April 16, 2023 • 44 mins
In this episode of The Onco'Zine Brief, Peter Hofland talks with two experts about their research and the impact the outcomes from these studies may have on the treatment of patients diagnosed with cancer.
First, Hofland talks with Christopher Heery, MD.
Dr Heery is a board-certified medical oncologist with primary expertise in the translational and clinical development of immunotherapies, including, but not limited to PD-L1 inhibitors, therapeutic cancer vaccines, immune suppressor modulator, adoptive NK cells, and other therapeutics.
As the chief medical officer at Arcellx, he is responsible for medical oversight, clinical strategy, medical affairs, and regulatory strategy for the company’s pipeline of novel – investigational drug.
In the second half of the program, Hofland talks with Srdan Verstovsek, Dr Srdan Verstovsek, MD, PhD., a Medical Oncologist and Professor in the Department of Leukemia at The University of Texas MD Anderson Cancer Center, about some of the developments in the treatment of myeloproliferative neoplasm, which are types of blood cancer that begin with an abnormal mutation or change, in a stem cell in the bone marrow. These change leads to an overproduction of any combination of white cells, red blood cells and platelets – and results in a number of diseases, including:
In a new episode of The Onco'Zine Brief, Peter Hofland talks with David M. Cognetti, MD, a Professor and Chair in the Department Head and Neck Surgery at Thomas Jefferson University Hospital in Philadelphia.
Hofland and Cognetti talk about head and neck cancer and a novel treatment approach called Photoimmunotherapy.
Head and Neck Cancer
According to the American Cancer Society, Head and neck cancer accounts for about 4% of all cancers in the United States. In the United States in 2023, an estimated 67,000 people will be diagnosed with head and neck cancer and about 15,000 patients are expected to die of the disease.
Today, many cancers of the head and neck can be cured, especially if they are found early. And while eliminating the cancer is the primary goal of treatment, preserving the function of the nearby nerves, organs, and tissues is also very important.
Beyond Current Treatment
Photoimmunotherapy is a recently developed hybrid cancer therapy to treat diseases by linking specific antibodies with photosensitizers to form photoimmunoconjugates.
But let’s go back to the beginning.
Surgery, radiation, and chemotherapy have dominated the treatment of oncologic. These therapies aim to eradicate cancer cells but, unfortunately, do that at the expense of normal, or healthy cells/ In turn, this can lead to severe and sometimes lethal side-effects.
Overall, the success of surgery, radiation and chemotherapy is measured by what we call a ‘therapeutic index.’
This ‘therapeutic index’ compares the potential benefits of treatment to the potential risks associated with treatment.
Unfortunately, the unintended, off-target side effects of these therapies can have profound effects on the health-related quality of life of patients.
For example, both radiation and chemotherapy sometimes preferentially kill lymphocytes much earlier than cancer cells because of the increased radiation sensitivity and high proliferation rate of lymphocytes, potentially leading to dose-limiting toxicity for some chemotherapy regimens.
To find a solution, researchers have developed new therapeutic strategies. And while these therapies have created an exciting new direction for the treatment of cancer therapy, there remain limitation to these novel approaches.
Now, in theory, the perfect cancer therapy would both directly destroy cancer cells to minimize residual cancer cells as well as activate the local host immune response to wipe out remaining cancer cells.
And while such a therapy would be highly selective for cancer cells but have minimal or no off-target effects in the tumor microenvironment.
First, Hofland talks with Christopher Heery, MD.
Dr Heery is a board-certified medical oncologist with primary expertise in the translational and clinical development of immunotherapies, including, but not limited to PD-L1 inhibitors, therapeutic cancer vaccines, immune suppressor modulator, adoptive NK cells, and other therapeutics.
As the chief medical officer at Arcellx, he is responsible for medical oversight, clinical strategy, medical affairs, and regulatory strategy for the company’s pipeline of novel – investigational drug.
In the second half of the program, Hofland talks with Srdan Verstovsek, Dr Srdan Verstovsek, MD, PhD., a Medical Oncologist and Professor in the Department of Leukemia at The University of Texas MD Anderson Cancer Center, about some of the developments in the treatment of myeloproliferative neoplasm, which are types of blood cancer that begin with an abnormal mutation or change, in a stem cell in the bone marrow. These change leads to an overproduction of any combination of white cells, red blood cells and platelets – and results in a number of diseases, including:
- Essential Thrombocythemia (ET) Is a rare blood disease in which the bone marrow produces too many platelets;
- Myelofibrosis, a rare disorder in which abnormal blood cells and fibers build up in the bone marrow;
- Polycythemia Vera (PV) – a disease in which too many red blood cells are made in the bone marrow and, in many cases, the numbers of white blood cells and platelets are also elevated.
In a new episode of The Onco'Zine Brief, Peter Hofland talks with David M. Cognetti, MD, a Professor and Chair in the Department Head and Neck Surgery at Thomas Jefferson University Hospital in Philadelphia.
Hofland and Cognetti talk about head and neck cancer and a novel treatment approach called Photoimmunotherapy.
Head and Neck Cancer
According to the American Cancer Society, Head and neck cancer accounts for about 4% of all cancers in the United States. In the United States in 2023, an estimated 67,000 people will be diagnosed with head and neck cancer and about 15,000 patients are expected to die of the disease.
Today, many cancers of the head and neck can be cured, especially if they are found early. And while eliminating the cancer is the primary goal of treatment, preserving the function of the nearby nerves, organs, and tissues is also very important.
Beyond Current Treatment
Photoimmunotherapy is a recently developed hybrid cancer therapy to treat diseases by linking specific antibodies with photosensitizers to form photoimmunoconjugates.
But let’s go back to the beginning.
Surgery, radiation, and chemotherapy have dominated the treatment of oncologic. These therapies aim to eradicate cancer cells but, unfortunately, do that at the expense of normal, or healthy cells/ In turn, this can lead to severe and sometimes lethal side-effects.
Overall, the success of surgery, radiation and chemotherapy is measured by what we call a ‘therapeutic index.’
This ‘therapeutic index’ compares the potential benefits of treatment to the potential risks associated with treatment.
Unfortunately, the unintended, off-target side effects of these therapies can have profound effects on the health-related quality of life of patients.
For example, both radiation and chemotherapy sometimes preferentially kill lymphocytes much earlier than cancer cells because of the increased radiation sensitivity and high proliferation rate of lymphocytes, potentially leading to dose-limiting toxicity for some chemotherapy regimens.
To find a solution, researchers have developed new therapeutic strategies. And while these therapies have created an exciting new direction for the treatment of cancer therapy, there remain limitation to these novel approaches.
Now, in theory, the perfect cancer therapy would both directly destroy cancer cells to minimize residual cancer cells as well as activate the local host immune response to wipe out remaining cancer cells.
And while such a therapy would be highly selective for cancer cells but have minimal or no off-target effects in the tumor microenvironment.
Mark as Played
Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:12):
This is the Agazine Brief with PeterHoffland. New Orleans. Without a doubt,
New Orleans is a one of akind destination, famous for its vibrant
culture and music, food, allreflecting the city's unique history of French,
Spanish, African and American culture.But the city is also known for its
(00:34):
many events, from sports to businessand of course, medical education. And
with this unique environment in mind,last December, New Orleans was the host
city of the American Society of Hermatology. This annual event brought the geither tens
of thousands participants from across the worldto present and discuss the results of studies
that ranged from initial hypothesis to practicechanging results. In this episode of the
(00:57):
Angazine Briefe, I talk with twoexpers about their research and the impact the
outcomes from these studies may have onthe treatment of patients diagnosed with cancer.
First, I talk with doctor ChristopherHerey. Doctor here is a Board certified
medical oncologist with primary expertise in translationaland clinical development of immunotherapies, including,
(01:18):
but let me emphasize not limited toPDL one inhibitors, therapeutic cancer vaccines,
immune suppressor modulators, adopted end casalsand other therapeutics. As Chief Medical Officer
of Arthenics, he is responsible formedical oversight, clinical strategy and medical affairs
and regulatory strategy for the company's pipelineof novel investigational drugs. In the second
(01:41):
half of the program, I'm talkingwith doctor certain for staff Sack. Doctor
for staff Sack is a medical oncologistand professor in the Department of Leukemia at
the University of Taxis MD Anderson CancerCenter. We talk about some developments in
the treatment of milo proliferative neoplasms.This type of cancer begins within normal mutation
or change in a stem cell inthe bone marrow. These changes leads to
(02:05):
an overproduction of any combination of whiteblood cells, red blood cells, and
platelets and results in a number ofdiseases, including essential tromboxytemia or ET,
a rare blood disease in which thebone marrow produces too much platelets, mylow
fibrosis, a rare disorder in whichabnormal blood cells and fibers built up in
the bone marrow, and polycythemia vera, a disease in which too many red
(02:30):
blood cells are made in the bonemarrow. And in many cases the number
of white blood cells and platelets arealso elevated. I'm Peter Hoffland and this
is the Youngesine Brief. The YoungasineBrief is developed in collaboration with our online
journal Oncosine that is onco zi nE where you can find additional information and
the latest news about cancer diagnosis andtreatment and cancer prevention. For more information
(02:54):
on how to support this program,visit our website at Oncosine that is o
nco zn dot com. And ifyou're living in the United States and want
to receive our newsletter, text towardsCancer to six six eight six six and
we will make sure that you'll receiveour newsletter, which includes an overview of
the latest news in oncology and hematology. This is the agazine Brief. For
(03:24):
the latest news about cancer and cancertreatment, visit our online journal on Gazine
at www dot kazine dot com.On the phone with me is doctor Christopher
Hey, the chief medical officer ofoursels. In this episode of the Youngashiin
Brief, we talk about some ofthe exciting developments in the field of cancer
research, in particular in carts celltherapies. Doctor Herry Chris, Welcome,
(03:49):
to the Youngishi in brief, thankyou so much for having me on the
podcast. Now we form, we'recoming to talk a little bit about the
developments that are presented at the annualmeeting of the American Society of Hematology.
