Evidence map›Paper›PMID 19927377›Full record

ArticleGenes, chromosomes & cancer2010

Definitive molecular cytogenetic characterization of 15 colorectal cancer cell lines.

Turid Knutsen, Hesed M Padilla-Nash, Danny Wangsa, Linda Barenboim-Stapleton, Jordi Camps, Nicole McNeil, Michael J Difilippantonio, Thomas Ried

Abstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
1.7field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 83 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Turid KnutsenSection of Cancer Genomics, Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892-8010, USA. knutsent@mail.nih.gov
Hesed M Padilla-Nash
Danny Wangsa
Linda Barenboim-Stapleton
Jordi Camps
Nicole McNeil
Michael J Difilippantonio
Thomas Ried
Center for Cancer Research · USNational Cancer Institute · US

Funding

Prediction of Therapy Response in Colorectal CancerZIABC010837 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RIED, THOMAS · 2009 to 2022
$8.9M
Cancer GenomicsZIABC010836 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RIED, THOMAS · 2009 to 2011
$1.8M
Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

In defining the genetic profiles in cancer, cytogenetically aberrant cell lines derived from primary tumors are important tools for the study of carcinogenesis. Here, we present the results of a comprehensive investigation of 15 established colorectal cancer cell lines using spectral karyotyping (SKY), fluorescence in situ hybridization, and comparative genomic hybridization (CGH). Detailed karyotypic analysis by SKY on five of the lines (P53HCT116, T84, NCI-H508, NCI-H716, and SK-CO-1) is described here for the first time. The five lines with karyotypes in the diploid range and that are characterized by defects in DNA mismatch repair had a mean of 4.8 chromosomal abnormalities per line, whereas the 10 aneuploid lines exhibited complex karyotypes and a mean of 30 chromosomal abnormalities. Of the 150 clonal translocations, only eight were balanced and none were recurrent among the lines. We also reviewed the karyotypes of 345 cases of adenocarcinoma of the large intestine listed in the Mitelman Database of Chromosome Aberrations in Cancer. The types of abnormalities observed in the cell lines reflected those seen in primary tumors: there were no recurrent translocations in either tumors or cell lines; isochromosomes were the most common recurrent abnormalities; and breakpoints occurred most frequently at the centromeric/pericentromeric and telomere regions. Of the genomic imbalances detected by array CGH, 87% correlated with chromosome aberrations observed in the SKY studies. The fact that chromosome abnormalities predominantly result in copy number changes rather than specific chromosome or gene fusions suggests that this may be the major mechanism leading to carcinogenesis in colorectal cancer.

Indexed as

Cell Line, TumorChromosome AberrationsChromosome BandingColorectal NeoplasmsComparative Genomic HybridizationCytogenetic AnalysisDNA Mismatch RepairHumansIn Situ Hybridization, FluorescenceKaryotypingTranslocation, Genetic

Identifiers

PMID19927377
PMCPMC2818350
OpenAlexW2149016664

What OpenQuestion holds

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Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.