Articles with the keyword: 
Once suspect protein found to promote DNA repair, prevent cancer
sea-maid submitted, created time 4 months 1 week (esciencenews.com)
An abundant chromosomal protein that binds to damaged DNA prevents cancer development by enhancing DNA repair, researchers at The University of Texas M. D. Anderson Cancer Center report online this week in the Proceedings of the National Academies of Science. The protein, HMGB1, was previously hypothesized to block DNA repair, senior author Karen Vasquez, Ph.D., associate professor in M. D. Anderson's Department of Carcinogenesis at the Science Park - Research Division in Smithville, Texas. 
Synergistic response to oncogenic mutations defines gene class critical to cancer phenotype
kavin submitted, created time 6 months 2 days (www.ncbi.nlm.nih.gov)
Here the authors show that a large proportion of genes controlled synergistically by loss-of-function p53 and Ras activation are critical to the malignant state of murine and human colon cells. Notably, 14 out of 24 'cooperation response genes' were found to contribute to tumour formation in gene perturbation experiments. In contrast, only 1 in 14 perturbations of the genes responding in a non-synergistic manner had a similar effect
Breast Tumor Cells Have This Molecular Characterization
jerry submitted, created time 6 months 2 weeks (ajp.amjpathol.org)
A detailed understanding of the assortment of genes that are expressed in breast tumor vessels is needed to facilitate the development of novel, molecularly targeted anti-angiogenic agents for breast cancer therapies.
This research found Of the 1176 genes that were differentially expressed between tumor and normal vascular cells, 55 had a greater than fourfold increase in expression level
Tumor cells share oncogenic receptors
sea-maid submitted, created time 6 months 3 weeks (www.jcb.org)
Mutant receptors made in one tumor cell can be passed to tumor cells lacking them.
In this study, the authors found that glioma cells expressing EGFRvIII transferred this errant receptor to nonexpressing cells via microvesicles--small plasma membrane buds. The microvesicles were produced in abundance by the mutant expressing cells and were widely taken up by receptor-negative cells
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