ArticleOncogene2002
A microarray-based, integrated approach to identify novel regulators of cancer drug response and apoptosis.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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.
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Who cites it
13 citing papers in PubMed, 35 citations in OpenAlex.
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- AMH protects the ovary from doxorubicin by regulating cell fate and the response to DNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Analysis of Secreted Proteins from Prepubertal Ovarian Tissues Exposed In Vitro to Cisplatin and LH.Cells · 2022Article
- Histopathologic, Genetic and Molecular Characterization of Endometrial Cancer Racial Disparity.Cancers · 2021Review
- Proteomic evidences for microcystin-RR-induced toxicological alterations in mice liver.Scientific reports · 2018Article
- Induction of microRNA-155 is TLR- and type IV secretion system-dependent in macrophages and inhibits DNA-damage induced apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Article
- Effects of ionizing radiation on self-renewal and pluripotency of human embryonic stem cells.Cancer research · 2010Article
- In praise of arrays.Pediatric nephrology (Berlin, Germany) · 2009Review
- A role for Drosophila in understanding drug-induced cytotoxicity and teratogenesis.Cytotechnology · 2008Article
- Tumor protein 53-induced nuclear protein 1 expression is repressed by miR-155, and its restoration inhibits pancreatic tumor development.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Colitis and colitis-associated cancer are exacerbated in mice deficient for tumor protein 53-induced nuclear protein 1.Molecular and cellular biology · 2007Article
- DNA microarrays: a powerful genomic tool for biomedical and clinical research.Molecular medicine (Cambridge, Mass.)Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA microarrays are powerful tools for the analysis of gene expression on a genomic scale. The importance of individual regulatory events for the process under study can however not be deduced unequivocally without additional experiments. We devised a strategy to identify central regulators of cancer drug responses by combining the results of microarray experiments with efficient methods for phenotypic testing of candidate genes. We exposed murine FL5.12 pro-B cells to cisplatin, camptothecin, methotrexate or paclitaxel, respectively and analysed the patterns of gene expression with cDNA microarrays. Drug-specific regulatory events as well as intersections between different apoptotic pathways, including previously studied responses to staurosporine and interleukin-3 (IL-3) deprivation, were identified. Genes shared by at least three pathways were chosen for further analysis. Ectopic expression of three such genes, TEAP, GP49B, and Lipin1 was found to have an anti-proliferative effect on pro-B cells. Interestingly, we identified hemoglobin alpha as a strong pro-apoptotic regulator. While hemoglobin-expressing cells were growing normally in the presence of IL-3, they displayed accelerated apoptosis with similar kinetics as Bax overexpressing cells upon IL-3 removal. The pro-apoptotic effect of hemoglobin was suppressed by Bcl-2 and was characterized by enhanced stimulation of caspase activity.
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