This is a difficult piece to understand. I am not a scientist but have done my
best to suss out the messages.
Part One in the series can be found here:
Two can be found
Three: chromium 6 metabolism and DNA
Four: Chromium (Cr)-DNA Adducts: http://www.mydepuyhiprecall.com/2013/01/genetic-and-epigenetic-mechanisms-in.html
Five: DNA Base Damage , Genomic Instability, Toxicity and Cr 6
Part Six: Chromium V1 as a Co carcinogen is below. This is the last in the series
p53 and MDM2 in renal cell carcinoma: biomarkers for disease progression and future therapeutic targets?
SourceDivision of Surgery and Oncology, School of Cancer Studies, University of Liverpool, Liverpool L69 3GA, United Kingdom.
If the TP53 gene is damaged, tumor suppression is severely reduced. . The TP53 gene can also be damaged in cells by mutagens (chemicals, radiation, or viruses), increasing the likelihood that the cell will begin decontrolled division. More than 50 percent of human tumors contain a mutation or deletion of the TP53 gene. Increasing the amount of p53, which may initially seem a good way to treat tumors or prevent them from spreading, is in actuality not a usable method of treatment, since it can cause premature aging. However, restoring endogenous p53 function holds a lot of promise. Loss of p53 creates genomic instability that most often results in the aneuploidy phenotype.