Highlights
I regard genetic screening as mandatory in all CLL patients, and by genetic screening I mean it is mandatory to have a FISH panel for the commonly involved chromosomes, so 11, 12, 13, 17 […] But further than FISH panel, I consider mandatory NGS mutational analysis, […] and I stress NGS because subclonal lesions, you cannot see them by Sanger.
If you have TP53 disruption you basically skip chemotherapy, so that’s the concept, the difference is that in this case you go immediately to let’s say ibrutinib plus or without rituximab, here we have a lot of arguing about if the patient is fit, so they’re not dying for rituximab I would say, I would give them an anti-CD20 in association, but otherwise there are not such strong data for the combination. But let’s say you use new drugs, ibrutinib, and later on venetoclax or whatever, if you have a patient with intact TP53, I still would like a little bit of additional information, so if I can apply my NGS panel I will. If the patient is carrying BIRC3 mutations as well, although these are rare, then I would consider, like for the TP53-mutated patients, to put them on targeted treatment immediately. Otherwise, the other patients without these mutations can receive chemo. Then, based on age and performance status, you can have either chlorambucil + anti-CD20 antibody, or you can have, for example now it’s relatively popular to also go with bendamustine + rituximab. We are not always doing FCR, so the fludarabine + cyclophosphamide + rituximab regimen, but this is also quite popular in CLL.
Overview
An Italy-based key opinion leader (KOL) provides insights into prescribing habits, key marketed brands, and late-phase pipeline therapies for CLL. Key pipeline assets highlighted include non-covalent BTK inhibitors, Brukinsa, and CD19-directed CAR-T therapies.