Clusters of CDK2, CCND1, and CMYC genes involved in cancers: Acute Lymphocytic Leukemia (ALL) as a model
Cancer is not a single disease but it involves changes in multifunctional genes, the causes for these changes remain less understood. It is now becoming clear that multiple genes orchestrate to turn on the carcinogenesis process. These genes involve several signaling pathways which then characterize uncontrolled cell divisions. Our aim was to study cell cycle genes CDK2, CCND1, and c-MYC to determine their clustering in the evolutionary pathway and to understand their diversions leading to continued cell division processes. Since Acute Lymphoblastic Leukemia (ALL) is the most prevalent form of cancer in children we took this as a model for analyzing the role of these genes in the leukemia process. The prevalence/spread of these genes was found to be very limited in the animal kingdom; hence the question is whether this may be due to the fact that during evolution in time there could have been loss of some functions or mutations in these genes which relates to the switch function of these genes. Alternatively, have they evolved in a way which we are unable to trace due to limited methodology? Further, with the results analyzed so far we can imagine that these species in which we found the presence of these genes across the animal kingdom could have had cancer like diseases during their lifetime. We conclude that each of these genes formed several clusters which were typical of their role/functions in ALL.