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IKBKE gene amplification is seen loud and clear in breast cancer tumors!
Primary paper:
Boehm, Jesse S. et al (2007). Integrative Genomic Approaches Identify IKBKE as a Breast Cancer Oncogene. Cell Press Vol.129, pp.1065-1079
Leukemia Patients with KIT-D816 Mutations.
Primary Paper:
Schnittger, S. et al (2006). KIT-D816 Mutations in AML1-ETO-Positive AML are associated with impaired event-free and overall survival.
At face value, what sparked the interest on reflecting on these two articles was the fact that they are both not only caused by mutations, which we know is what gives rise to cancer, but they both can be linked to specific oncogenes. These particular mutations give rise to types of breast cancer and acute myeloid leukemia that can be categorized as “gain-of-function” mutations as opposed to “loss-of-function” which is the category that for instance a tumor suppressor gene would fall under because the gene can no longer suppress the growth or development of tumors. In studying any type of cancer it is important to maybe make this a primary distinction in order to conduct more focused research.
The mutation being examined in breast cancer occurs in the IKBKE caused by gene amplification leading it to function as an oncogene. In terms of acute myeloid leukemia, KIT is a proto-oncogene that when converted causes the D816 which becomes KIT –D816. It is important to note that both IKBKE and KIT-D816 starts off as normal genes. Mutations cause for these once normal genes to become oncogenes which are directly linked to development of any type of cancer. This is one of the first points emphasized in Cancer Biology.
After reading both these blogs a few questions did rise such as if these mutations are only specific to specific forms of breast cancer and leukemia? This then leads me to wonder how many types of these cancers exist. Are there any studies that are looking at the factors that contribute to the occurrence of these mutations; are they environmental or genetic or both?
Monday, February 18, 2008
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