New targeted treatments for blood cancers: Multiple myeloma, non-Hodgkin lymphoma, genomic marker mismatch repair and myelofibrosis
Dr Merry-Jennifer Markham - University of Florida, Florida, USA
You, like I, have been listening to Dr Usmani talking here. Now he was pretty wide-eyed with wonder at the results of introducing an immunotherapy in multiple myeloma which has lacked this sort of approach. As a doctor, what do you make of those results initially with daratumumab?
I think it’s very exciting to have an immune therapy that can have an almost one in three patient response in a refractory patient population. These are patients who typically aren’t going to respond well to treatment and this opens up a really exciting new door for multiple myeloma.
And these patients had had all of the transplants and the top-line therapies that we’ve heard so much about in recent years and still refractory. What did you make of the fact that it’s deepening these deep responses that he was talking about?
I think it’s very intriguing and it offers… it really gives evidence to the fact that these are very novel therapies that are giving us responses that are unexpected but very exciting.
Dr Sehn was talking about results on obinutuzumab with bendamustine. First of all, what was that study all about? What was the main point here coming out of it from your point of view?
These were patients who were refractory to rituximab, which is a very standard therapy in indolent non-Hodgkin’s lymphoma. In her study she looked at obinutuzumab combined with bendamustine and the results were very exciting in this patient population who are already refractory to rituximab. Obinutuzumab functions in a very similar way, it’s an anti-CD20 monoclonal antibody.
So is it a sort of super-rituximab, then?
It is, it is actually like a very, very potent rituximab.
What did you make of that? Is this serious competition, then, for rituximab?
I don’t think it’s competition, I think it’s just a different agent that we will have in our arsenal of agents to use in indolent non-Hodgkin’s lymphoma. Rituximab still has a very important role and will not be going away.
So what do you think doctors should be taking home from this in the context of indolent non-Hodgkin’s lymphoma?
I think this just gives us another major drug that we can really use in our patient population who are not responsive to rituximab. It’s just another in the growing arsenal of agents for our patients.
And why is it so valuable because it’s indolent non-Hodgkin’s lymphoma?
So these are patients who have an incurable cancer and their response is very much driven, their length of life is very much driven by their ability to respond to the drug rituximab. When they no longer respond to rituximab their prognosis tends to be shorter. This drug is changing that.
Now ibrutinib is something that has entered the scene and we had some very interesting results with a huge clear separation with a hazard ratio of 0.2 from Dr Khan. What did you make of those studies, and that was in chronic lymphocytic leukaemia.
So ibrutinib is established in chronic lymphocytic leukaemia already. This is novel in that it’s pairing with a traditional chemotherapy regimen, bendamustine and rituximab. I think what’s exciting is that repairing a novel therapy with a very standard therapy and getting some very amazing results. So this opens up all new doorways for our patients with CLL.
There was a big separation in the curves. What should doctors be making of that?
I think this is very exciting. It’s not yet standard of care but once that final publication comes out I think this definitely will become a standard of care option for patients.
Now, looking at patients with myelofibrosis, which is a very interesting disease and it can result from different origins. Could you tell me what you thought of the pacritinib study that Dr Mesa was referring to just now?
I think this is also very intriguing. These are patients who are very symptomatic from their disease and many of them may not be able to receive other therapies because of low platelet counts. In this study patients with low platelet counts were included and still were able to have good improvement in their disease and in their symptoms related to enlarged spleen, for example.
And what did you make of the primary endpoint of splenomegaly, that presumably is clinically very significant?
I think it makes sense in a disease that we’re not able to cure but instead palliate and relieve symptoms. It’s a very reasonable endpoint.
And your take home for doctors on this?
I think this does offer patients who have low platelets in myelofibrosis a very viable option eventually.
And they could have freedom from transfusion, things like this?
So it’s symptomatic big improvements?
So this is going to improve quality of life of our myelofibrosis patients.