Secrets of Cancer-Fighting Gene Uncovered

[ThreeWs]

Welcome progress for the poor prognosis folks.

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biosciencetechnology.com/ne...

[Kwenda]

Excellent progessive Australian research yet AGAIN,.

Dick

[AussieNeil Partner Administrator in reply to Kwenda]

Yes, Venetoclax arose from research from the same place: healthunlocked.com/cllsuppo....

Coincidentally, Chris Cllcanada just posted about related research specific to CLL being done by Dr Anna Schuh:

healthunlocked.com/cllsuppo...

[Peggy4]

Wow!😀

Peggy

[Mystic75]

Great article - thanks for sharing!

[Bubnojay]

So much hope for the future.

Bubnjay1

[Momlyn]

Could someone explain how this affects those of us who have 17p deletion and TP53 deletion?

[ThreeWs in reply to Momlyn]

Hi Momlyn,

The importance of the TP53 tumor suppressor gene is unquestioned BUT this gene or any other gene is not a lone actor. Think of any marker that we get from FISH testing or other lab results that identifies specific biomarkers that help define how aggressive or indolent our CLL is likely to be. Each patient has a unique palette of these markers many correlated to known chromosomes and many that are considered not important enough to report or are unknown. Dysfunctional genes are in the form of deletions, fusions and mutations of varying amounts of DNA.

TP53 gene is a high “judge” in our biochemical court system for determining the fate of whether a cell lives or is given signals to die. TP53 presides over whether or not a damaged cell can be repaired or must go the way of Apoptosis (programed cell death). If the TP53 gene is itself damaged or deleted it allows for cancer or defective (oncogene) cells to escape apoptosis and for chemo to be ineffective for killing off cancer cells.

Think of TP53 as important but only one data point Dot in a puzzle that is CLL. Every gene that is connected to and “talks” to other genes in a complex of dots. To complete the puzzle you need all the dots and how they network.

In the goal of not just CLL but all cancers, is to not get the cancer in the first place and secondly, if you get it you want a cure. The finding touted in this eye-candy finding, if correct, leads to a newly discovered understanding of the faulty repair work of damaged DNA overseen by the TP53 gene. Think of all the patients who have familial CLL and the anxiety for their offspring. In that scenario it suggests a faulty DNA repair mechanism that just might be part of an defective inherited TP53 gene and or one or more of the genes it communicates with. I am speculating here as the great-uncredentialed-one🙃 but having a better understanding for DNA repair and how it links to TP53 would be a big deal.

The worst cases of CLL are CK (Complex Karyotype) with 3 or more chromosomal aberrations and in second place 17p- patients because that is where TP53 resides. DNA repair is critical and in the example of a rare flavor of DLBCL (Diffuse Large B-Cell Lymphoma) called PMLBCL (Primary Mediastinal Large B-Cell Lymphoma) which is very deadly and therapy resistant – researchers state: ”we detected abundant chromosomal alterations, including loss of parts of 2p, 6p, 20q, 22q, and gain of an X. The 2p region lost contains MSH2 and MSH6 loci that, along with MLH1, MLH3, MSH3, PMS1, and PMS2genes, work coordinately in sequential steps to initiate repair of DNA mismatch.” & “findings raise the possibility that the extreme mutability of this patient's tumor is related to deficiency of DNA repair genes.” “DNA repair genes are known to be mutated in DLBCL and in lymphomas non‐responsive to chemotherapy suggesting that mutations in DNA repair genes could be the cause of their refractoriness to therapy.” Ref: onlinelibrary.wiley.com/doi...

Note the number of “dots” and that MLH1 is but one in a family of several repair genes as is often the case with singled out markers.

Speculating that MLH1 is the key player and eventually we could detect and correct this key dot, might the cancer not develop for a number of people? Bench to clinic application is likely to take awhile but the pace of interventions is increasing. Stay tuned.

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