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Catalog of chromosome aberrations in cancer
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TLDR
This poster presents a probabilistic procedure to count the number of chromosomes in the nucleus using a simple “spatially aggregating” procedure called “spot-spot analysis”.Abstract:
Chromosome 1-22 Chromosome X Chromosome Y Homogeneously Staining Regions (HSR) Ring Chromosomes (R) Double Minute Chromosomes (DMIN).read more
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Journal ArticleDOI
A characteristic sequence of trisomies starting with trisomy 7 in benign thyroid tumors
TL;DR: The cytogenetic results from a series of 113 thyroid hyperplasias and adenomas are reported; 15 showed clonal karyotypic alterations and it is concluded that a subset of lesions characterized by polysomies may be an example of a more common genetic pathway in human solid tumors.
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Genome imprinting and carcinogenesis.
TL;DR: Data from human pediatric tumors, transgenes in the mouse and variegating position-effects in Drosophila, indicate that the net effect of modifier loci is the inactivation of alleles at affected loci, which provides a mechanism by which differential genome imprinting may be accomplished.
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Genomic structure of the human MAD2 gene and mutation analysis in human lung and breast cancers.
Akihiko Gemma,Yoko Hosoya,Masahiro Seike,Kazutsugu Uematsu,Futoshi Kurimoto,Suguru Hibino,Akinobu Yoshimura,Masahiko Shibuya,Shoji Kudoh,Mitsuru Emi +9 more
TL;DR: The results suggested that the hMAD2 gene is not commonly mutated in either lung nor breast cancers, and its genomic structure and intronic primers designed to amplify the entire coding region will facilitate future studies to determine the full spectrum and frequency of the genetic events that can affect expression of the h mad2 gene in human tumors.
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Abnormalities involving chromosome 6 in newly diagnosed patients with non-Hodgkin's lymphoma
TL;DR: The results suggest that chromosome 6, especially the long arm, carries important information for the clinical behavior of NHL and it is necessary to resolve the molecular defects.
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Allelotyping of acute myelogenous leukemia: loss of heterozygosity at 7q31.1 (D7S486) and q33-34 (D7S498, D7S505).
TL;DR: The smallest commonly deleted regions are identified to be at 7q31.1 (D7S486) and 7q33-34 (D 7S498, D7S505) suggesting that alterations of a TSG in each region have an important role in de novo AML.