Dr. Brian Durie:
I would very much like to welcome Dr. Abonour, who
will talk about frontline therapy, the initial therapy for myeloma patients. Very,
very important first step for myeloma patients, so very pleased that Dr. Abonour can be with
us today to present this topic. Welcome Rafat. Dr. Rafat Abonour:
Thank you, Brian. Good afternoon and good evening wherever you are. Thank you so
much, Brian. This is an exciting time in multiple myeloma. We've been doing this for a while. And
we hav
en't seen such amazing drugs and amazing results in a long time, so it's a good time I
guess. And hopefully I'll show you some of the progress that we've made in upfront therapy. Okay,
so we are going to try to move the slide flicking. Dr. Brian Durie:
There you go. Dr. Rafat Abonour:
Here we go. I guess when you diagnosed with multiple myeloma, what are the goals of
therapy? I mean, I think two things. Obviously you are diagnosed because you have symptoms related to
the myeloma. You have bo
ne pain, you have anemia, you have kidney failure. We're so excited about
the slide here. Let's see what's going on. Let's go back to the previous slide. My clicker does not
want to cooperate. Okay, previous slide please. Previous, previous, yeah, let's go here. All
right. Symptoms control. That's really important, so we need to get you under control quickly. And
probably part of the important thing is that if you have kidney failure, high calcium, we're
going to hydrate you, we're going to
give you steroid. Believe me, steroids are very important
in the first month or two of therapy. After that, we can ditch them. And obviously you want to
control the disease, you want to make sure that you get rid of as much myeloma as you
can and you want to minimize the toxicity. And the goal is to live as long as possible and we
need to achieve that. So I think what's evolving is that the depth of response matters, how much
myeloma you get rid of is very important. In the old days, the b
est we could do is partial
response, get rid of 50% of your myeloma. And when that happens, the patient didn't live that
long. The median survival 20 years ago used to be two to three years and then 10 years ago, five
to seven years, and now it's getting better. Why? I believe because of the depth of response.
Because look at it. If you leave PR here, that's partial response on the left. What you're
seeing is that it's taking not much that long to go back to where you started. But if you ge
t rid
of it, complete remission is going to take longer. But if you start getting rid of a lot of
myeloma, stringent complete remission, your myeloma protein is gone, your free light chain
is normal, no myeloma cells in the bone marrow, it's going to take much longer to relapse. But
then what happened we start looking at something you heard from Dr. Brian Durie, minimal residual
disease detections, we start improving on that. And when we improve on that and we get rid of the
majority of mi
nimal residual disease, you can see the curve. It takes much longer to relapse And
hopefully when you reach these amazing minimal residual disease undetectable, your relapse may
not happen for 30 years and that means hopefully you are cured, so getting to that level of
response I think is really very important. Okay. So for some reason it is... Dr. Brian Durie:
It's working, it's working, yeah. Dr. Rafat Abonour:
It's working? Dr. Brian Durie:
Yeah, there's a slight delay I think. Dr. Rafat A
bonour:
Yeah, there is delay. I don't know why. Anyway, so basically what we're trying to do here is to how
we detect minimal residual disease. And there are two ways to do it, but why is it important to get
minimal residual disease? I think it's emerging as an important marker of lasting clinical benefit,
so when we look at clinical trials that have looked at minimal residual disease, patients
who achieve minimal residual disease tend to have longer remission and longer survival. And
we us
e two ways. One is a flow cytometry that the IMF really sort of brought to America from Europe.
The flowcytometry using eight colors and 10 colors flowcytometry has a decent sensitivity of one in a
hundred thousand. And in good hands it can be even one in a million. And it's really nice because
what the pathologists, when they're doing the flow, they're looking at actually abnormal plasma
cells and they can tell you if they have one cells in a million or 10 cells in a million. And that's
us
ually informative and it's easy because you don't have to have your initial bone marrow
to know that you have abnormal plasma cells. Abnormal plasma cells are there when you are
diagnosed, when you relapse, and when you still have disease. The other more sensitive assays
is the next-generation sequencing. You have to have the original myeloma samples When you are
diagnosed, we generate a sequence specific for your disease and then we follow you. And that's
after transplant, we can use these
sequences to look at these cells and find them. And the
sensitivity is usually one in a million, so one log more sensitive, so why is MRD useful?
