Received results from Foundation one, and we need help understanding the results.

[benninger]

Genomic Findings: ATM L807, MYC amplification, KDM6A R219fs*33, MCL1amplification, RAD21 amplification . Biomarker Findings: Microsatellite Status-MS-stable, Tumor Mutational Burden-TMB-intermediate (16 Muts/Mb Ductal Adenocarcinoma. Currently his PSA is .01 on Zytiga, prednisone and Loupron. Finished chemo in March. We should have asked questions. Dr. only gave us first three pages of report .

[Hidden]

From what you posted, the only "actionable" mutation that I know of would be the ATM, but I'm not very knowlegable on this subject. I read this on ATM: Approximately 5% of prostate cancer specimens exhibit somatic ATM alterations including some 1% of pathogenic germline mutations. ATM acts a controller of cell cycle checkpoint signalling pathways that are required for cell response to DNA damage and for genome stability. ATM has been reported to be highly activated in prostatic intraneoplasia and some missense variants of the ATM gene confer a moderate increased risk of prostate cancer, ATM mutations were observed in affected individuals who achieved clinical responses to PARP inhibition and predicted to benefit from this therapy.

My understanding is that as long as you are getting a good response from your second-line ADT Zytiga you would continue that and do a targeted treatment based on the gene mutations later. That concludes my knowlege on the subject. So these are some things you could discuss with your doctor. Good luck and let us know what he/she says.

[benninger in reply to Hidden]

Thank you...Dr. said we were good until zytiga stopped working. He said PARP inhibitors for the ATM l807* and Pd-1mAb for the tumor mutations but he didn't say anything else and when I got home the mind thinks of a hundred things and I couldn't find much or UNDERSTAND what I did find. Thank you for taking the time to reply

[Hidden in reply to benninger]

I agree with your doctor.

Unfortunately, there are not enough targeted treatments available at this time for the various mutations. PARP inhibitors are useful for several of them. Hopefully the Zytiga will work for a long time and if that's the case you might consider doing the genetic testing again. Probably not something you want to hear, but these mutations develop over time do to the "survival of the fittest" cancer cells that occurs during treatment. Sadly, fighting this disease is a lot like "whack a mole".

[benninger in reply to Hidden]

Thank you , You are so right it is just like a game and everyday we all face a different challenge. best of luck and lots of prayers your way