Tell me a little bit about yourself, about your background and how are you
caught here? Sure well, Itrained as a medical oncologist. My training
was of course, in internal medicinefirst and then medical oncology. I did
(04:13):
the medical oncology training at the NationalCancer Institute method to Maryland. After finishing
that part of the required training,I stayed there at the National Cancer Institute
for a total of about seven years, and in my time there, my
primary responsibility was to be the clinicallead of a translational team that was focused
(04:34):
almost exclusively on off the shelf immunotherapeutics. And so during my time in that
role, I saw patients, enrolledpatients on clinical trials, managed those clinical
trials from an administrative standpoint and alsoa regulatory standpoint, analyzed data, published
(04:54):
data, etc. And most ofthose studies were in the field of checkpoint
in ahibition or vaccines or cytokines.But at the NCI, you cannot be
there and not be aware of SteveRosenberg's group. So you know, some
of my closest friends worked in doctorRosenberg's lab, so I was well aware
(05:15):
of what was going on in theself therapy group. You know, was
a reviewer on protocols, sometimes onthe data safety monitoring boards, etc.
And when I left NCI, Ijoined a company called Bavarian Nordic as a
chief medical officer, which is avaccine company, but was interested in using
vaccines for cancer therapeutics. After thatwent to a company called Precision Biosciences,
(05:35):
which is primarily focused on gene editing. That they have a unique gene editing
tool separate from crispur cast. Andwe had an alogenetic cart platform. So
I was leaving that cart platform.And then about a year and a half
ago, was approached by our CEO, Rami Elgandor, and he asked if
(05:58):
I'd be willing to come and joinour celes as a chief medical officer.
And you know, at the timeI had not heard of oursels very much.
I only knew it because I hada former colleague who had who had
gone to work at our CELS.But I had a chance to review some
of the clinical data that would bepresented at the upcoming ASCO meeting at that
time, which is in twenty twentyone, and it looked incredibly compelling.
(06:23):
It's been about a year and Ihad a little over a year and a
half, and in that time we'vetaken what was sort of this early clinical
data at our celex that looked reallycompelling and really tried to turn the company
from an early stage r indeed companyinto a company that was prepared to go
into a commercial setting with that product. So it's been a pretty significant change
(06:46):
in the company over the last yearand a half, largely attributable to some
decisions by the board, and that'swhy they brought in Rami and then me
and then other members of the leadershipteam. Now our seals it's a boutech
company focusing on college. Right,you refer to off the shelf products,
and these are basically the standard drugtherapies that we use right now in most
cases in a clinic. Right,that's right. And then with our cells,
(07:11):
you're actually developing something else, cartcell therapies. Now, our audience
has often heard about cart cell therapies, but tell me in short, what
makes these drugs so unique. There'sa number of things that are unique about
cart cell therapies, and specifically,when I say cart cells, what I
mean is autologous cart cells that areindividually manufactured for each patient. And so
(07:33):
what makes it truly unique is thatfor each patient, we have to remove
the immune cells from the patient's bloodthrough a process called aphoresis. Those cells
are then shipped to a facility wherethey are modified genetically using a virus,
and then they are grown into largerquantities. They are then frozen and then
(07:57):
shipped back and then infused back tothe patient. So, as you can
imagine, having a therapy that isindividually manufactured for each patient does create some
level of complexity that may not bethere for historical cancer therapeutics as we think
of them broadly. So that iswhat you're focusing on, and it is
(08:18):
also part of what you're presented atthe annual meeting of the American Society of
Hermatology right in December. Can youtell me a little bit more about these
studies and ongoing research, because ifI understand this correctly, you are presented
a number of studies, including theresults of a Phase two clinical trial and
a phase one clinical trial. Tellme a little bit more about these studies
(08:39):
and their outcomes. Sure, yeah, well we are. We are really
only presenting data from the phase onetrial, but we have also recently announced
that we have begun enrollment of ourphase to pivotal trial. So yeah,
let me start with the phase onebecause that is what led us to everything
else. The Phase one trial wasinitially designed to evaluate what is we believe
(09:01):
a unique version of autologous CART cells. And what is unique about our CAR
T cells is the binding domain.So for any listener that isn't aware of
what a CART cell really is,it is a normal T cell that we
have modified so that it expresses somethingthat we call a CAR. A CAR
is a chimeric antigen receptor. Andagain that might not mean anyone to mean
(09:24):
anything to someone who doesn't know whatthat is, so I'll describe it.
What that means is that on theexternal surface there is something that will bind
to something on a tumor cell,and then it is connected to signaling pathways
that tell the cell to become activeand kill. And we have seen over
(09:45):
the last about fifteen years some reallyremarkable changes in our understanding of these types
of cells. So, starting atabout two thousand and nine, there were
two different groups, one at Universityof Pennsylvania and one at the National Cancer
Institute who both started clinical trials thatturned out to be now approved drugs and
(10:05):
are having a huge impact in lymphomaand pediatric all So these therapies are really
changing the way we think about whatwe can achieve with cancer therapy. Let's
take a break. If you're justjoining us in today's episode of The Youngersine
Brief, I'm talking with doctor ChristopherHeary, the chief medical officer at Oursels.
(10:26):
I'm Peter Hoffland, and Dish isToongusine Brief. Each day researchers make
new discoveries. They bring us closerto the moment when all cancer patients can
become survivors. Some days they takesmall steps, others, huge discoveries lead
(10:48):
to giant leaps forward. This progress, both small steps and giant leaps,
happens with the help of clinical trials. Clinical trials are a fundamental path to
progress and the brightest torch researchers haveto light their way towards better treatments.
And if you've been diagnosed with cancer, they may be your brightest ray of
hope. Clinical trials introduce new hopein addition to the current standard of care
(11:11):
by allowing researchers to provide participants accessto cutting edge and potentially life saving treatments.
So if you're interested in exploring newtreatment options while helping to light the
path for other patients, clinical trialsmay be the best choice for you.
Speak with your doctor and visit standUp to cancer dot org slash clinical Trials
(11:31):
to learn more about clinical trials.Together, we can stand up for all
of us. This is the YoungGazine Brief with Peter Hoffland and welcome back.
(11:54):
This is the Young Gushian Brief.If you're just joining us. In
today's episode of The Young Gusian Brief, I'm talking with doctor Christopher Herey,
the chief medical officer at their Cells. So what we have is just sort
of we think of it as anext generation or a slight difference in that
those original cart cells that have alreadybeen improved, most of them use a
(12:15):
binding domain that is called an scFvor a single chain variable fragment, and
those binding domains are sort of they'rebased on the antibodies that our body makes
normally, what we have done isactually used a binding domain that is based
on a synthetic protein. The questionmight be why would you do that,
And the reason is that those certainsynthetic proteins have characteristics that make them potentially
(12:43):
really good as a binding domain.And so in this case, we call
this binding domain the D domain.And what makes it really really nice for
this purpose is that it's very verysmall and very very stable. And so
what that means is that cells canmake KIT very consistently and at a very
high rate. So if you justthink of a cell as a little protein
(13:07):
factory and that all of the functionsof that cell are the result of how
well it can make that protein,they can make D domains very efficiently.
And then once they make them thoseproteins, the D domains are actually very
very stable, even when they're onthe outside of the cell. And so
we believe, based on what weknow the preclinical experiments and what we've seen
(13:30):
in the clinic that D domain basedcart cells had some potential advantages, And
in the clinic so far, inthe thirty eight patients we're presenting, we
see very compelling clinical evidence that thesecells work really well. So I'll tell
you about those now, so thirtyeight patients have a dosed. Every single
one of those patients has how toresponse. About seventy percent of the patients
(13:54):
so far have reached a complete response. And interestingly, when we look at
those patients who were dosed eighteen monthsago or twelve months ago, the complete
response rate is actually about eighty percentin those in that group of patients.
