The role of plasma cell biology in multiple myeloma

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Published: 18 Feb 2011
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Dr William Matsui - Sidney Kimmel Comprehensive Cancer Center, Baltimore, USA
Dr William Matsui speaks about plasma cell biology and how this affects cancer growth. In multiple myeloma, malignant plasma cells make up the vast majority of tumour cells and are thought to be responsible for tumour growth. Dr Matsui speaks about the aims and challenges facing his work evaluating if rituximab can be used to treat multiple myeloma and looking to see if signalling pathways can be targeted to prevent cancer development.

Matsui

 

2010 American Society of Hematology Annual Meeting 3rd - 7th December

Interview with Dr William Matsui - Sidney Kimmel Comprehensive Cancer Center, Baltimore, USA

The role of plasma cell biology in multiple myeloma 

 

IV               Interviewer

WM            William Matsui

 

 

 

 

IV               So, thank you for joining us here at ASH; can you tell me a bit about what you’ve been talking about at this conference?

 

WM            So, the… I was part of an ad-hoc session, a scientific session on plasma-cell biology; and so the disease that we’re interested in studying is a disease called multiple myeloma; and really what my lab is interested in, what the session was about, was whether or not there are specific cells that we’d like to call cancer stem cells, within this disease, multiple myeloma. And there were three speakers, and I was one of the speakers, and really, what my research is interested in is whether or not these cells actually exist; whether you can, sort of, target them and eliminate them; and whether it actually matters to the outcome of patients. It’s really… the idea is based on the idea that there are some of these cells within every tumour; and that they are the cells that are actually responsible for making the tumour grow. So, if you don’t get rid of those then the tumour will come back and continue to grow; if you eliminate them, then the tumour stops growing; so that’s really the, sort of… the premise… the clinical premise of the whole concept.

 

So what I described today was just some of the work that we’ve been doing trying to identify the cells, and characterise them, and then give just a couple of examples of how we’re starting to move this idea actually from the lab into the clinic.

 

IV               So, what are some of those examples, and how can we use this?

 

WM            So, right now what we’ve done is we’ve done a couple of trials where we used… what we find is that in myeloma – so, myeloma’s a disease of plasma cells, and plasma cells are the cells that make antibodies; and they come from B-cells. So B-cells are actually the cells that make up things like lymphomas, so there are a lot of drugs that you can use in lymphomas - that are being used in lymphoma - and the question is whether you can use those same drugs actually in a different disease: in myeloma, because the stem cells look like B-cells.

 

So we have… I talked about a trial that we had done in the past using an antibody against B-cells called Rituximab; and using that in multiple myeloma patients; and then the other, sort of, idea that we’ve had is that there are certain signalling pathways that are important in developing from an embryo – while you’re an embryo – and so if you think about cancer as, sort of, a new organ being generated, then it involves embryo-genesis, and so we look at specific pathways involved in development to see if they’re applicable to cancer; and that’s the other approach we’ve started taking.

 

IV               Mm-hmm; so, what’s the endgame for the clinic here; what’s…?

 

WM            So, I think that since the stem cells… it’s a bit of an unusual situation because the stem cells represent maybe one in 1,000, or one in 100,000 cancer cells; so if we eliminate them, you actually don’t see the tumour shrink right away; it’ll take some time; so really, the… we have the clinical trials where we’re testing some of these agents, but the biggest question, or barrier, for us is how do we actually measure that the drugs are effective? So, most therapies, you give the patient the medication, you do something like check an x-ray to see if the tumour gets smaller; and we can’t do that because we are hitting such a small percentage of the cells.

 

So really, right now, our challenge is, how do we know that we’re actually doing what we are intending to do; and a lot of what the lab does is try to figure out, well, what are different ways we can detect this small population of tumour cells.

 

IV               Mm-hmm. So, when are your trials looking to report?

 

WM            So, we have… we had a trial that we reported out about a year ago at the ACR; that was using this antibody Rituximab; and we have a couple of other trials that are, I think, in the phases… or, probably within the next six to 12 months we’ll see some early data.

 

IV               Okay; it’ll be interesting to follow that.

 

WM            Yes.

 

IV               Thank you very much.

 

WM            Thanks.