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Catalog of chromosome aberrations in cancer
01 Jan 1985-
TL;DR: 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).
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TL;DR: There is now evidence that most cancers may indeed be genetically unstable, but that the instability exists at two distinct levels, and recognition and comparison of these instabilities are leading to new insights into tumour pathogenesis.
Abstract: Whether and how human tumours are genetically unstable has been debated for decades. There is now evidence that most cancers may indeed be genetically unstable, but that the instability exists at two distinct levels. In a small subset of tumours, the instability is observed at the nucleotide level and results in base substitutions or deletions or insertions of a few nucleotides. In most other cancers, the instability is observed at the chromosome level, resulting in losses and gains of whole chromosomes or large portions thereof. Recognition and comparison of these instabilities are leading to new insights into tumour pathogenesis.
4,121 citations
TL;DR: Because patients with APL can be induced into remission with high dose RA therapy, it is proposed that the nonliganded PML-RAR protein is a new class of dominant negative oncogene product.
1,429 citations
TL;DR: A novel role for a trithorax-homologous protein in multilineage human leukemias that may be mediated by DNA binding within the minor groove at AT-rich sites is suggested, implicated to play an important role in bacterial IHF, yeast datin-, and mammalian HMG-mediated gene activation.
967 citations
TL;DR: Not only is the POD a novel structure, but it can be ascribed an imputed function such that its disruption leads to altered myeloid maturation; this may represent a novel oncogenic target.
804 citations
TL;DR: Comparative genomic hybridization was applied to 5 breast cancer cell lines and 33 primary tumors to discover and map regions of the genome with increased DNA-sequence copy-number, indicating that these chromosomal regions may contain previously unknown genes whose increased expression contributes to breast cancer progression.
Abstract: Comparative genomic hybridization was applied to 5 breast cancer cell lines and 33 primary tumors to discover and map regions of the genome with increased DNA-sequence copy-number. Two-thirds of primary tumors and almost all cell lines showed increased DNA-sequence copy-number affecting a total of 26 chromosomal subregions. Most of these loci were distinct from those of currently known amplified genes in breast cancer, with sequences originating from 17q22-q24 and 20q13 showing the highest frequency of amplification. The results indicate that these chromosomal regions may contain previously unknown genes whose increased expression contributes to breast cancer progression. Chromosomal regions with increased copy-number often spanned tens of Mb, suggesting involvement of more than one gene in each region.
772 citations