And the reason for that is veryspecific to multiple miloma, but it's something
that is fairly consistently seen in effectivetherapeutics in multiple miloma, which is that
(14:18):
the responses tend to deepen with morefollow up in some percentage of patients.
So additionally to that, what wasnew at the ASH meeting because we've presented
data on this study before, Sowhat was new at this meeting is we
had about seven more patients than wepresented at ASCO earlier this year. But
we were also able to take alook at the percentage of patients who had
(14:41):
not had progression or otherwise referred toas the progression free survival rate at intervals
like six months, twelve months,and eighteen months. And you know,
there were many people who were wonderingwhether we would see that a high proportion
of patients remained in in response ateighteen months, because that is a strong
(15:03):
indicator of the durability of these responses, and we were very happy to present
that about sixty five percent of patientshad progression free survival, meaning they had
not progressed at eighteen months in ouranalysis in this presentation. So the last
point that I think is still reallyimportant is that in addition to that efficacy
(15:26):
data, we also have seen afairly impressive or unusual it might be a
good way to say, a safetyprofile, and that we haven't seen any
grade three cytokine release syndrome, whichis a syndrome that is associated with CARTI
cells and typically what happens people willget high fevers or they can have low
(15:48):
blood pressure. We haven't seen anyof those grade three events in the dose
that we're going to be taking intothe Phase two trial. And we've had
only one event of what's called eyecans or neurotoxicity, where patients will have
a syndrome related to cyto kinds aswell, where they can be confused or
you know, unable to answer questionsand things like that. So we've only
(16:11):
had one of those events out ofthirty two patients at that dose level that
we're taking forward. So taken together, what we believe is that this product
has a unique mix of excellent abilityto eliminate cancer cells without the high risk
(16:32):
features of historical card T cells thatmight drive some of these toxicities. That
definitely sounds very impressive. So clincurrculationswith these results, that must say,
now, this product you have rightnow in a phase one clinical study,
based on the outcomes, you arestarting a phase two clinical trial, right,
tell me a little bit more aboutthat. That is exactly right.
So we have actually already initiated aphase two trial that will be we believe
(16:59):
based on our conversations with FDA thatthis will be our pivotal trial that should
allow us to file a BLA BLAfor the listeners is essentially the request to
get an approval for the drug tobe used as a commercial product. And
yeah, so that study is underway. There are a number of sites coming
online, some already are, andwe expect to be enrolling very very quickly
(17:23):
over the next seven to nine months. Roughly A lot of work remains now
in other developments. The company recentlyannounced a partnership with Kite. Tell me
a little bit more about that.Yeah, Well, one of the things
that is difficult, as we mentionedabout autologous carti cell therapies, is that
there's a very large startup cost tobuild all the facilities to manufacture at the
(17:48):
scale you need to treat all thepatients you would like to treat, and
there's no better company at doing thatthan Kite. So on Friday, we
announced, right before the ASH meeting, announced that we had established a partnership
with Kite, in which the veryvery broad strokes are that Kite was going
to essentially take the majority or allactually all of the responsibility related to manufacturing
(18:15):
of our product, and in returnthey gave us some upfront money. But
I think the thing we're really excitedabout is this remains a partnership. We
both companies have roles and responsibilities,and we want to continue to build our
cels as well, and so thisallows us to sort of remove some of
the need to continue to raise alot of money to be able to do
(18:38):
the things we want to do.But the other thing it does is it
allows us to potentially accelerate all ofthe development of the program because Kite has
so many capabilities in terms of manufacturingand commercialization and distribution channels that we don't
now we do not have to recreatethose, So it's really an ideal partnershi
(19:00):
for us, and we're really excitedabout it. Well, I totally can
imagine the excitement, and in thatcontext, I can see how this may
help the company. But I canalso see that on the learn ren and
with the manufacturing power of Kite tosupport you, how patients may benefit from
the therapist you're developing while you,on the other hands, can focus on
ongoing didruct development. Now, youwere at the ASH meeting where so many
(19:22):
interesting study weis also were presented.Before we're going to talk about that,
can you tell me a little bitmore about the company's pipeline. What are
some of the agents you're advancing throughthe clinic right now, but also looking
beyond what is being presented at ASH, what are some of the other exciting
developments and study outcomes being presented.Sure, yeah, I'll just touch on
something that we haven't touched on aboutour celes before going there, which is
(19:47):
that our pipeline right now is filledwith another sort of next generation version of
autologous CART cells, and those productsare what we would call a universal CART
cell. And so the idea isthat the CART cell itself doesn't bind the
tumor target. It binds to atag on a protein, and then we
(20:11):
infuse proteins that have that tag butalso have the binding domain that attaches to
the tumor antigen. So you canthink of this as sort of like an
activation step. We give the patientthese cells that we call cells, and
then we infuse these proteins that wecall sparks, and so the arc and
(20:33):
the spark have to be present togetherin order to attach to the tumor cell
and cause the cell to be activatedand killed. And the reason we do
that is because there are certain situationswhere you want to be able to go
after multiple targets on a tumor cell. You don't want just one target.
And it also, at least intheory, allows us to think about maybe
(20:56):
controlling those card T cells so thatthey're not constantly activated, which might improve
adverse event profiles, for instance.So there's a lot of reasons why we
think this is a really interesting platform. That that platform went into the clinic
earlier this year, and we're actuallylaunching soon another phase one with that platform
(21:17):
in AML or MDS, and sothat will be targeting CD one twenty three.
So as we look around the ASHconference, you know, we obviously
the leadership team has been very busyfinalizing this deal with Kite and a number
of other things, but we haveyou know, many of our people going
(21:38):
to the poster halls and things lookingfor anything related to cart cells of course,
anything related to BCMA, target attherapeutics, anything in mL, anything
targeting CD one twenty three, etc. You know, and then there are
also things that are just of generalinterest that we pay attention to. Any
there's always an interest in what's goingon in the treatment lands tape of multiple
(22:00):
miloma and AML as well, andthere are plenty of things that keep track
of at this meeting. I assumethat more information about your pipeline and the
study outcomes presented at ASH and atlater meetings can be found on your company's
website. Right of course, DoctorChristopher herey, thank you so much for
being with us here at the Youngishimbridgetoday. After the break, I'm back
(22:22):
with doctor certain for stof Doctor forStaffsak is a medical oncologist and professor in
the Department of Leukemia at the Universityof Texas MD Anderson Cancer Center, and
we will be talking about some ofthe developments in the treatment of miloproliferative neoplasms.
Don't go away, Stay tuned.Sarcoma odds are you've never heard that
(22:49):
word before, but for the fortypeople diagnosed with sarcoma every day, it
is a life changing word, lifechanging and devastating because sarcoma is cancer.
Sarcoma is a cancer of bone andsoft tissue, more prevalent in children than
in adults. More than six thousandpeople lose their lives to sarcoma each year.
(23:10):
Treatment options for sarcoma are limited,and new therapies are desperately needed.
More research and increased awareness is necessaryto find a cure for a cancer that
you probably didn't even know existed untilnow. Through awareness, advocacy, and
research, the Sarcoma Foundation of Americais determined to help those affected by this
forgotten cancer. To bring hope tothe children and adults whose lives are forever
(23:33):
changed by a word they had neverheard before. Please help us in the
fight to find the cure for sarcoma. For more information on sarcoma and the
work of the Sarcoma Foundation of America, please go to Cure Sarcoma dot org.
(23:56):
This is the Young Gazine Brief withPeter Hoffland and welcome back. In
the second half of the program,I'm talking about doctor certain for Stapsac.
Doctor for Stafsak is a medical oncologistand professor in the Department of Leukemia at
the University of Taxis MD Anderson CancerCenter, and we'll be talking about some
(24:18):
of the developments in the treatment ofMILO proliferative neoplasms. Doctor for Staffsak,
Welcome to the Agoshi In Brief.Before we're going to talk about your research,
can you tell me a little bitmore about MILO proliferative neoplasms. Milo
proliferative neoplasms are a group of diseasesof the bone marrow and blood where the
cells in the bone marrow grow withoutcontrol. That's what myloid stands for for
(24:44):
bone marrow cells proliferative MILO proliferative growingwithout control and there are several different types.
Classic diseases are essential trauma, sytemia, high platelets. That's what mean.