Because it predicts the outcome. Here there are two data's showing if the patients achieve,
this is a large set of patients, if you achieve minimal residual disease negative, you are going
to enjoy a better time without relapse and you're going to enjoy a longer survival. That one on
the right is looking at overall survival. And on the one on the
left, that graph is looking at
progression-free survival, those times without relapse. And the more sensitive the assay, the
results are more actually important and reliable. Okay, so now the thing about it is that if you
get minimal residual disease, it may lead you to enjoy a very long progression-free survival,
living without the disease. And what you can see on top is that even patients with high risk
disease who achieve minimal residual disease are behaving like patients, what we call
standard risk
myeloma, so when we say you are high risk versus standard risk, risk of what? The risk is for a
short remission and short survival and you can overcome that by getting rid of the myeloma to
a level undetectable by these sensitive assay. Because if you don't have the myeloma cells
around you get rid of the high risk clone, that's a good thing because they're not going to
become more aggressive and cause relapse quickly, so that's very important things. Obviously when
you don'
t achieve that you're going to have a sort of shorter time to relapse, so we need to
work on that group of patient to try to improve their outcome. And the next slide, basically these
are data showing effect of sort of maintenance. And this is a study that was done in France
looking at patients who had received induction treatment, high-dose chemotherapy, and
autologous stem cell transplant. And if they achieve MRD negativity, they enjoy and
they had a longer time with good survival. And wh
at it means that achieving MRD negativity
can save the patient taking medication, side effect related to the medications,
and also cost, so this is great things. So most patients with just a year of maintenance
enjoy that. Again, the thing about it is that there is a great benefit of maintenance
but can be a downside for it. And that's why for example some of the work that is
being done, and I'll show you example of clinical trials that focus on achieving minimal
residual disease that is s
ustained and showed that actually that's maybe a different way of
managing patients. All right? And this is just, I'm trying to make the case that minimal residual
disease negativity is very important. And again, when you achieve a sustained minimal residual
disease, the survival is.. Look, it's flat. I mean there's nothing better than seeing a curve
that is flat, when you start seeing a drop-off when people are not doing well either relapsing
or not surviving, that's a not good thing, so M
RD negativity is so important for
improving overall survival. All right, so you saw a similar slide earlier. The evolution
of myeloma therapy is incredible and you can see when few years ago we used to say RVd is a good
thing, Revlimid/ Velcade, Kyprolis/Revlimid, things like that. Now we start using instead
of three drug regimen, we're using four drug regimens. We're seeing amazing result. A lot of
patients still getting consolidation with stem cell transplant and then they post-transplant
setting, you're getting maintenance. It used to be Revlimid alone. Now Revlimid/Daratumumab and
you can see the number of immunotherapies. So we've been around for a long time and we
used to say okay, if we look at Revlimid, it used to be in the relapse setting now is
upfront. Revlimid and Velcade used to be in the relapse setting. Now upfront DARA used to
be just in the relapse setting is now upfront. I really think some of these drugs in the
relapse setting, in the rescue setting, becau
se we understand how well they work and
because we understand their side effect profiles, we probably going to move a lot of these drugs
that Dr. Usmani is going to talk about, earlier on in the course of the disease. And I think that
will generate better responses, more patient getting minimal residual disease undetected, and
hopefully we can cure a large number of patient. What's really important is that in the old days we
used to think about, okay, let's sequence drugs, okay we're going
to use Revlimid Dex first and
then maybe use Velcade Dex. But the most important thing is that using combination therapy.
