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The p53 gene demystified -revealing some truths about the p53’s behavior and why it mutates leading to cancer genesis

Author: 
Dr. Isa-Allean Blacksher, N.D., OMD
Subject Area: 
Health Sciences
Abstract: 

It is known that within normal cells, genetic mutations don’t occur and normal cells don’t develop into cancer cells, but within abnormal cells if genetic mutations do develop, the p53 tumor protein should normally monitor this and guard the body from these dangerous cells developing or being replicated – like with cancerogenesis and tumorigenesis. This tumor protein known as the “guardian of the genome” or “cell cycle police” is normally extremely sensitive to cellular abnormalities - its true job is to protect the integrity, genetic growth and development of future daughter cells, thus protecting cellular development in the body overall. Policing, securing and preventing cells from carrying on dangerous genetic mutations with “cell-cycle arrest” and “induced apoptosis” is vitally the most important role of the normal p53 - but just as fraud and corruption is a regular occurrence with authority, these “gene police” can also mutate and become corrupt, immoral and start helping cancer cells progress instead of stopping them. When the p53 starts allowing cell mutation and supporting abnormal cell development this contradictory, reprehensible behavior becomes an obviously incriminating focal point within the genetic “cancer equation” for researchers to question. Asking why and how this change occurs is relevant because this specific moment is connected to “cancer’s start-up.” Detailing this occurrence and all of the pathomechanisms involved in this “switch of the p53” needs to occur so that it can be stopped! Just like with any form of fraud or corruption, exposing and elucidating this inconspicuous shrouded “moment” and identifying all causative factors involved is necessary but difficult for cancer researchers. Due to the striking similarities of this situation to interrogating a corrupt official – this issue similarly needs a non-biased “internal affairs” type of investigation – to dig down deep and bring out all relevant factors into the light. So far, this p53 investigation has been labeled as “difficult to understand” or as “having an unknown cause” but with honest appraisal, the true cause can be identified. Therefore, this article is about exposing the cause of the p53’s switch, examining the p53 from different perspectives and going beyond any traditionally occluded views to find the truth. The benefits of this interrogation will help in the development of new p53 based cancer treatments.

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