It means essential trauma, sytemia andthen polystimia. Vera is another one
where everything grows red blood cells andwhites and platelets. And the most difficult
one is the mile of fibrosis.That the name that is derived by the
(25:08):
description of the bone marrow again myloidand then fibrosis right scarring tissue in the
bone marrow. So instead of havingtoo many cells, most of the patients
mulfords too few. It's kind ofcontraintuitive. Anemia is widely recognized as a
problem. Some patients have a lotof platelets and the bone marrow is not
(25:29):
working well, leading to the reactionof the body of Maulfurous patients in terms
of enlargement of the spleen. Hugespleen huge deliver bad quality of life and
short life expectancy, while ET andPV are more benign. We call them
benign. Life expectancy is good fifteentwenty years sixty five year old test average
age a diagnosis. This is notbad for a mile of fibrosis patients in
(25:53):
five years, so we are preoccupiedwith that deadly disease. But they interpret
approaches overlap while we control the bloodsaccount. Because it's too many cells and
that leads to trombosis in IT andPV, and we worry about the life
expectants in alphaberlities. There are manymedications that overlap and can help all of
(26:14):
these groups or some. Now whereyou look at these group of diseases,
there are a variety of treatment options, some with overlap. But what is
the approach? What is the bestapproach chemotherapy, biologics? What is your
goal in treatment? Is it yourgoal to eliminate these diseases completely or is
it and there's also a very goodoption to control these diseases. So for
(26:38):
example, and to build on standardpractice to explain where the needs. Hydroxyr
is a chemotherapy by mouth Hill thatyou give to patients with it to lower
the flicteds, decrease the white cells, improve the quality of life in a
spleen. Is it all factors associatewith at and make life less complicated,
(26:59):
say, and decrease the trombotic riskblood clot risk by decreasing those blood counts.
Similarly, hydria is used in PVfor the same purpose and in early
stage malphabologies as well. In advancedphase of malphabrosis, it would shrink the
spleen perhaps an improved quality of life. So a different scope of goal with
the same medications in different scenarios,and the scope of work is to control
(27:26):
the disease. As you can see, right, we don't have medications that
would eliminate disease. Jack inhibitors.There are medications again pills that are given
to patients with malphabololities or PV.Sometimes even it is another class of drug
which is non specific for malignan clone. They inhibit the protein inside the BOMU
(27:47):
cells that is important for cell growth, is hyperactive. That's all you call
it. Jack inhibitors. They're notspecific for malignant cells or mutator jack.
So they would decrease the growth,improve the inflammation and again useful in ETPV
and malfulus, but no elimination ofthe disease. The goal is to control
disease signs and symptoms. Right now, when you look at this group of
diseases and the standard of care,which may in each case be different,
(28:11):
what are the unmade medical needs forthese patients? So unmade medical need is
to have a medication that to deliminatedisease makes sense, right, complete response,
You have no disease there are noissues with blood count symptoms or splean
well Planty session an ASH twenty twentytwo gave us a clue about where is
the future, what's coming. Therewas a presentation in our session on the
(28:36):
development of an antibody, a proteinthat would be attaching itself to another protein
on the surface of malignal cells inpatients with malfabrosis or ET. Now,
how can suddenly that be possible?Well, in about a third of the
patients with ET or malfabrosis, theyhave a mutation energene called color reticulin c
(28:57):
A l R. This is oneof the major mutations in these patients,
and the mutation and gene makes aprotein. The protein gets out of the
cells and attaches itself from the outsideto the surface of the cells and does
different things, make cells grow withoutcontrol among many Well, it's on the
(29:17):
surface of the cells, so immunesystem can recognize it or antibody a structure
that was presented in this or planarysession can recognize it and attach itself to
the surface of these malign cells anddestroy or prevent it from functioning, so
the cells dies off. That's probablybetter description, and so that would be
targeted therapy formal legal clone in aboutthird of the patients with ET and AS.
(29:41):
That's why this was planary session andASH because we don't have anything like
that at all. Usually it's justcontrolling science symptoms and that's completely different ball
game. Like I said, atneed of elimination of disease potential exists.
It was not even a phase oneto study. It was the pre clinical
but it's so important it made itto planarty session. Now that's definitely unique,
(30:04):
something that we don't see very oftenthat outcomes of preclinical development are presented
so early in the drugs development ata major medical meeting. It's really something
that shows the importance of this development. But what are your expectations at this
time? And I realize that thisis very hard to predict. Do you
expect that this will also result inthe fast path to development. I assume
(30:27):
that we should expect that this drugcandidate will be for the foreseeable future in
clinical trials. Right, and talkingabout clinical studies, when do you think
these studies will start? I hopethe study will open actually in twenty twenty
three. Now, as you know, many drugs are being tested. I
don't know whether this will work ornot. The hope is very high.
(30:48):
It will take some time for thisto be tested properly in a third of
the patients. Is not for everybody. But what is coming and it's perhaps
more important to talk about right nowbecause kind of imminent is a new medication
for all patients with malo hebrosis calledmom latiniv. I presented some of the
findings on this drug at as myselfand led the overall developmental program of this
(31:14):
drug. This is another pill.It is again controlling decision signs, but
much better than anything else so far. Typically in malfabros, we have three
problems. You recall the description ofthe patients being explined not feeling well,
anemia. Well, no drug existsso far that will do everything right usually
have a control of the splein andsymptoms at the expense of worsening anemia,
(31:36):
for example. So we have tofind this balance between the benefit and risk.
This particular drug has been tested ina phase the random my study,
and now we have presentations of multipledifferent ones on how long the therape is,
how safe it is. It issafe, it's easy to give it,
no problems, simple, safe andeffective. In other words, for
control of anemia, symptoms and thespleen all of it to a degree possible,
(32:00):
of course, and it may becomeone of the major new drugs.
We expect this to be approven nextsummer in the United States. May become
readily used because it's safe, effectiveand simple, so we are looking forward
to that. Now, some additionalinformation for our listeners. Momolotonip is a
small molecule oral inhibitor of JACK oneand JACK two. Now, an interesting
(32:22):
observation is that patients diagnosed with Miloverbrosis had the clinically significant improvement in disease
related symptoms, including anemia and spleenenlargement when treated with this drug. And
this conclusion is based on the outcomesfrom the international Phase three Momentum trial led
by researchers at University of Taxis MdnswerCancer Center. These findings were published in
(32:45):
late January twenty twenty three in thelandset and support the use of momolotonip over
the standard therapy in treatment of Miloverprocess. Patients get very resilient, refractory
or intolerant to first line therapy,especially symptomatic patients and those with anemia.
This is the youngers in Brief.If you're just joining us in today's episode
(33:05):
of The Youngers in Brief, I'mtalking about doctor certain for Stuff Sack.
Doctor for Staff Sack is a medicaloncologist and professor in the Department of Leukemia
at the University of Texas MD AndersonCancer Center, and we are talking about
some of the developments in a treatmentof patients diagnosed with milo prolifictive neoplasms.
I'm Peter Hoffland and this is TheYoungers in Brief. My name is Jiujean.
(33:40):
I'm the chair of a computational biologydepartment as say Je Children's Research Hospital
that I feel so excited about seeingthe potential impact not only on the kids
treated as Saint Jude, but acrossthe world. One of the major advantage
we have in Saint Jude is thatbecause of resources we have, we were
(34:00):
able to utilize the most comprehensive wayof profiling genals through the study. As
a data scientist, I feel verypassionate about sharing data. We also want
to enable talented scientists to analyze datausing the innovative tools and making new discoveries
on top of what we have made. And I think this is a great
(34:22):
use of the trust we got fromour donors finding cures saving children. Learn
more at Saint Jude dot org.This is the Young Gazine Brief with Peter
(34:45):
Hoffland and welcome back. This isthe Young Maasine Brief. If you're just
joining us in today's episode of theYoung Cuisine Brief, I'm talking about doctor
Cerdin for stuff sec doctor for Staffsakis a medical oncologist and professor in the
Department of Leukemia at the University ofTaxis MD Anderson Cancer Center. One thing
(35:07):
that stands out is that MOMOLUTINEP andmost of the drugs that you've mentioned as
part of the available treatment options areoral medications, and I wonder oral therapy
introduces a new variable in treatment,that of patient adherents, because, unlike
traditional infusion oncology, where doctors,nurses, and pharmacists directly oversee the dosing
(35:29):
of administration of the drug, oraltherapy requires the patients themselves to correctly administer
the drugs, and various studies havesuggested that patients may not always adhere to
oral medications. Outcomes of a numberof publish studies have shown lower rates of
oral CHEMOTHERA adherents. These studies suggestmore than fifty percent will adhere to prescribe
(35:52):
therapy. However, in some instances, these studies indicate that adherent's rates are
as low as sixteen percent compared withpatients under the supervision of clinicians delivering infusion,
and decreased adherence leads to poorer outcomeswith an increased in morbidity and mortality.
Now, when you look at yourpatients, the patients that you're treating,
(36:14):
are you worried about this? Idon't worry about this too much because
why do you treat the patients.It's to eliminate the symptoms, and if
you don't take the pill, youdon't feel well, so the compliance is
rather high. It would be extraordinarythat medications like a lot or other JACK
inhibitors that include the symptoms, nothydria, which is chemo therapy, with
(36:37):
others that are JACK inhibitors that decreasethe inflammation and proliferation. It would be
unusual for people not to take fora week, because in a week they
feel bad, very bad. Theother thing is, if we are looking
to the future and we potentially havelikely the antibody that I described earlier on
medication that would potentially eliminate disease.The comp is high again and I'll give
(37:00):
you example in invent because if youdon't take it, disease is there.