Combination therapy, that's what made the difference in the survival of patients. Just using
one or two drugs is not enough, three drugs is a great and using four drugs is maybe even better
like adding Daratumumab to RVd, Revlimid/Velcade, it's a great thing, so I think more to come
and it's going to change quickly here, okay. All right, so you heard about the trial that
Dr. Brian Durie
actually led and presented several times now, it's basically we used to say Revlimid Dex is a
good induction treatment for patient not going to transplant. Can we use Velcade/Revlimid Dex? Is
it three drugs better than two drugs? And yeah, I mean you know you saw earlier results that he
Dr. Brian and 101 showed you and basically what you can see is that time to relapse and overall
survival was in favor of using a three-drug regimen, so that makes the case, yes, we need a
t
hree drug regimen because we need to try to get rid of all the different clones that the patient
has because not all myeloma patients have the same sort of correct, the baby, the myeloma
cells coming from the original cells, they don't all behave the same way,
so some will benefit from drug A but not drug B and vice versa, so the
combination therapy makes a difference. The next thing was, okay, can we add something
called Daratumumab, the monoclonal antibody that bind to CD38 cells to Revli
mid Dex, would it be
better than Revlimid Dex? And so this is called the MAIA trial and was done mostly in Europe
and also in North America. But these patients were not transplant eligible, they thought they
are now going to be able to get a transplant, so can we improve their survival? And basically
what it showed here is that there is significant improvement in the duration of response and the
overall response, and a lot of patients who were able to stay on therapy without having to stop
treatment. If you look at the overall response that mean how many patient responded well to the
combination of Dara/Revlimid Dex, you can see it's 93% versus 81%. But if you look at the quality of
the response was much better when Daratumumab was added that mean you're getting more patient into
complete remission, stringent complete remission. And so the initial data looks great and the follow
up data looks even good and better. For example, if you look at complete remission and stringent
complete remission was 51% versus 30% in the Revlimid arm, so clearly combination therapy does
make a difference, does lead to a better response, deeper response. And again translates to better
time without having to worry about relapse of your disease. You can see that the difference
was at 60 months of follow up, yes five years of follow up was 52% versus 28%, so a lot of
patients in the Revlimid arm have relapsed and a lot of patients in the Daratumumab-Revlimid
arm, the combination of t
hree drugs led to a better duration of response and it does look
like it translated to improvement in overall survival. More patients are alive when they get
the three drug regimen versus two drug regimen. And they follow them for some times and the median
time to next treatment, that mean because you can judge the regimen is that how long it took
you to get to a different line of therapy? You know progress because you're not responding
was the DARA arm was only 42 months before you needed
something. I mean not reach for the
DARA arm and for the Revlimid was 42 months, so clearly you can stay without needing a new
therapy much longer when you use a three drug regimen versus two drug regimen. All right?
That's I think an important observation, and the subsequent therapy is just based
on what's available in these countries. All right, so I think the conclusion is that
I think Daratumumab added to Revlimid Dex does improve overall survival and does improve
time without disease
and it takes much longer to needing a new therapy, all right?
Now we are going to go to see the patient who will probably need a transplant
and we already established that RVd, the regimen that Dr. Brian Durie studied is a
really good treatment compared to Revlimid Dex. Can we make it even better? Can we add Daratumumab
to it, the monoclonal antibody to it? Can we make the results better? And this is a sort of
phase two randomized study called the GRIFFIN, Dr. Usmani and his colleagues or w
ere the
leader when he was in North Carolina on this. And basically what they did is that
they added Daratumumab to RVd and compare it to a group of patient who get just RVd
and they give him induction, four cycles, consolidation with two cycles with
transplant in the middle between the induction and consolidation and the patient
get maintenance Revilmid Dex versus Revlimid. And this study's been going on for a while so
we have some mature results, so what does this mature result show? So
first of all, let me show
you the DARA arm is on the left here. The kind of purplish color and the orange-ish color is on the
right is the just Revlimid/Velcade/Dexamethasone. And what you can see is that with each step
the number of patients getting stringent complete remissions increasing and after one
year it reached 63% and at two years 66%. In the RVd arm that stringent complete remission
is lower, so this regimen adding now Daratumumab to RVd for drug regimen is inducing more
respons
es that are deep quality responses. And this is the result of minimal
residual disease testing we talked about earlier that MRD negativity is very
important and what you can see here is that getting MRD negativity increased with each step
in DARA arm from 22% to 64% in the Revilmid arm went from 80% to 30%. So twice as many patients
after two years of therapy are achieving minimal residual disease. That's unheard of, I mean so I
think it makes sense that the four drug regimen are producing
deeper response to a level that
is undetectable in the bone marrow. All right. Dr. Brian Durie:
Okay. Dr. Rafat Abonour:
I have to figure out my clicker here and you can see the time to MRD and activity
is faster in DARA/Revlimid arm and you can see larger and more patients achieved that
while the people who just get Revlimid Dex, they get there but not as high the percentage and
not as fast. So basically the beta duration to MRD negatively was 8.5 months in DARA RVd and took 34
months for
the Revilmid/Valcade Dex to get there, so you get there, you get MRD negativity
faster, and more patient gets that, okay? Dr. Brian Durie:
All right. Dr. Rafat Abonour: I may have done something to my, and obviously
