL. To understand the role, if any, of the AML1 amplification in leukemogenesis, further studies are needed.

119 citations

Journal Article
TL;DR: The data suggest that one or more putative tumor suppressor genes may reside on chromosome 1p, and have cloned the entire region of interest at 1p31 in yeast artificial chromosomes.
Abstract: The short arm of chromosome 1 is frequently affected by rearrangements in a variety of human malignancies. Genetic alterations, predominantly deletions, which are indicative of the presence of a putative tumor suppressor gene at chromosome 1p, are observed in breast cancer. In order to define the altered locus, eleven highly polymorphic microsatellite markers on chromosome 1p were used to detect loss of heterozygosity. We analyzed 52 cases of breast cancer and found 4 common deleted regions at chromosome 1p. Twenty-two of 52 (42%) informative patients showed at least 1 affected locus. The region most frequently exhibiting loss of heterozygosity was 1p31 (11/39; 28%); the other three common deleted regions were 1p36 (10/44; 23%), 1p35-36 (5/40; 13%), and 1p13 (8/39; 21%). These data suggest that one or more putative tumor suppressor genes may reside on chromosome 1p. We have cloned the entire region of interest at 1p31 in yeast artificial chromosomes. This yeast artificial chromosome contig can be used for fine mapping of the region and cloning of the candidate tumor suppressor gene.

119 citations

Journal ArticleDOI
01 Nov 1980-Genetics
TL;DR: These localizations should assist in the construction of additional useful chromosome marker stocks, especially since several of these enzyme loci lie in regions that were previously poorly mapped.
Abstract: Linkage relationships of 19 enzyme loci have been examined. The chromosomal locations of eight of these loci are formally reported for the first time in this paper. These localizations should assist in the construction of additional useful chromosome marker stocks, especially since several of these enzyme loci lie in regions that were previously poorly mapped. Six loci are on the long arm of chromosome 1. The arrangement is (centromere)—Mdh4-mmm-Pgm1-Adh1-Phi-Gdh1, with about 46% recombination between Mdh4 and Gdh1.—Linkage studies with a2 and pr have resulted in the localization of four enzyme genes to chromosome 5 with arrangement Pgm2-Mdh5-Got3-a2-(centromere)-pr-Got2. Pgm2 lies approximately 35 map units distal to a2 in a previously unmapped region of the short arm of 5, beyond ameiotic.—Approximately 23% recombination was observed between Mdh4 and Pgm1 on chromosome 1, while 17% recombination occurred between Mdh5 and Pgm2 on chromosome 5. Similarly, linkages between Idh1 and Mdh1, about 22 map units apart on chromosome 8, and between Mdh2 and Idh2, less than 5 map units apart on chromosome 6, were observed. Thus, segments of chromosomes 1 and 5 and segments of 6 and 8 may represent duplications on nonhomologous chromosomes.

118 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202320
202259
202147
202061
201943
201858