You die. I'm sorry that's harsh, but that's how it is. So
there is another milopliftive neoplasm that isvery rare. It has a complicated name.
It's called myloid lymphoid neoplasm. It'sa combination of lymphauma, al miloma
(37:22):
or all kinds of clinical presentations likeMPNCMML. But it is caused by a
specific abonnormality in gene called FGFR fibroplastgrowth factor receptor FGFR. And this is
a very good case to say howmuch we advanced in development of new drugs.
(37:42):
Very rare condition but driven by thisgenetic abnormality which makes them bed protein
method at FGFR. So far youwould die within a year ear and a
half. Now, we in Augustthis year got approval of FGFR inhibitor pay
me gutt a name, and thatwas one of the presentations that ash longer
follow up on patients. In majorityof patients ninety plus percent, you eliminate
(38:06):
disease. You don't take the drug. It's not going to go away right,
or you'll stop taking drug, itwill come back and your life is
short. So there are different reasonswhy I am not that what it in
MPN that people would be not takingpills. So basically, you're dealing with
a group of very motivated patients,patients that really want to improve their health
(38:28):
related quality of life and make surethat these therapies, if these therapies can
eliminate the disease or cure them,at least can help in controlling disease so
that they can continue living exactly exactly. The annual meeting of the American Society
of Hermatology is being held over manydays. In addition to what you're focusing
on, are there other interesting studieswe need to pay attention to. Well,
(38:52):
I'm focused one hundred percent on mildprolivative neopolisms, and one of the
major points on several medic presentation wasthat we should perhaps find a middle ground
between controlling the signs and symptoms,how you feel, how bigger splin is
or how is your anemia and completeemission, which would be eliminational disease,
and look at the other benefits,which we call a molecular response decreasing the
(39:16):
number of cells, decreasing, perhapsnot eliminating, decreasing number of cells that
patients are affected by, which transfersto benefits of fewer progressions some patients progress
them also decreasing progression to acutukemia orfrom ATMPV to malifibrosis. So progression free
survival is being built as an endpointfor some therapies through modification of the mutational
(39:43):
profile or a number of cells affectiveat different mutations. So kind of stepwise
advance from just how you feel towhat's your molecular response? Can we prevent
progression to maybe with the antibody eliminationof the disease. And in each step,
in each part of the patient's journey, you're looking at how these developments
may contribute to improving their health relatedquality of life. Right, that's priority
(40:07):
to number one. And then youwant to have a longevity. My goal
is to get the people to feelgood and live longer. And with that,
thank you so much, doctor forstaff Sack for joining me today in
the angusime Brave. I think we'velearned a lot about the disease and treatment
options, as well as really goodnews in improving treatment outcomes. Absolutely,
(40:29):
we are making strikes. This isenhancing our ability to tackle the problem with
the disease biology so much so thatthere will be a number of new therapists
with the next five years. Sothank you very much for having on the
program today. In this episode ofthe angusin Brave, I spoke with doctor
(40:52):
Christopher Here. Doctor Here is aboard certified medical oncologist with primary expertise in
the translational andical development of immune therapiesincluding, and let me emphasize this not
limited to PDL one inhibitors, therapeuticcancer vaccines, immune suppressor modulators, adoptive
ndcase cells, and many other therapeutics. As the chief medical officer of our
(41:15):
selics, he is responsible for medicaloversight, clinical strategy, medical affairs,
and regulatory strategy for the company's pipeline. For more information about the company and
what they are developing, go totheir website at wwwar slix dot com.
That is aar ce llx dot com. And I also spoke with doctor certain
(41:37):
for staff Sec. Doctor for staffSec is a medical oncologist and professor in
the Department of Leukemia at the Universityof Texas MD Anderson Cancer Center and we
spoke about some of the developments ina treatment of miloprolibative neoplasms. For more
information about this group of diseases,go to the website of the Leukemia and
(41:58):
Lymphoma Society at LLS dot org.Another great resource about this group of diseases
with additional disease information, educational information, helpful of resources and tips, and
community activities, as well as opportunitiesfor patients and caregivers to share their stories
and spread awareness. Go to thewebsite Voice of MPN dot com. That
(42:21):
is Voices of MPN dot com.And if you are a US based healthcare
professional treating patients diagnosed with MILO proliferiveneoplasms or MPN, take some time to
explore the insights and the expertise fromexperts at mpnconnect dot com. For more
information about the studies presented in thisprogram, please go to our online journal
(42:45):
Oncoisine at oncoisine dot com. I'mPeter Hoffland and this is the youngessin Brave.
For us here at the oncsin Brave, we want to thank you,
our listeners, sponsors, and advertisersfor your ongoing support. Your support makes
it possible that you can hear thisprogram via PRX Public Radio Exchange and in
the United Kingdom and mainland Europe viaUK Health Radio. And you can also
(43:07):
download our program via podcast and streamingmedia including iTunes, Spotify, Audible,
Stitcher, SoundCloud, and nearly anywhereyou can find the podcast. For more
information about supporting the On Cuisine Brief, visit our website on Cuisine at on
cuisine dot com. If you're livingin the United States and want to receive
our newsletter, text the word cancerto six six eight six six, that
(43:30):
is six six eight six six,and we will make sure that you'll receive
our newsletter, which includes an overviewof the latest news in oncology and tematology.
Thank you all, and thank youfor listening, and join us again
for our next episode. I'm PeterHoffland and this is the Youngusine Brief.
(43:58):
The Ongazine Brief global medical educational servicefrom the publishers of on Gazine and ADC
Review, the Journal of Antibody DrugConjugates. Support for the Ongazine Brief comes
from our commercial underwriters and advertisers andthe listeners to this station. For more
information about advertising, underwriting and sponsoringoptions, visit on Gazine at www dot
(44:20):
Oncazine, dot com, Forward Slashpodcasts. The on Gazine Brief contains health
and medicine related information and is providedfor educational and entertainment purposes only. The
content in this program is not intendedas a substitute for professional medical or health
advice, and does not replace yourdoctor's advice and guidance. Your doctor is
the best person to answer questions aboutyour personal health. If you hear something
(44:43):
in this program that doesn't agree withwhat your doctor has told you, ask
him or her about it.
This is the Agazine Brief with PeterHoffland. New Orleans. Without a doubt,
New Orleans is a one of akind destination, famous for its vibrant
culture and music, food, allreflecting the city's unique history of French,
Spanish, African and American culture.But the city is also known for its
(00:34):
many events, from sports to businessand of course, medical education. And
with this unique environment in mind,last December, New Orleans was the host
city of the American Society of Hermatology. This annual event brought the geither tens
of thousands participants from across the worldto present and discuss the results of studies
that ranged from initial hypothesis to practicechanging results. In this episode of the
(00:57):
Angazine Briefe, I talk with twoexpers about their research and the impact the
outcomes from these studies may have onthe treatment of patients diagnosed with cancer.
First, I talk with doctor ChristopherHerey. Doctor here is a Board certified
medical oncologist with primary expertise in translationaland clinical development of immunotherapies, including,
(01:18):
but let me emphasize not limited toPDL one inhibitors, therapeutic cancer vaccines,
immune suppressor modulators, adopted end casalsand other therapeutics. As Chief Medical Officer
of Arthenics, he is responsible formedical oversight, clinical strategy and medical affairs
and regulatory strategy for the company's pipelineof novel investigational drugs. In the second
(01:41):
half of the program, I'm talkingwith doctor certain for staff Sack. Doctor
for staff Sack is a medical oncologistand professor in the Department of Leukemia at
the University of Taxis MD Anderson CancerCenter. We talk about some developments in
the treatment of milo proliferative neoplasms.This type of cancer begins within normal mutation
or change in a stem cell inthe bone marrow. These changes leads to
(02:05):
an overproduction of any combination of whiteblood cells, red blood cells, and
platelets and results in a number ofdiseases, including essential tromboxytemia or ET,
a rare blood disease in which thebone marrow produces too much platelets, mylow
fibrosis, a rare disorder in whichabnormal blood cells and fibers built up in
the bone marrow, and polycythemia vera, a disease in which too many red
(02:30):
blood cells are made in the bonemarrow. And in many cases the number
of white blood cells and platelets arealso elevated. I'm Peter Hoffland and this
is the Youngesine Brief. The YoungasineBrief is developed in collaboration with our online
journal Oncosine that is onco zi nE where you can find additional information and
the latest news about cancer diagnosis andtreatment and cancer prevention. For more information
(02:54):
on how to support this program,visit our website at Oncosine that is o
nco zn dot com. And ifyou're living in the United States and want
to receive our newsletter, text towardsCancer to six six eight six six and
we will make sure that you'll receiveour newsletter, which includes an overview of
the latest news in oncology and hematology. This is the agazine Brief. For
(03:24):
the latest news about cancer and cancertreatment, visit our online journal on Gazine
at www dot kazine dot com.On the phone with me is doctor Christopher
Hey, the chief medical officer ofoursels. In this episode of the Youngashiin
Brief, we talk about some ofthe exciting developments in the field of cancer
research, in particular in carts celltherapies. Doctor Herry Chris, Welcome,
(03:49):
to the Youngishi in brief, thankyou so much for having me on the
podcast. Now we form, we'recoming to talk a little bit about the
developments that are presented at the annualmeeting of the American Society of Hematology.
