Transcriptional Deregulation Hypothesis

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Synopsis
Scientists believe that one of the more probable ways for cancer to occur is through the process of transcriptional deregulation. Experiments were conducted by a group of researchers to conclude whether this hypothesis was one of merit or one that should be revised. These analysts first stated the process by which cancer can occur based on multitudes of mitotic genes and proteins. One way oncogenic cells are able to form, based off of the original hypothesis, is through transcriptional malfunctions during mitosis. The tumor suppressors that are used in cellular division lose their function due to mutations, and the genes that have the ability to become cancerous due to over expression and/or mutations become more highly functioning. This gain and loss of function results in the instability of the chromosomes undergoing the process of cellular division. Some genes and proteins that may be mutated or deregulated include, but are not limited to, Plk1, E2F, SAC, Cdc20, STAG2,
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Ghatak, and P. Das (the scientists mentioned previously) conducted included the study of 526 genes accessed from a list that included 572 verified mitotic genes found on a COSMIC v67 database. The percent mutation for each gene was calculated and resulted in two separate, testable hypotheses. One stated that a mutation in the SAC (Sacisn Molecular Chaperone; gene used to encode sacsin, which is predominantly found in the nervous system) genes, as well as similar genes, inhibited pivotal checkpoints in mitosis, allowing mutated cells to continue replication. The other stated that a mutation that resulted in the deactivation of any gene vital to the cell would cause the cell to kill itself in a process called apoptosis. They were also able to reason that mutations in the checkpoint genes themselves were not the cause for the unusual checkpoints in cancerous cells; these mutations simply change the protein levels in the new

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