Example sentences for: oncogenes

How can you use “oncogenes” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • For example, the expression of a number of oncogenes, proto-oncogenes, and reduced or absence of expression of recessive oncogenes has been postulated to provide diagnostic and/or prognostic information in human cancers [e.g.

  • Indeed, since tumor necrosis factor alpha (TNFα) is known to suppress hepatic apoptosis [ 9 ] , a function which is considered a safeguard mechanism against neoplasia [ 10 11 ] , the reported ability of RU486 to elevate hepatic TNFα production in vivo and to enhance cell sensitivity to its toxic effects is alarming [ 12 ] . Glucocorticoids also inhibit hepatocellular proliferation [ 13 14 15 ] and modulate the expression of oncogenes and tumor suppressor genes [ 11 ] , via mechanisms involving the glucocorticoid receptor [ 16 17 18 ] , further supporting the notion that inhibiting these receptors may result in harmful effects.

  • The cell surface expressed integrins can control this process by physically interacting with the extracellular matrix proteins and other cell surface proteins on endothelial cells lining the blood vessel wall [ 1 ] . These integrins signal adhesion and migration by communicating with several tyrosine kinases inside the cell, including the Focal Adhesion Kinase (FAK) and Src family kinases [ 1 2 ] . Src kinases control the activation of FAK, as well as the tyrosine phosphorylation of critical substrates that regulate adhesion and migration [ 3 ] . Indeed, colon cancer cells with high metastatic potential have elevated levels of Src activity or activating mutations in the Src gene [ 4 5 ] . One Src substrate that is involved in regulating an important signaling node in this process is the adaptor protein p130 cas (Cas) [ 6 7 8 9 10 ] . Cas appears to play a central role in the transformation process by several oncogenes including ras, ornithine decarboxylase (ODC), v-Src, v-crk, and Bcr-Abl, as these tumors all have elevated levels of tyrosine phosphorylated Cas [ 6 11 12 13 ] . Cells from mice that lack Cas have much reduced migration and are resistant to transformation by v-Src, while expression of Cas anti-sense RNA in cells transformed with ras, v-Src or ODC result in reversion of the transformed phenotype [ 11 14 15 ] . Furthermore, increased expression of Cas can rescue cell migration and adhesion in cells expressing the tumor suppressor PTEN, and can enhance cell migration and adhesion in normal cells, with a major role being played by the substrate domain [ 16 17 ] .

  • There were oncogenes and there were tumour suppressor genes.

  • Indeed this may be universal for oncogenes, since we are not aware of instances when anchorage dependent cells fail to enter a plateau phase in tissue culture.


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