I looked through Nature/Cell/Science papers and found people liked to present their results that contained the most well-known cancer drivers in their final results. And they tended to be cautious when they made their conclusions. And this way will lead to a wider acceptance of the readers. But it does little help for affluent new findings when we used HIGH-throughput datasets.
So I would like to know how many cancer drivers we can obtain now. Does anyone have some suggestions?
Cancer is a very complex, cell-type specific pathological condition which is an outcome of a multi-hit, multistage disease process, so researchers are cautious about the results and conclusions they make. But of course if your results are coming from data that is reproducible and statistically significant you may come out with the new findings. And today with available high through-put data analysis with more sophisticated software tools with network and pathways analysis, one can identify tumour type-specific passenger and drivers' gene networks that may hold future answers for tumour diagnostic and/or therapeutic biomarkers for complex aggressive tumours or unknown biomarkers for new types of tumours identified, so new informations will help acheive such goals.
I add two recent refs which will help you for with their information to proceed with your thoughts and queries, if you haven't already read them. Good Luck!
1. Br J Cancer. 2012 Mar 13;106(6):1107-16. doi: 10.1038/bjc.2011.584. Epub 2012 Feb 16.
A network-based, integrative study to identify core biological pathways that drive breast cancer clinical subtypes.
Dutta B, Pusztai L, Qi Y, André F, Lazar V, Bianchini G, Ueno N, Agarwal R, Wang B, Shiang CY, Hortobagyi GN, Mills GB, Symmans WF, Balázsi G.
Source
Department of Systems Biology - Unit 950, The University of Texas MD Anderson Cancer Center, 7435 Fannin Street, Houston, TX 77054, USA.
2. http://www.cancernetwork.com/triple-negative-breast-cancer/content/article/10165/2056401
Another paper that could be useful is:
Mutational heterogeneity in cancer and the search for new cancer-associated genes by Michael S. Lawrence, Petar Stojanov, Paz Polak et al. published on Nature (2013) doi:10.1038/nature12213
...and a review:
"Cancer Genome Landscapes" by Bert Vogelstein et al. Science 339, 1546 (2013)
FYI - Foundation Medicine is one of a few labs that tries to keep up on all cancer alterations that seem like they might have any potential value, but this is more than just "drivers" (i.e., ones whose effect, if reversed, would stop the cancer at least for a while). I think they update their list about every 6 months so there will be more soon. It's a handy pretty-comprehensive list, though:
http://www.foundationmedicine.com/pdf/resources/ONE-I-002-20130529_FoundationOne_Technical.pdf
The shortcut in the tumor cell is a proliferative mutation that allows replication. These genes are important, all other mutations are secondary events. Tumor formation becomes easy to understand.
Riede,I. (2012)
Inhibition of Apoptosis in ALL-1 Leukemic Cell Lines: Allowance of Replication, Constant Repair Replication, Defect DNA Damage Control
J Cell Sci Ther 3:133
doi:10.4172/2157-7013.1000133
http://www.omicsonline.org/2157-7013/2157-7013-3-133.php?aid=10462
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