2007 they thought it was a worthy marker of cell progression to malignancy
http://ar.iiarjournals.org/content/27/2/979.full.pdf2008 they thought that it was a good prognosticator of better survival, useful enough to suggest that increased aggressive treatment in patients with its expression wasn't needed
http://cebp.aacrjournals.org/content/17/2/414.full2009 they thought it didn't mean crap and was an unreliable marker
http://www.ncbi.nlm.nih.gov/pubmed/191920552011 they found p16 may not be useful for distinguishing hyperplastic oral epithelium from dysplastic oral epithelium (no predictive value)
http://www.scielo.br/scielo.php?pid=S1806-83242011000100007&script=sci_arttextAnd in a review of a ton of articles (a three page bibliography), the Brits found the
P16 regulatory gene has been extensively studied (no shit) and is a promoter of hypermethylation common in OSCC (p16:76%) however, no significant correlation with clinicopathological characteristics or prognosis has been observed. Further, these epigenetic aberrations have also been shown in �normal� and dysplastic oral lesions, (which mean that it is worthless as a marker) BUT after stating that clearly they go on to conclude the exact opposite, that it may be involved in the early stages of carcinogenesis and related to exposure to alcohol and tobacco. So separate for the whole
HPV issue they conclude that it is more tied to the tobacco carcinogenesis pathway.
http://research-archive.liv.ac.uk/288/2/05-047-draft9-26-5-05.pdfI could go on here, but in the end, this is the contradictory nature of research, interpreting what it means, whose studies have bias in them, whose have too few participants or samples to be meaningful, and so much more BS.
MY OPINION, stated above is that after reading these things about p16 till I am almost blind for 5 years, is stated in the previous post:
There is much debate about what all this means in finite terms, and lots of speculation from researchers with grossly different findings in what are mostly animal studies and small human studies. Some say that it NOT a reliable marker for oral cancers, others the opposite. We will know soon. If it is indeed a marker that has value, recent research from about two years ago shows that the good news is that the prognostic significance of tumor
HPV status in oropharyngeal cancer treated with chemoradiation, (which is that there is a survival advantage) also shows that p16 identifies a larger group with an improved prognosis as well. The
HPV negative, but p16 positive population also has a better prognosis compared to patients with
HPV neg/p16 neg tumors. So clearly (really? after reading all that) it has prognostic value, some of which is good to hear, some of which is on the not so good side of things. It is not a stand alone prognosticator, it does not significantly impact treatment decisions at major institutions, and depending on which researcher you listen to with glazed eyes over these cell modulating proteins you will come away with a different answer today. Tomorrow is going to be different because they have been beating this marker to death looking for a Holy Grail of prognostic opportunity, and they soon will thumbs up or down it as a meaningful component of the question.
I think it is going to be just another small piece of the tumor suppressor protein/gene puzzle and never be a stand alone marker of significance, without considering the many other contributions of the many other cell regulators (p53, RB etc.) at the same time.
