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Hello. My name is Dr. Paul Richardson.
I'm the RJ Corman Professor of Medicine at Harvard Medical School,
and I serve as the Clinical Program Leader and Director of
Clinical Research at the Jerome Lipper Multiple Myeloma Center,
Dana-Farber Cancer Institute in Boston, Massachusetts.
It's my pleasure to talk to you today about
the evolving role of novel and next-generation therapies
in multiple myeloma and to share with you today
current status and future directions in our field.
0:27
First, I want to show you my next slide,
which simply is disclosures.
These are my relevant disclosures to the discussion
today and reflect my service on advisory committees,
as well as research funding.
0:40
Now, in the context of multiple myeloma it's
important to recognize that this is not just one disease.
Clearly, multiple myeloma as it sounds is many different diseases.
There's enormous variance between patients and, in fact,
within a patient, disease can change over time.
This recognition of what we call clonal heterogeneity has been
essential in our understanding of what we call risk stratification.
Fortunately, with the advent of novel therapies over the last three decades,
there's been an ability to individualize treatment.
1:12
So as we consider the complexity of multiple myeloma biology,
it's very important to appreciate that not only is
multiple myeloma truly multiple and what
that means is very traumatically between patients,
but it's also important to appreciate that it varies and ebbs and flows and
changes within a patient during the course of the natural history of the disease,
and in this slide I seek to capture that by illustrating to
you the clonal evolution and the matched genetic events
that myeloma evolves from its precursor states of MGUS and
smoldering disease to active disease and then to its relapsed refractory form.
Then the far right of the slide,
I really wanted to emphasize here,
and I think quite seminal work from my colleague Dr. Nikhil Munshi
looking at whole genome sequencing in the top slide of one of our patient's diagnosis.
As you can see, there are 5,000 mutations in this patient's disease at that time.
This patient then undergoes induction remission treatment,
autologous transplant, consolidation, and maintenance and then relapses.
As you can see in the bottom slide, at relapse,
the patient is challenged by 12,000 mutations in his disease.
This I think points to
the extraordinary mutagenic thrust of this illness and how we need to understand
better all the clinical implications of
such genetic instability and what that means for a patient over time,
especially as we now blessed fortunately with
multiple new treatments and modalities that can hopefully improve outcome.
