There is nothing cool about colorectal cancer

News Article:
Drug Week (May 19, 2006).Colorectal cancer c-fes protein- Tyr kinase functions in growth suppression.

Primary Scientific Article:
Delfino, F.J, Stevenson, H., Smithgall, T.E. (2006).A Growth-suppressive Function for the c-Fes Protein- Tyrosine Kinase in Colorectal Cancer. J Biol.Chem., Vol.281, Issue 13, pg 8829-8835.

Articles that cite the primary article:

Naba, A., Reverdy, C., Louvard, D., Arpin, M. (2008). Spatial recruitment and activation of the Fes Kinase by ezrin promotes HGF-induced cell scattering. The EMBO Journal 27, 38–50, doi:10.1038/sj.emboj.7601943.

Pasder, P., Salem, Y., Yaffe, E., Shpungin S., Nir, U. (2007). FER as a novel intervening target for cancer therapy. Prous Science DOI: 10.1358/dof.2007.032.01.1065737. Drugs of the future 32(1): 61 ccc 0377-8282

Voisset, E., Lopez, S., Dubreuil, P., De Sepulveda, P, (2007). The tyrosine kinase Fes is an essential effector of KIT D816V proliferation signal. Blood, 1 Vol.110, No.7, pp.2593-2599.


Summary

In the United States colorectal cancer is the second leading cause of cancer related death. Researchers have found protein-Tyr Kinase in colorectal cancer operates as a growth suppressor (yeast study). C-fes has been identified as an encoded non-receptive protein that has only seven genes with domain mutations caused by Kinase. The four mutant groups (M704V, R706Q, V743M, S759F) has reduced the C-fes “autophosphorylation and phosphorylation in STAT3 TYR-705 in contrast with the Fes wild type.

Through out the researchers experiment they have found Fes endogenous at the base of the colonic crypts is strongly expressed where it then “co-localizes with epithelial cells” where Musashi-1 a progenitor cell marker. In colon tumors and proteins the Fes gene has been showed to be either low or absent in some patients. Introducing Fes lines into soft agar suppressed the growth. The researchers have named the tumor suppressor gene- protein -tyrosine Kinase. Also it will not be noted as a dominant oncogene for colorectal cancer.

There was a global screening for genomic Kinase in colorectal cancer in relationship with mutations. There were 138 kinase domains and one of the genes C-fes out of seven was consistent in mutations in 182 tumors that were analyzed. Researchers have not been able to find the Fes Kinase Activity in Fes in relationship with colorectal cancer. Another test that was performed was the yeast study. The yeast study was for growth suppression. Fes Kinase activity is blocked by colon cancer mutations.

The secondary source was basically a direct citation and quotes from the primary source. The secondary source just talked about the primary sources abstract. The secondary source was very brief and confusing. I prefer the primary source because it went into more details along with experiments. I trust both sources but the primary more that the secondary because the secondary was exact copy of the primary source.

My additional questions are:
1. Who are at higher risks for colorectal cancers men or women?
2. What ethnicity/race is more prone to colorectal cancer and why?