ArticleBritish journal of cancer1993
Susceptibility to apoptosis is differentially regulated by c-myc and mutated Ha-ras oncogenes and is associated with endonuclease availability.
Article in British journal of cancer, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 124 citations in OpenAlex.
- Wild-type K-ras has a tumour suppressor effect on carcinogen-induced murine colorectal adenoma formation.International journal of experimental pathology · 2014Article
- A microarray method for identifying tumor antigens by screening a tumor cDNA expression library against cancer sera.Human vaccines & immunotherapeutics · 2013Article
- Activation of K-RAS by co-mutation of codons 19 and 20 is transforming.Journal of molecular signaling · 2011Article
- Mutated K-ras(Asp12) promotes tumourigenesis in Apc(Min) mice more in the large than the small intestines, with synergistic effects between K-ras and Wnt pathways.International journal of experimental pathology · 2009Article
- Conditional expression of mutated K-ras accelerates intestinal tumorigenesis in Msh2-deficient mice.Oncogene · 2007Article
- Stem cell gene expression changes induced specifically by mutated K-ras.Gene expression · 2007Article
- Article
- Loss of p21WAF1/CIP1 accelerates Ras oncogenesis in a transgenic/knockout mammary cancer model.Oncogene · 2000Article
- Restricted 12p amplification and RAS mutation in human germ cell tumors of the adult testis.The American journal of pathology · 2000Article
- Suppression of P-gp induced multiple drug resistance in a drug resistant gastric cancer cell line by overexpression of Fas.World journal of gastroenterology · 2000Article
- Genetic determinants of response to chemotherapy in transgenic mouse mammary and salivary tumors.Oncogene · 2000Article
- Induction of mammary gland hyperplasia in transgenic mice over-expressing human Cdc25B.Oncogene · 1999Article
- B-Raf inhibits programmed cell death downstream of cytochrome c release from mitochondria by activating the MEK/Erk pathway.Molecular and cellular biology · 1999Article
- A farnesyltransferase inhibitor induces tumor regression in transgenic mice harboring multiple oncogenic mutations by mediating alterations in both cell cycle control and apoptosis.Molecular and cellular biology · 1998Article
- Increased tumor proliferation and genomic instability without decreased apoptosis in MMTV-ras mice deficient in p53.Molecular and cellular biology · 1997Article
- Apoptosis of human BEL-7402 hepatocellular carcinoma cells released by antisense H-ras DNA--in vitro and in vivo studies.Journal of cancer research and clinical oncology · 1997Article
- Apoptosis -- the story so far....Experientia · 1996Review
- Ras signaling in tumor necrosis factor-induced apoptosis.The EMBO journal · 1996Article
- Cell fusion to study nuclear-cytoplasmic interactions in endothelial cell apoptosis.The American journal of pathology · 1996Article
- Massive programmed cell death in intestinal epithelial cells induced by three-dimensional growth conditions: suppression by mutant c-H-ras oncogene expression.The Journal of cell biology · 1995Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncogenes and oncosuppressors can deregulate cell replication in tumours, and recently have been shown to influence the probability of apoptosis. The effects of human c-myc and mutated (T24) Ha-ras oncogenes on susceptibility to apoptosis were investigated by introducing them into immortalised rat fibroblasts. The resulting family of transfectants showed closely similar measures of proliferation, but widely divergent rates of apoptosis, differing by up to fifteen-fold, that correlated inversely with population expansion rates in vitro. T24-ras transfectants with moderate or high p21ras expression showed reduced apoptosis, and this was reversed by pharmacological inhibition of membrane localisation of p21ras by mevinolin. In contrast, c-myc stimulated apoptosis, and this was further enhanced by serum deprivation. Inducibility of effector proteins represents one possible mechanism of genetic control of the susceptibility to apoptosis, and its investigation showed that c-myc was associated with expression by viable cells of latent calcium/magnesium sensitive endonuclease activity characteristic of apoptosis. In contrast, endonuclease activity was not detected in viable cells of a T24-ras transfectant expressing high levels of p21ras. Thus, there appeared to be differential regulation of susceptibility to apoptosis, positively by c-myc and negatively by activated ras, and this was associated with availability of endonuclease activity. Genetic modulation of apoptosis in human neoplasms is likely to influence net growth rate, retention of cells acquiring new mutations and response to certain chemotherapeutic agents.
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