I read a post today that it’s more common that patients on Abiraterone (Zytiga) are more prone to their Prostate Cancer morphing into Neuroendocrine Carcinoma?
Is this true?
Any other Medications that are prone to have it Morp into Neuroendocrine Carcinoma ?
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Shorehousejam
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Emerging evidence suggests that NEPC develops as a transdifferentiation from prostate adenocarcinoma, in response to androgen deprivation therapy and/or treatment with inhibitors targeting AR signaling pathways (5). During NEPC development, cells lose their granular structure and demonstrate small cell neuroendocrine-like morphology, positive for typical neuroendocrine markers such as chromogranins, synaptophysin (SYP), and neurospecific enolase (NSE) but little or very low levels of AR and AR-regulated gene expression (6). Since AR signaling is required for epithelial cell differentiation during prostate development, inhibition of AR pathway likely initiates developmental reprogramming of prostate adenocarcinoma to neuroendocrine tumors through a transdifferentiation mechanism (7). Unlike prostate adenocarcinoma, neuroendocrine tumors are very aggressive with median cancer-specific survival is less than 2 years (8). Conventionally, neuroendocrine prostate cancers have been managed clinically with cisplatin-based chemotherapy regimens, however further identification and understanding of the oncogenic drivers of this phenotype necessitates the development of novel targeted therapies.
It appears so, but it's not 100% of the time. I remember a study by Aargawahl that said 20% of one study population had so-called "treatment-emergent" NEPC that had been taking AA.
No. Whoever wrote that didn't understand that the chances of treatment-emergent NE increases after any treatment. Kill off enough cancer cells and what's likely to be left over is impervious to whatever you've used to treat it. That might be NE or it might be something worse.
Exactly right! The androgen independent cells will take advantage of a non competitive environment and start multiplying and using different available pathways and or mutate as in NEC.
That is why i am doing BAT, in order to keep the beast fed intermittently but caged in the hopes that the beast is content to stay in its cage.
I hope it works for you, and that you are doing it as part of a clinical trial. So far, it has only been advantageous in men with certain androgen receptor characteristics.
I certainly hope it works also! Not part of clinical trial as i am HSPC. I don’t like the idea of but understand the rigidity of clinical trials but i am adjusting my cycles per my PSA responses. That can’t be done in the present BAT trial formats. My OC at MGH is monitoring me, plus data is going to Denmeade at JOHNS HOPKINS.
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