I havent seen much posted re the important issue of impact/understanding/treatment of methylation of our Pca related genetics. I saw the following article
Although its a statistically based analysis, I hoped it would help in understanding this potentially important way our genes can be negatively affected by the process of methylation.
In my case, Dr Snuffy Myers, after he had 2 Caris lab genetic tests (2014 & 2016) done on my removed prostate, he reported that I had a mutation on my ERBB2 gene and although my PTEN gene showed as unmutated, it had been silenced by hyper methylation - losing an important Pca braking function.
With Dr Myers retired and a need to review my Pca clinical background, I reread both of the Caris lab reports as well as the referral letter, describing my case, to Dr Drake. Neither the Caris lab reports nor the referral letter mention the PTEN methylation issue. To be sure, I called Caris labs and they said they didnt have any other info regarding my case. Also, all Guardant360 blood biopsies tests have been negative.
As a result, I was interested if anyone knows any other way the Dr would have known or inferred that my PTEN was hyper methyalated?
Also, if anyone has other such articles that hopefully, dont depend upon just statistical analysis for this important part of our Pca risk profile?
Written by
podsart
To view profiles and participate in discussions please or .
But, be aware that this class of drugs is associated with numerous serious adverse reactions including anemia, immune suppression, hepatic and renal toxicity, hypokalemia, congestive heart failure, etc.
It seems that ERBB2 mutation is the ERBB2/HER2 mutation.
"ERBB2/HER2, best known for its role in breast cancer tumorigenesis, can be targeted by two types of pharmacological manipulation: antibody therapy against the extracellular receptor domain and small molecule compounds against the intracellular tyrosine kinase domain.""
""The HER2 (official name ERBB2) gene encodes a membrane receptor in the epidermal growth factor receptor family amplified and overexpressed in adenocarcinoma. Activating mutations also occur in several cancers. We report mutation analyses of the HER2 kinase domain in 7497 histologically diverse cancers.""
It is about my pay grade, but perhaps Dr Myers mentioned PTEN because PTEN and ERBB2 participate in the regulation of the PIK3/AKT pathway.
""Phosphatase and tensin homolog deleted on chromosome 10 (PTEN)/phosphatidylinositol 3-kinase (PI3K)/AKT constitute an important pathway regulating the signaling of multiple biological processes such as apoptosis, metabolism, cell proliferation and cell growth.""
""The HER2-PI3K pathway is the one of the most mutated pathways in cancer. Several drugs targeting the major kinases of this pathway have been approved by the Food and Drug Administration and many are being tested in clinical trials for the treatment of various cancers""
""Phosphoinositide 3-kinase (PI3K) activity is stimulated by diverse oncogenes and growth factor receptors, and elevated PI3K signaling is considered a hallmark of cancer. Many PI3K pathway-targeted therapies have been tested in oncology trials, resulting in regulatory approval of one isoform-selective inhibitor (idelalisib) for treatment of certain blood cancers, and a variety of other agents at different stages of development.""
Tango.... You do a lot here yet don't get that much credit. Therefore I give you lots and lots of credit. Keep up the help..... we all need it.. Thank you!!!
Content on HealthUnlocked does not replace the relationship between you and doctors or other healthcare professionals nor the advice you receive from them.
Never delay seeking advice or dialling emergency services because of something that you have read on HealthUnlocked.
DNA Methylation Readers and Cancer: Mechanistic and Therapeutic Applications
