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Chromosome

About: Chromosome is a research topic. Over the lifetime, 17538 publications have been published within this topic receiving 660077 citations. The topic is also known as: chromosomes & GO:0005694.


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Journal ArticleDOI
TL;DR: Recent studies show that a unique form of chromatin, based on the histone-H3-like protein CENP-A and homologues, provides a conserved foundation for this mechanical chromatin domain.

168 citations

Journal ArticleDOI
TL;DR: Previous cytogenetic results from primary Hodgkin's tumors suggest an important pathogenic role of REL and JAK2 in this disease, and provide evidence for a novel cytogenetics pathomechanism leading to increased copy numbers of putative oncogenes from terminal chromosomal regions, most probably in the course of chromosomal stabilization by telomeric capture.
Abstract: Four Hodgkin's lymphoma cell lines (KM-H2, HDLM-2, L428, L1236) were analyzed for cytogenetic aberrations, applying multiplex fluorescence in situ hybridization, chromosome banding and comparative genomic hybridization. Each line was characterized by a highly heterogeneous pattern of karyotypic changes with a large spectrum of different translocated chromosomes (range 22–57). A recurrent finding in all cell lines was the presence of chromosomal rearrangements of the short arm of chromosome 2 involving the REL oncogene locus. Furthermore, multiple translocated copies of telomeric chromosomal segments were frequently detected. This resulted in a copy number increase of putative oncogenes, e.g., JAK2 (9p24) in 3 cell lines, FGFR3 (4p16) and CCND2 (12p13) in 2 cell lines as well as MYC (8q24) in 1 cell line. Our data confirm previous cytogenetic results from primary Hodgkin's tumors suggesting an important pathogenic role of REL and JAK2 in this disease. In addition, they provide evidence for a novel cytogenetic pathomechanism leading to increased copy numbers of putative oncogenes from terminal chromosomal regions, most probably in the course of chromosomal stabilization by telomeric capture. © 2002 Wiley-Liss, Inc.

168 citations

Journal ArticleDOI
TL;DR: It is proposed that H2A.Z plays an integral role in organizing centromere structure, and is identified as a new structural component of the Centromere.
Abstract: Mammalian centromere function depends upon a specialized chromatin organization where distinct domains of CENP-A and dimethyl K4 histone H3, forming centric chromatin, are uniquely positioned on or near the surface of the chromosome. These distinct domains are embedded in pericentric heterochromatin (characterized by H3 methylated at K9). The mechanisms that underpin this complex spatial organization are unknown. Here, we identify the essential histone variant H2A.Z as a new structural component of the centromere. Along linear chromatin fibers H2A.Z is distributed nonuniformly throughout heterochromatin, and centric chromatin where regions of nucleosomes containing H2A.Z and dimethylated K4 H3 are interspersed between subdomains of CENP-A. At metaphase, using the inactive X chromosome centromere as a model, complex folding of this fiber produces spatially positioned domains where H2A.Z/dimethylated K4 H3 chromatin juxtaposes one side of CENP-A chromatin, whereas a region of H2A/trimethyl K9 H3 borders the other side. A second region of H2A.Z is found, with trimethyl K9 H3 at the inner centromere. We therefore propose that H2A.Z plays an integral role in organizing centromere structure.

168 citations

Journal Article
TL;DR: The results suggest that renal cell carcinoma may be cytogenetically classified into 3 categories: tumors with changes of chromosome 3: (b) tumors with other clonal aberrations; and (c) tumors without clonal changes.
Abstract: A method combining an enzymatic technique and short term culture was applied to 27 tumor tissues from 22 patients with nonfamilial renal cell carcinoma in order to establish the chromosome changes in these tumors. Chromosome analyses were successfully carried out in quinacrine mustard-Hoechst 33258 and G-banded preparations of 14 tumors from 12 patients, including 2 cases in which established cell lines were obtained after 43 and 64 days in culture and maintained for 25 and 30 passages in an in vitro system, respectively. The modal chromosome numbers ranged from 38–46 in 11 samples, involving chromosomes in structural and numerical changes and 72 chromosomes in one case, with the remaining 2 samples showing a variety of chromosome numbers. Banding analysis revealed 45 clonal aberrations in 11 tumor samples from 10 patients and nonclonal aberrations in the remaining 3 samples from 2 of the patients. Rearrangements of chromosome 3 were observed in 12 tumors, with the breakpoints on this chromosome almost totally clustered from p11 to p21. In one case both primary and metastatic tumors were studied, and an isochromosome for the long arm of chromosome 1 was observed as clonal in origin in the metastatic tissue. Two cases showed nonclonal changes. The remaining case had one clonal abnormality, i.e. , deletion of 6q. Of the remaining 33 clones, chromosomes 1, 2, 6, 11, and 17 were frequently involved. These results suggest that renal cell carcinoma may be cytogenetically classified into 3 categories: ( a ) tumors with changes of chromosome 3; ( b ) tumors with other clonal aberrations; and ( c ) tumors without clonal changes. Rearrangements of chromosome 3 may be possibly associated with the genesis and/or progression of renal cell carcinoma.

168 citations

Journal ArticleDOI
01 Nov 1986-Nature
TL;DR: It is speculated that the same enzymatic mechanism is responsible for the t(8; 14) translocations in African Burkitt's lymphoma and pre-B cell ALL.
Abstract: The reciprocal chromosome translocation, t(8;14), involving the heavy chain locus on chromosome 14 and the c-myc oncogene on chromosome 8 is a characteristic of the B-cell malignancies Burkitt's lymphoma and acute lymphoblastic leukaemia (ALL). We have cloned and sequenced the t(8; 14) breakpoints of an African Burkitt's lymphoma cell line, P3HR-1, and a pre-B cell ALL cell line, 380. In each case the region of chromosome 8 involved has recombined with a JH region on chromosome 14. The two sites of breakage on chromosome 8 lie within 70 base pairs (bp) of one another. At each joining site, sequences homologous to the signal sequences thought to be recognized by the V-D-J recombinase were identified, as were N regions. In B-cell chronic lymphocytic leukaemias (B-CLL) carrying the t(11; 14) chromosome translocation and in follicular lymphomas carrying the t(14; 18) translocation, the V-D-J recombinase is implicated in the mechanism of chromosomal translocations. We speculate that the same enzymatic mechanism is responsible for the t(8; 14) translocations in African Burkitt's lymphoma and pre-B cell ALL.

168 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20241
2023862
20221,198
2021368
2020359
2019365