the progression-free survival based on intention to treat was also in favor of the patient who
get DARA RVd, you can see almost a flat line. The majority of the patients have sustained a sort
of lasting remission, so that's what we want. We want to get more patients getting MRD n
egative
and more patients have a sustained control of their disease. We don't want a patient start
relapsing in a year or two, the longer the better, all right? The second thing I think that
is really exciting is this approach by Dr. Luciano Costa from Alabama a very, he recruited
other academic centers and came up with this trial called the MASTER trial and I start calling
him Master Luciano because I think it's really a beautiful way of looking at how we should be
treating multiple myelo
ma. And basically what he did is that, all right we know that four drug
regimen is good and we believe that Carfilzomib is a very good PI, so can we use Daratumumab,
Carfilzomib, Lanalidomide, and Dexamethasone, a combination in a way that will use it for
induction followed by transplant and then get guided by MRD negativity to decide what we
are going to do next, okay, so what did he do? What did he do? Basically what he did is four cycles of induction
with this four drug regimen DARA, Car
filzomib, Lanalidomide, and Dexamethasone followed by
autologous stem cell transplant. He did check MRD after each sort step but didn't make a
decision what to do until after transplant. And if you got MRD assure or MRD-SURE that means
you know get tested twice you're MRD negative, we are going to just watch you. But if you still
have MRD positive cells, minimal residual disease still detected in the bone marrow, he gives
another consolidation four cycles and then decided he's going to do f
our more cycle of induction.
And if they are MRD negative, we're going to call it a day. But if you still have disease,
you're going to get Lanalidomide maintenance, so what happened? Let's see what happened. First of all, if you look at all patients by
sensitive next-generation sequencing assay, he's getting a lot of patients who achieve MRD
negativity and when he looked at patients who use several, the top is the flow, the red and
the blue is the next-generation sequencing. And what he sh
owed is that you're getting
really large numbers of patients getting MRD negativity. And if you look at patients
who have no high risk cytogenetic or one high risk cytogenetic like 17p Deletion,
the response is still really good. The patients who do not achieve such good
results are the patient who have what we call double head myeloma that mean they are two
different kind of high risk features present. And so if you look at the patients who
in term of progression-free survival, the patien
ts who have one high risk cytogenetic or
none actually looks like majority of them stayed without progression with the now follow up of
a couple years or more, but the people who have high risk still not enjoying the same duration of
disease free survival. And the overall survival looks better for the patients who have standard
risk myeloma or one high risk cytogenetic, so the majority of the patients are benefiting
from such approach that is MRD directed go or no go based on where you are
after you get your
induction in transplant, so this is an opportunity for us to say does everybody need maintenance?
Does everybody need consolidation? I think it's generating a lot of questions that ought to be
tested in a bigger trial and I think there's a lot of interest in those kind of trials and
a lot of cooperative group are testing that. I think the conclusion from the MASTER trial is
that next-generation sequence response adaptive therapy is feasible in the majority of the
patient
s and in the multicenter and 72%, 72% of the patient enrolled on this
trial achieve what we call MRD-SURE. And patient with standard high-risk
cytogenetic have similar depth of response and low risk MRD, so I think this is a good
group. If you have one high-risk cytogenetic, you're going to do good and that's an
improvement because we use this thing that these patients are going to relapse in
a year or two, so I think quadruple therapy achieving MRD negative will able to explore this
conce
pt. Where are we still struggling I think, is the ultra high risk when you have for
example, gain a point Q and 17B deletion or a P deletion or some of the translocation 4;14
and things like I mean the 6;14 and like that. I think it's a really amazing trial, so we don't
have really time to talk about all the trials that have been going on, but I'm trying to give
you a flavor of some of the other things that are going on. For example, this is going on in
Germany where they added isatuximab i
s the other anti‐CD38 antibody to the RVd regimen in newly
diagnosed patients, so what did the German show? So basically randomized them a large number of
patients to induction, stem-cell transplant, and then maintenance either with Revlimid alone
or with Revlimid and the antibody Cetuximab. And the goal is to see how many patients will
achieve minimal residual disease. And you can see that by next-generation sequence
flow, which is detecting one cells in a hundred thousand cells. What you
can see is
that when you use the four drug regimen, a monoclonal antibody with RVd, you're getting more
patients enjoying a better overall response rate. And with each step the number of patient
achieving complete remission is increasing. And you see in when you add an antibody,
there are more patients achieving very good partial response, more patients achieve stringent
complete remission, so it is again another trial showing that four drug regimen improve overall
response rate and improv
e the depth of response. And this is just a sort of a breakdown of some of
the side effect that we're seeing. And obviously when you add more drugs, you're going to see
more side effect. Some of it is related to drop in a blood count, some of the related
to infection. For example, in the four drug regimen you're going to see more, for example
infection 43% versus 34%. But I think we are aware that this is happening and we can manage
those things safely. Okay, where are we next? I really thi
nk, I mean the upfront
therapy is evolving and I didn't say, I mentioned to you trials that was testing
three drugs in transplant ineligible patients. I show you trials that testing for drugs in
transplant eligible patients where the induction is for drug regimen and followed by transplant.