Tell me a little bit about yourself, about your background and how are you
caught here? Sure well, Itrained as a medical oncologist. My training
was of course, in internal medicinefirst and then medical oncology. I did
(04:13):
the medical oncology training at the NationalCancer Institute method to Maryland. After finishing
that part of the required training,I stayed there at the National Cancer Institute
for a total of about seven years, and in my time there, my
primary responsibility was to be the clinicallead of a translational team that was focused
(04:34):
almost exclusively on off the shelf immunotherapeutics. And so during my time in that
role, I saw patients, enrolledpatients on clinical trials, managed those clinical
trials from an administrative standpoint and alsoa regulatory standpoint, analyzed data, published
(04:54):
data, etc. And most ofthose studies were in the field of checkpoint
in ahibition or vaccines or cytokines.But at the NCI, you cannot be
there and not be aware of SteveRosenberg's group. So you know, some
of my closest friends worked in doctorRosenberg's lab, so I was well aware
(05:15):
of what was going on in theself therapy group. You know, was
a reviewer on protocols, sometimes onthe data safety monitoring boards, etc.
And when I left NCI, Ijoined a company called Bavarian Nordic as a
chief medical officer, which is avaccine company, but was interested in using
vaccines for cancer therapeutics. After thatwent to a company called Precision Biosciences,
(05:35):
which is primarily focused on gene editing. That they have a unique gene editing
tool separate from crispur cast. Andwe had an alogenetic cart platform. So
I was leaving that cart platform.And then about a year and a half
ago, was approached by our CEO, Rami Elgandor, and he asked if
(05:58):
I'd be willing to come and joinour celes as a chief medical officer.
And you know, at the timeI had not heard of oursels very much.
I only knew it because I hada former colleague who had who had
gone to work at our CELS.But I had a chance to review some
of the clinical data that would bepresented at the upcoming ASCO meeting at that
time, which is in twenty twentyone, and it looked incredibly compelling.
(06:23):
It's been about a year and Ihad a little over a year and a
half, and in that time we'vetaken what was sort of this early clinical
data at our celex that looked reallycompelling and really tried to turn the company
from an early stage r indeed companyinto a company that was prepared to go
into a commercial setting with that product. So it's been a pretty significant change
(06:46):
in the company over the last yearand a half, largely attributable to some
decisions by the board, and that'swhy they brought in Rami and then me
and then other members of the leadershipteam. Now our seals it's a boutech
company focusing on college. Right,you refer to off the shelf products,
and these are basically the standard drugtherapies that we use right now in most
cases in a clinic. Right,that's right. And then with our cells,
(07:11):
you're actually developing something else, cartcell therapies. Now, our audience
has often heard about cart cell therapies, but tell me in short, what
makes these drugs so unique. There'sa number of things that are unique about
cart cell therapies, and specifically,when I say cart cells, what I
mean is autologous cart cells that areindividually manufactured for each patient. And so
(07:33):
what makes it truly unique is thatfor each patient, we have to remove
the immune cells from the patient's bloodthrough a process called aphoresis. Those cells
are then shipped to a facility wherethey are modified genetically using a virus,
and then they are grown into largerquantities. They are then frozen and then
(07:57):
shipped back and then infused back tothe patient. So, as you can
imagine, having a therapy that isindividually manufactured for each patient does create some
level of complexity that may not bethere for historical cancer therapeutics as we think
of them broadly. So that iswhat you're focusing on, and it is
(08:18):
also part of what you're presented atthe annual meeting of the American Society of
Hermatology right in December. Can youtell me a little bit more about these
studies and ongoing research, because ifI understand this correctly, you are presented
a number of studies, including theresults of a Phase two clinical trial and
a phase one clinical trial. Tellme a little bit more about these studies
(08:39):
and their outcomes. Sure, yeah, well we are. We are really
only presenting data from the phase onetrial, but we have also recently announced
that we have begun enrollment of ourphase to pivotal trial. So yeah,
let me start with the phase onebecause that is what led us to everything
else. The Phase one trial wasinitially designed to evaluate what is we believe
(09:01):
a unique version of autologous CART cells. And what is unique about our CAR
T cells is the binding domain.So for any listener that isn't aware of
what a CART cell really is,it is a normal T cell that we
have modified so that it expresses somethingthat we call a CAR. A CAR
is a chimeric antigen receptor. Andagain that might not mean anyone to mean
(09:24):
anything to someone who doesn't know whatthat is, so I'll describe it.
What that means is that on theexternal surface there is something that will bind
to something on a tumor cell,and then it is connected to signaling pathways
that tell the cell to become activeand kill. And we have seen over
(09:45):
the last about fifteen years some reallyremarkable changes in our understanding of these types
of cells. So, starting atabout two thousand and nine, there were
two different groups, one at Universityof Pennsylvania and one at the National Cancer
Institute who both started clinical trials thatturned out to be now approved drugs and
(10:05):
are having a huge impact in lymphomaand pediatric all So these therapies are really
changing the way we think about whatwe can achieve with cancer therapy. Let's
take a break. If you're justjoining us in today's episode of The Youngersine
Brief, I'm talking with doctor ChristopherHeary, the chief medical officer at Oursels.
(10:26):
I'm Peter Hoffland, and Dish isToongusine Brief. Each day researchers make
new discoveries. They bring us closerto the moment when all cancer patients can
become survivors. Some days they takesmall steps, others, huge discoveries lead
(10:48):
to giant leaps forward. This progress, both small steps and giant leaps,
happens with the help of clinical trials. Clinical trials are a fundamental path to
progress and the brightest torch researchers haveto light their way towards better treatments.
And if you've been diagnosed with cancer, they may be your brightest ray of
hope. Clinical trials introduce new hopein addition to the current standard of care
(11:11):
by allowing researchers to provide participants accessto cutting edge and potentially life saving treatments.
So if you're interested in exploring newtreatment options while helping to light the
path for other patients, clinical trialsmay be the best choice for you.
Speak with your doctor and visit standUp to cancer dot org slash clinical Trials
(11:31):
to learn more about clinical trials.Together, we can stand up for all
of us. This is the YoungGazine Brief with Peter Hoffland and welcome back.
(11:54):
This is the Young Gushian Brief.If you're just joining us. In
today's episode of The Young Gusian Brief, I'm talking with doctor Christopher Herey,
the chief medical officer at their Cells. So what we have is just sort
of we think of it as anext generation or a slight difference in that
those original cart cells that have alreadybeen improved, most of them use a
(12:15):
binding domain that is called an scFvor a single chain variable fragment, and
those binding domains are sort of they'rebased on the antibodies that our body makes
normally, what we have done isactually used a binding domain that is based
on a synthetic protein. The questionmight be why would you do that,
And the reason is that those certainsynthetic proteins have characteristics that make them potentially
(12:43):
really good as a binding domain.And so in this case, we call
this binding domain the D domain.And what makes it really really nice for
this purpose is that it's very verysmall and very very stable. And so
what that means is that cells canmake KIT very consistently and at a very
high rate. So if you justthink of a cell as a little protein
(13:07):
factory and that all of the functionsof that cell are the result of how
well it can make that protein,they can make D domains very efficiently.
And then once they make them thoseproteins, the D domains are actually very
very stable, even when they're onthe outside of the cell. And so
we believe, based on what weknow the preclinical experiments and what we've seen
(13:30):
in the clinic that D domain basedcart cells had some potential advantages, And
in the clinic so far, inthe thirty eight patients we're presenting, we
see very compelling clinical evidence that thesecells work really well. So I'll tell
you about those now, so thirtyeight patients have a dosed. Every single
one of those patients has how toresponse. About seventy percent of the patients
(13:54):
so far have reached a complete response. And interestingly, when we look at
those patients who were dosed eighteen monthsago or twelve months ago, the complete
response rate is actually about eighty percentin those in that group of patients.
And the reason for that is veryspecific to multiple miloma, but it's something
that is fairly consistently seen in effectivetherapeutics in multiple miloma, which is that
(14:18):
the responses tend to deepen with morefollow up in some percentage of patients.
