With all the new options for therapy in Prostate cancer, one may wonder if there is still interesting topics and areas of unknown in Prostate cancer. One thing is for certain, there is no definitive cure for Prostate Cancer and therefore research and progress in this field remain to be accomplished. And with each conference, one continue to learn new areas of research emphasis. In Prostate cancer, data free Zones continue to abound as discoveries are made!
Areas of Data free Zone!
------------------------------This is where in clinical practice things are done although there is no clear data to support our practice.
1.Although we all know that patient who fail Lupron should go onto "withdraw", there is no biomarkers to determine who should be chosen for this option. Often we bypass this withdraw as an option to jump now to Abiraterone or Enzalutamide because we can! This is however an important period of no therapy that our patients can enjoy with no therapy or side effects!
2.How to determine the most efficacious treatment? or what are the most predictive Bio-markers?
3.Are combination therapy better than sequential use of major therapeutic options
4.Is deterioration of performance status a clear indication of exclusion of spileucel-T use since this drug may take up to 6 months before the curb separation to indicate benefit, should Performance status be used for early initiation of chemotherapy...?
4.what is the role of new immune markers?
CD54 upregulation has been used for the appropriateness of use of spileucel-T? what about CTC - ARv7 the so called "negative Predictor Biomarker"?
5.Given the impact of the marrow, should RAD 223 come always prior to Chemotherapy or after this? should documented radiological progression in the bone be the indicator of RAD 223 in a pain bearing patient with metastatic Prostate cancer patient? And how to interpret PSA fluctuation in RAD 223 treated patient? Should we always continue to associate Lupron or other anti-androgen treatment that adress non bone disease (or visceral disease) while on RAD 223?
6. What in hell is "liquified semen" while on treatment for Prostate cancer? And now the role of Eosinophilia in so called "good responders" ? should alkaline Phosphatase, or PAP be better biomarker in patient treated will spileucel-T. Or is-it PA-2024? Could proof of long term memory by T-cell be evidence of further role for a boost in Spileucel-T. What is the role of "Antigen spread"? and what that has to do with Cancer preservation and resistance?
7Notion of AR Variant that apparantly lack a binding domain for membrane area activity but can still act deeper into the Nucleus, and is -t here that Enzutamide may be more effective since it impairs deep localisation at AR cellular path...and what are the co-factors allowing this deep action of the variant AR. Should we really look for AKT/PI3K upregulation in resistant diseases? And actually which gene cross-talk with the AR in resistant cancers? And the role of combination therapy in these setting...
8.Instead of fighting all these side effect, should we just push further Orchiectomy?
9.role of Gleason once treatment has been started?
10. Is testosterone level <50ng better than 20ng to define hormone resistance disease?
11. how to appreciate cardiac risk in patient on treatment for metastatic Prostate cancer
EH! patient on Abiraterone, always use Prednisone
but you don't have to for Enzalutamide
and always use GCSF while on Cabazitaxel because the one who died fron this chemotherapy did so after the first cycle of chemotherapy! experimenting without it at your own risk!
etc...and I can go on for days...at CRBCM, we keep ourselves informed! still a lot of work even in Prostate cancer....
No comments:
Post a Comment