And basically what I'm showing you here is that right now I think commonly used in the US for
patients who are going through transplant, at least a four drug regimen, you add a
monoclonal antibody again
st CD38 to VRD or KRD and we have the thing is feasible with
limited toxicity, you're getting deeper response and you're getting more patients achieving
minimal residual disease, negative disease. And I think MRD is becoming an important
measures that we probably start to include it in our assessment of how well our patient
is doing and use it maybe to escalate, deescalate the therapy and guide us where to go
with high risk disease that's still a challenge, but it seems like maybe not your
typical high
risk, the ultra high risk continue to be a group of patients that need more attentions, more
clinical trials to try to answer the question. And I didn't spend a lot of time about transplant.
Is it important? I think if you look at all of the study that's showing much deeper response, more
MRD negativity, better overall survival has really included transplant high-dose melphalan
still play a role until we have better trials in the era of better induction treatments and
better m
onitoring, it still has a room for it, so we still recommend it to our patients who are
eligible. The question is that will we replace it one day with something else? We don't know.
We don't have the data yet, so we still include it. I think that may be my last slide. Let
me see. Okay, so let me just go to one more sort of futuristic trial that is called
the MASTER-2 and it just addresses what I was saying earlier here in the last slide is
that can we now say okay, what he did is that he us
ed consolidation when he doesn't get MRD
negative after the induction and transplant. Well you're going to hear from Dr. Usmani about
the bispecific and the CAR T-cells and he's going to tell you how we are able now to manage a side
effect. How can we control cytokine release and neurotoxicity? They would becoming familiar with
these side effect. We can manage them and we can probably bring those therapy early on. Why should
we wait until the patient has a horrible myeloma that we cannot co
ntrol? If we have a high risk
patient's double head myeloma, we are not getting m MRD negativity, we can consider some of these
new therapy because you're going to hear about the mechanisms of action. They're totally different
than the drug we use upfront. If you're going to keep using the same image, the same monoclonal
antibody, you're just not changing anything, you're not changing the biology. But when you
use the T-cell specific by specific engagement, for example, what you're doing he
re is that you
are making the immune cells work in your favor. You're trying to get your myeloma cells to be
recognized by the T-cells. You're making the T-cells angry, get rid of the myeloma cells
and hopefully get rid of all the ugly cells that are left behind and the patient then will
achieve a sustained MRD negativity and perhaps cured, why not? All right, I think I am here
toward the end, I have to figure out why. Okay, so you better watch it myeloma, so we are going to
take care of y
ou. And so there are three myeloma patients here and one guy trying to pretend
that he's a cyclist, but we're going to take care of myeloma. I think this is a really exciting
time. Some of the drug you hear from Dr. Usmani, I really think they should be used early on
and we start thinking about myeloma as history, not as a continuum that we have to deal
with all the time. With that, I'm done. Dr. Brian Durie:
All right, so thank you so much Rafat, and a number of questions have been coming i
n
and most of them you've touched on and made it clear that they are actually still questions.