So additionally to that, what wasnew at the ASH meeting because we've presented
data on this study before, Sowhat was new at this meeting is we
had about seven more patients than wepresented at ASCO earlier this year. But
we were also able to take alook at the percentage of patients who had
(14:41):
not had progression or otherwise referred toas the progression free survival rate at intervals
like six months, twelve months,and eighteen months. And you know,
there were many people who were wonderingwhether we would see that a high proportion
of patients remained in in response ateighteen months, because that is a strong
(15:03):
indicator of the durability of these responses, and we were very happy to present
that about sixty five percent of patientshad progression free survival, meaning they had
not progressed at eighteen months in ouranalysis in this presentation. So the last
point that I think is still reallyimportant is that in addition to that efficacy
(15:26):
data, we also have seen afairly impressive or unusual it might be a
good way to say, a safetyprofile, and that we haven't seen any
grade three cytokine release syndrome, whichis a syndrome that is associated with CARTI
cells and typically what happens people willget high fevers or they can have low
(15:48):
blood pressure. We haven't seen anyof those grade three events in the dose
that we're going to be taking intothe Phase two trial. And we've had
only one event of what's called eyecans or neurotoxicity, where patients will have
a syndrome related to cyto kinds aswell, where they can be confused or
you know, unable to answer questionsand things like that. So we've only
(16:11):
had one of those events out ofthirty two patients at that dose level that
we're taking forward. So taken together, what we believe is that this product
has a unique mix of excellent abilityto eliminate cancer cells without the high risk
(16:32):
features of historical card T cells thatmight drive some of these toxicities. That
definitely sounds very impressive. So clincurrculationswith these results, that must say,
now, this product you have rightnow in a phase one clinical study,
based on the outcomes, you arestarting a phase two clinical trial, right,
tell me a little bit more aboutthat. That is exactly right.
So we have actually already initiated aphase two trial that will be we believe
(16:59):
based on our conversations with FDA thatthis will be our pivotal trial that should
allow us to file a BLA BLAfor the listeners is essentially the request to
get an approval for the drug tobe used as a commercial product. And
yeah, so that study is underway. There are a number of sites coming
online, some already are, andwe expect to be enrolling very very quickly
(17:23):
over the next seven to nine months. Roughly A lot of work remains now
in other developments. The company recentlyannounced a partnership with Kite. Tell me
a little bit more about that.Yeah, Well, one of the things
that is difficult, as we mentionedabout autologous carti cell therapies, is that
there's a very large startup cost tobuild all the facilities to manufacture at the
(17:48):
scale you need to treat all thepatients you would like to treat, and
there's no better company at doing thatthan Kite. So on Friday, we
announced, right before the ASH meeting, announced that we had established a partnership
with Kite, in which the veryvery broad strokes are that Kite was going
to essentially take the majority or allactually all of the responsibility related to manufacturing
(18:15):
of our product, and in returnthey gave us some upfront money. But
I think the thing we're really excitedabout is this remains a partnership. We
both companies have roles and responsibilities,and we want to continue to build our
cels as well, and so thisallows us to sort of remove some of
the need to continue to raise alot of money to be able to do
(18:38):
the things we want to do.But the other thing it does is it
allows us to potentially accelerate all ofthe development of the program because Kite has
so many capabilities in terms of manufacturingand commercialization and distribution channels that we don't
now we do not have to recreatethose, So it's really an ideal partnershi
(19:00):
for us, and we're really excitedabout it. Well, I totally can
imagine the excitement, and in thatcontext, I can see how this may
help the company. But I canalso see that on the learn ren and
with the manufacturing power of Kite tosupport you, how patients may benefit from
the therapist you're developing while you,on the other hands, can focus on
ongoing didruct development. Now, youwere at the ASH meeting where so many
(19:22):
interesting study weis also were presented.Before we're going to talk about that,
can you tell me a little bitmore about the company's pipeline. What are
some of the agents you're advancing throughthe clinic right now, but also looking
beyond what is being presented at ASH, what are some of the other exciting
developments and study outcomes being presented.Sure, yeah, I'll just touch on
something that we haven't touched on aboutour celes before going there, which is
(19:47):
that our pipeline right now is filledwith another sort of next generation version of
autologous CART cells, and those productsare what we would call a universal CART
cell. And so the idea isthat the CART cell itself doesn't bind the
tumor target. It binds to atag on a protein, and then we
(20:11):
infuse proteins that have that tag butalso have the binding domain that attaches to
the tumor antigen. So you canthink of this as sort of like an
activation step. We give the patientthese cells that we call cells, and
then we infuse these proteins that wecall sparks, and so the arc and
(20:33):
the spark have to be present togetherin order to attach to the tumor cell
and cause the cell to be activatedand killed. And the reason we do
that is because there are certain situationswhere you want to be able to go
after multiple targets on a tumor cell. You don't want just one target.
And it also, at least intheory, allows us to think about maybe
(20:56):
controlling those card T cells so thatthey're not constantly activated, which might improve
adverse event profiles, for instance.So there's a lot of reasons why we
think this is a really interesting platform. That that platform went into the clinic
earlier this year, and we're actuallylaunching soon another phase one with that platform
(21:17):
in AML or MDS, and sothat will be targeting CD one twenty three.
So as we look around the ASHconference, you know, we obviously
the leadership team has been very busyfinalizing this deal with Kite and a number
of other things, but we haveyou know, many of our people going
(21:38):
to the poster halls and things lookingfor anything related to cart cells of course,
anything related to BCMA, target attherapeutics, anything in mL, anything
targeting CD one twenty three, etc. You know, and then there are
also things that are just of generalinterest that we pay attention to. Any
there's always an interest in what's goingon in the treatment lands tape of multiple
(22:00):
miloma and AML as well, andthere are plenty of things that keep track
of at this meeting. I assumethat more information about your pipeline and the
study outcomes presented at ASH and atlater meetings can be found on your company's
website. Right of course, DoctorChristopher herey, thank you so much for
being with us here at the Youngishimbridgetoday. After the break, I'm back
(22:22):
with doctor certain for stof Doctor forStaffsak is a medical oncologist and professor in
the Department of Leukemia at the Universityof Texas MD Anderson Cancer Center, and
we will be talking about some ofthe developments in the treatment of miloproliferative neoplasms.
Don't go away, Stay tuned.Sarcoma odds are you've never heard that
(22:49):
word before, but for the fortypeople diagnosed with sarcoma every day, it
is a life changing word, lifechanging and devastating because sarcoma is cancer.
Sarcoma is a cancer of bone andsoft tissue, more prevalent in children than
in adults. More than six thousandpeople lose their lives to sarcoma each year.
(23:10):
Treatment options for sarcoma are limited,and new therapies are desperately needed.
More research and increased awareness is necessaryto find a cure for a cancer that
you probably didn't even know existed untilnow. Through awareness, advocacy, and
research, the Sarcoma Foundation of Americais determined to help those affected by this
forgotten cancer. To bring hope tothe children and adults whose lives are forever
(23:33):
changed by a word they had neverheard before. Please help us in the
fight to find the cure for sarcoma. For more information on sarcoma and the
work of the Sarcoma Foundation of America, please go to Cure Sarcoma dot org.
(23:56):
This is the Young Gazine Brief withPeter Hoffland and welcome back. In
the second half of the program,I'm talking about doctor certain for Stapsac.
Doctor for Stafsak is a medical oncologistand professor in the Department of Leukemia at
the University of Taxis MD Anderson CancerCenter, and we'll be talking about some
(24:18):
of the developments in the treatment ofMILO proliferative neoplasms. Doctor for Staffsak,
Welcome to the Agoshi In Brief.Before we're going to talk about your research,
can you tell me a little bitmore about MILO proliferative neoplasms. Milo
proliferative neoplasms are a group of diseasesof the bone marrow and blood where the
cells in the bone marrow grow withoutcontrol. That's what myloid stands for for
(24:44):
bone marrow cells proliferative MILO proliferative growingwithout control and there are several different types.
Classic diseases are essential trauma, sytemia, high platelets. That's what mean.
It means essential trauma, sytemia andthen polystimia. Vera is another one
where everything grows red blood cells andwhites and platelets. And the most difficult
one is the mile of fibrosis.That the name that is derived by the
(25:08):
description of the bone marrow again myloidand then fibrosis right scarring tissue in the
bone marrow. So instead of havingtoo many cells, most of the patients
mulfords too few. It's kind ofcontraintuitive. Anemia is widely recognized as a
problem. Some patients have a lotof platelets and the bone marrow is not
(25:29):
working well, leading to the reactionof the body of Maulfurous patients in terms
of enlargement of the spleen. Hugespleen huge deliver bad quality of life and
short life expectancy, while ET andPV are more benign. We call them
benign. Life expectancy is good fifteentwenty years sixty five year old test average
age a diagnosis. This is notbad for a mile of fibrosis patients in
(25:53):
five years, so we are preoccupiedwith that deadly disease. But they interpret
approaches overlap while we control the bloodsaccount. Because it's too many cells and
that leads to trombosis in IT andPV, and we worry about the life
expectants in alphaberlities. There are manymedications that overlap and can help all of
(26:14):
these groups or some. Now whereyou look at these group of diseases,
there are a variety of treatment options, some with overlap. But what is
the approach? What is the bestapproach chemotherapy, biologics? What is your
goal in treatment? Is it yourgoal to eliminate these diseases completely or is
it and there's also a very goodoption to control these diseases. So for
(26:38):
example, and to build on standardpractice to explain where the needs. Hydroxyr
is a chemotherapy by mouth Hill thatyou give to patients with it to lower
the flicteds, decrease the white cells, improve the quality of life in a
spleen. Is it all factors associatewith at and make life less complicated,
(26:59):
say, and decrease the trombotic riskblood clot risk by decreasing those blood counts.
