Expression of c-myc oncogene in coeliac disease.

Author:

Ciclitira P J,Stewart J,Evan G,Wight D G,Sikora K

Publisher

BMJ

Subject

General Medicine,Pathology and Forensic Medicine

Reference12 articles.

1. Cellular oncogenes and retroviruses. Ann Rev Biodifferentiate into mature cells.'3 Cell loss in coeliac disease, as measured by DNA from the washings from perfused segments of small bowel, shows a sixfold increase above normal.'4 There is a concomitant chem;Bishop, J.M.,1983

2. Expression of c-myc changes during differentiation of mouse erythroleukaemic cell lines;Lackman, A.M.; Skonltchi, A.L.;Cancer Res,1984

3. The detection of the increase in cell production in untreated disease, due to c-myc oncogene product in testicular cancer. Br J Cancer a higher number of proliferating cells and a doubling of the rate of cell division. The c-myc gene and its product p62cImYc have been 1985; 52;Sikora, K.; Evan, G.; Stewart, J.; Watson, J.V.

4. Chemically synthesized peptides predicted from the nucleotide sequence of the hepatitis B virus genome elicit implicated in the control of cell cycle activation and differentiation. The activation or expression of p62c/mYc, probably in combination with other oncogene products, is in part responsible for the increase antibodies reactive with the native envelope protein;Lerner, R.A.; Green, N.; Alexander, H.; Lin, F.T.; Sutcliffe, J.G.; Shinnick, T.M.,1981

5. Isolation of monoclonal antibodies specific for the human and mouse c-myc proto-oncogene products. Molecular and cellular Biology in the rate of cell proliferation, decrease in cell cycle time, and abnormal differentiation. The true nature of the regulating mechanism, whereby gluten challenge results in an increase in the rate of cell loss;Evan, G.; Lewis, C.K.; Ramsey, G.; Bishop, J.M.,1985

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