One question is about high risk. Were high risk patients included in the GRIFFIN study? And then
obviously the MASTER trial really evaluated high risk with the finding that the ultra-high
risk really still need extra attention, so maybe you and Asad might want to
comment on the current status of high risk. I think earlier you mentioned Asad
that there were seven trials for high risk going on. Som
ebody wanted to know,
well, where are those seven trials? Dr. Saad Usmani:
I'd mentioned that there have been seven trials that have been reported and there
are others that are actively being planned. And we will have three frontline high-risk studies open
in the United States by early part of next year. One is going to be a cellular therapy based
concept or clinical trial where we are going to use CAR-Ts in early alliance. There's another
one which will incorporate bispecific antibodies. A
nd then there's a third a consortium
platform study which will be exploring different questions, whether we need
to change something in induction, whether we need to change something in
consolidation, so I think those are coming, so there's a lot of hope for high risk patients,
but yeah, I mean some of the newer therapies that I'll talk about for relapse patients, we are going
to be moving them up for high risk patients soon. Dr. Brian Durie:
Yeah, maybe you can just touch on that as you go
through a variety
of those new therapies in a moment. Yeah. Rafat, any other comments? I mean the two
comments really are the role for autologous stem cell transplant and basically you've said
that we're still doing that for the time being because it prolongs remission. There was a
question actually which was indicating that maybe the high-dose melphalan increases
genomic damage, which is something that one of our colleagues, Dr. Richardson frequently
talks about. I don't know if there ar
e real pros and cons to doing the stem cell transplant,
but you are still recommending it, right? Dr. Rafat Abonour:
Yeah, I mean I was still recommended it. I mean obviously some of the data on the genomic
instability is probably related to having cells to become genomically unstable. I mean, getting rid
of it to a minimal residual disease undetected, you're not going to worry about genomic
instability, so if you look at all the trials that really had a high level of MRD negativity,
includ
ed induction with four drug regimen followed by transplant and maybe some consolidation or
maintenance, and that's when you're not going to see that, so I really think it's not totally
wrong to say that there's genomic instability. What I really think is wrong is to
think about myeloma is a disease, that we are going to be able to deal with
continuous therapy that also will generate genomic instability. Having myeloma cells around,
they're not going to be behaving. I mean, I always say that
when you live in a bad neighborhood,
you're going to become bad, so you know want to get rid of these cells, so that's why
I sort of like the idea that if it's feasible with a limited duration of treatment to get MRD
negatively, why not? What do you think, Asad? Dr. Saad Usmani:
Yeah, no, I agree with you. I think there are two important things and when we listen
to other experts, it's very important. People say things in passing, so I want to be very specific
about the data. What we comme
nt on is this observation that actually came from the Memorial
Sloan Kettering data set, actually. It was a paper that was published by us in collaboration with
the Arkansas group, some European colleagues and with Ola and Francesca Mora in Miami now. And the
observation is that high-dose melphalan increases the gene mutations in myeloma cells, but there
is no data to suggest that that's a bad thing. Why? Because the PFS is always better
on the transplant arms. And the issue is that transpl
ant has set such a high bar of
progressions free survival. It's going to be very, it's a high bar and we'll have to beat it with
frontline studies, which we do not have now, so until then we have to follow the data because
if anything, one can actually argue the other case that if you have more genomic instability,
you actually create more new antigens that the immune system can take those cancer cells
out better, so I think that there are a few different ways in which we can look at that
data, but I support what Dr. Abonour was saying. Dr. Brian Durie:
All right. Great. Great. I'm going to cut you on, there's a couple of questions. Why
is MRD status not standardized? Well, I think that the definition of MRD negative is standardized in
that we have 10 to the minus five as the cutoff. You're not supposed to be MRD negative unless
you're at least 10 to the minus five. But what I would say is the reporting of it is all across the
board, 10 to the minus four, 10 to the minus five
, 10th of the minus six. And so 10 to the minus six
is obviously better in terms of outcome versus 10 to the minus five. But really we should not be
reporting MRD negative unless one has achieved at least 10 to the minus five, either by NGF
or by NGS. Then a question about the timing. I think that the best timing for doing MRD testing
is still a little bit up in the air. However, one question and some of the data you saw is
that with ongoing therapy response deepens and so about 10 to 15% o
f patients will achieve
their best level of MRD negative after or during the maintenance period. And so actually overall,
one of the best times to do an MRD test is after about 12 months of treatment where the maximum
number of patients will have had an opportunity to achieve MRD negative, if they're going to do
that. In a relapse setting, it is probably a good idea to test the MRD a little bit sooner
more in the six to nine month timeframe, so that maybe covers some of the things. What is
PFS? Yeah, some of these basic questions.
What is PFS? Progression-free survival. This is basically the time that a patient stays in
remission without the myeloma progressing, progression-free survival. How do we know
for high risk? That is based on either the fish testing, which shows those problems
with chromosome 17, chromosome number 1, 414, things like that. Or if relapse has
occurred in that one year timeframe or if some other things have happened like
plasma cell leukemia with myelo
ma in the blood or myeloma in soft tissue areas,
what we call extramedullary myeloma.
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