mCRPC in focus
Transcript: PLATIPARP
Dr Neeraj Agarwal, Professor Karim Fizazi, Dr Bárbara Vieira Lima Aguiar Melão, and Professor Axel Merseburger
All transcripts are created from interview footage and directly reflect the content of the interview at the time. The content is that of the speaker and is not adjusted by Medthority.
So with that, we'll go back to Dr Fizazi. So, Karim, this is a trial, is a phase 2 study of induction docetaxel and carboplatin in patients with mCRPC with homologous recombination and DNA repair deficiency followed by maintenance therapy with rucaparib, so I thought that trial design was interesting. Please, would you like to share your views on this abstract?
Sure, unfortunately, this is a rather small trial, not the investigators for [indistinct] obviously. It's simply, that Clovis that developed rucaparib actually bankrupt, and so during the course of a trial so that they could not treat more patients. But really, the concept indeed is an interesting one.
This is based on what we're doing in ovarian cancer, where typically we are treating patients with cisplatin or carboplatin-based chemotherapy, and then we're using PARP inhibitors as a maintenance strategy, especially in patients with DNA repair defects. And basically, we're using response to chemotherapy as a biomarker to indicate that a PARP inhibitor is likely to work and help these women.
So, for a while there is, you know, the idea that we should do the same in prostate cancer. I know there are efforts and ongoing trial probably at MD Anderson, for example, doing that. But I think this was really the first trial testing the hypothesis. Again, unfortunately, the number of patient is too small to tell. What we show with that, number one, it's doable as expected, but number two also, it appears that the PARP inhibitor is not able to circumvent resistant to taxane plus platin combo suggesting that the mechanism of a resistance between the two, or three maybe, are similar. And actually, this is supported by my own experience the other way around. I've been treating some patients who had, with DDR alterations, mostly BRCA patients who had exhausted a PARP inhibitor with a platin, mostly carboplatin progression. And it's, in my experience, it's been rarely successful with I think just one or two patients benefiting out of probably 20 or 25 patients we've been treating so far. So, again, mechanism of resistance may be really common to the two families of agents, unfortunately.
But I have to applaud the investigators for doing this trial. Again, not sure we can do much with this, but again, not their fault really. We'll need probably more data and more trial to figure out whether instead of testing for mutations for BRCA for example or something else, we should actually treat all the patients with a platin and then select platin-sensitive patients to get a PARP inhibitor. Again, as we do in ovarian cancer, this still needs to be addressed in prostate cancer. We don't know at this point.
That's great, so drawing analogy, learning from ovarian cancer treatment paradigm and applying to metastatic prostate cancer.
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