Similarly, hydria is used in PVfor the same purpose and in early
stage malphabologies as well. In advancedphase of malphabrosis, it would shrink the
spleen perhaps an improved quality of life. So a different scope of goal with
the same medications in different scenarios,and the scope of work is to control
(27:26):
the disease. As you can see, right, we don't have medications that
would eliminate disease. Jack inhibitors.There are medications again pills that are given
to patients with malphabololities or PV.Sometimes even it is another class of drug
which is non specific for malignan clone. They inhibit the protein inside the BOMU
(27:47):
cells that is important for cell growth, is hyperactive. That's all you call
it. Jack inhibitors. They're notspecific for malignant cells or mutator jack.
So they would decrease the growth,improve the inflammation and again useful in ETPV
and malfulus, but no elimination ofthe disease. The goal is to control
disease signs and symptoms. Right now, when you look at this group of
diseases and the standard of care,which may in each case be different,
(28:11):
what are the unmade medical needs forthese patients? So unmade medical need is
to have a medication that to deliminatedisease makes sense, right, complete response,
You have no disease there are noissues with blood count symptoms or splean
well Planty session an ASH twenty twentytwo gave us a clue about where is
the future, what's coming. Therewas a presentation in our session on the
(28:36):
development of an antibody, a proteinthat would be attaching itself to another protein
on the surface of malignal cells inpatients with malfabrosis or ET. Now,
how can suddenly that be possible?Well, in about a third of the
patients with ET or malfabrosis, theyhave a mutation energene called color reticulin c
(28:57):
A l R. This is oneof the major mutations in these patients,
and the mutation and gene makes aprotein. The protein gets out of the
cells and attaches itself from the outsideto the surface of the cells and does
different things, make cells grow withoutcontrol among many Well, it's on the
(29:17):
surface of the cells, so immunesystem can recognize it or antibody a structure
that was presented in this or planarysession can recognize it and attach itself to
the surface of these malign cells anddestroy or prevent it from functioning, so
the cells dies off. That's probablybetter description, and so that would be
targeted therapy formal legal clone in aboutthird of the patients with ET and AS.
(29:41):
That's why this was planary session andASH because we don't have anything like
that at all. Usually it's justcontrolling science symptoms and that's completely different ball
game. Like I said, atneed of elimination of disease potential exists.
It was not even a phase oneto study. It was the pre clinical
but it's so important it made itto planarty session. Now that's definitely unique,
(30:04):
something that we don't see very oftenthat outcomes of preclinical development are presented
so early in the drugs development ata major medical meeting. It's really something
that shows the importance of this development. But what are your expectations at this
time? And I realize that thisis very hard to predict. Do you
expect that this will also result inthe fast path to development. I assume
(30:27):
that we should expect that this drugcandidate will be for the foreseeable future in
clinical trials. Right, and talkingabout clinical studies, when do you think
these studies will start? I hopethe study will open actually in twenty twenty
three. Now, as you know, many drugs are being tested. I
don't know whether this will work ornot. The hope is very high.
(30:48):
It will take some time for thisto be tested properly in a third of
the patients. Is not for everybody. But what is coming and it's perhaps
more important to talk about right nowbecause kind of imminent is a new medication
for all patients with malo hebrosis calledmom latiniv. I presented some of the
findings on this drug at as myselfand led the overall developmental program of this
(31:14):
drug. This is another pill.It is again controlling decision signs, but
much better than anything else so far. Typically in malfabros, we have three
problems. You recall the description ofthe patients being explined not feeling well,
anemia. Well, no drug existsso far that will do everything right usually
have a control of the splein andsymptoms at the expense of worsening anemia,
(31:36):
for example. So we have tofind this balance between the benefit and risk.
This particular drug has been tested ina phase the random my study,
and now we have presentations of multipledifferent ones on how long the therape is,
how safe it is. It issafe, it's easy to give it,
no problems, simple, safe andeffective. In other words, for
control of anemia, symptoms and thespleen all of it to a degree possible,
(32:00):
of course, and it may becomeone of the major new drugs.
We expect this to be approven nextsummer in the United States. May become
readily used because it's safe, effectiveand simple, so we are looking forward
to that. Now, some additionalinformation for our listeners. Momolotonip is a
small molecule oral inhibitor of JACK oneand JACK two. Now, an interesting
(32:22):
observation is that patients diagnosed with Miloverbrosis had the clinically significant improvement in disease
related symptoms, including anemia and spleenenlargement when treated with this drug. And
this conclusion is based on the outcomesfrom the international Phase three Momentum trial led
by researchers at University of Taxis MdnswerCancer Center. These findings were published in
(32:45):
late January twenty twenty three in thelandset and support the use of momolotonip over
the standard therapy in treatment of Miloverprocess. Patients get very resilient, refractory
or intolerant to first line therapy,especially symptomatic patients and those with anemia.
This is the youngers in Brief.If you're just joining us in today's episode
(33:05):
of The Youngers in Brief, I'mtalking about doctor certain for Stuff Sack.
Doctor for Staff Sack is a medicaloncologist and professor in the Department of Leukemia
at the University of Texas MD AndersonCancer Center, and we are talking about
some of the developments in a treatmentof patients diagnosed with milo prolifictive neoplasms.
I'm Peter Hoffland and this is TheYoungers in Brief. My name is Jiujean.
(33:40):
I'm the chair of a computational biologydepartment as say Je Children's Research Hospital
that I feel so excited about seeingthe potential impact not only on the kids
treated as Saint Jude, but acrossthe world. One of the major advantage
we have in Saint Jude is thatbecause of resources we have, we were
(34:00):
able to utilize the most comprehensive wayof profiling genals through the study. As
a data scientist, I feel verypassionate about sharing data. We also want
to enable talented scientists to analyze datausing the innovative tools and making new discoveries
on top of what we have made. And I think this is a great
(34:22):
use of the trust we got fromour donors finding cures saving children. Learn
more at Saint Jude dot org.This is the Young Gazine Brief with Peter
(34:45):
Hoffland and welcome back. This isthe Young Maasine Brief. If you're just
joining us in today's episode of theYoung Cuisine Brief, I'm talking about doctor
Cerdin for stuff sec doctor for Staffsakis a medical oncologist and professor in the
Department of Leukemia at the University ofTaxis MD Anderson Cancer Center. One thing
(35:07):
that stands out is that MOMOLUTINEP andmost of the drugs that you've mentioned as
part of the available treatment options areoral medications, and I wonder oral therapy
introduces a new variable in treatment,that of patient adherents, because, unlike
traditional infusion oncology, where doctors,nurses, and pharmacists directly oversee the dosing
(35:29):
of administration of the drug, oraltherapy requires the patients themselves to correctly administer
the drugs, and various studies havesuggested that patients may not always adhere to
oral medications. Outcomes of a numberof publish studies have shown lower rates of
oral CHEMOTHERA adherents. These studies suggestmore than fifty percent will adhere to prescribe
(35:52):
therapy. However, in some instances, these studies indicate that adherent's rates are
as low as sixteen percent compared withpatients under the supervision of clinicians delivering infusion,
and decreased adherence leads to poorer outcomeswith an increased in morbidity and mortality.
Now, when you look at yourpatients, the patients that you're treating,
(36:14):
are you worried about this? Idon't worry about this too much because
why do you treat the patients.It's to eliminate the symptoms, and if
you don't take the pill, youdon't feel well, so the compliance is
rather high. It would be extraordinarythat medications like a lot or other JACK
inhibitors that include the symptoms, nothydria, which is chemo therapy, with
(36:37):
others that are JACK inhibitors that decreasethe inflammation and proliferation. It would be
unusual for people not to take fora week, because in a week they
feel bad, very bad. Theother thing is, if we are looking
to the future and we potentially havelikely the antibody that I described earlier on
medication that would potentially eliminate disease.The comp is high again and I'll give
(37:00):
you example in invent because if youdon't take it, disease is there.
You die. I'm sorry that's harsh, but that's how it is. So
there is another milopliftive neoplasm that isvery rare. It has a complicated name.
It's called myloid lymphoid neoplasm. It'sa combination of lymphauma, al miloma
(37:22):
or all kinds of clinical presentations likeMPNCMML. But it is caused by a
specific abonnormality in gene called FGFR fibroplastgrowth factor receptor FGFR. And this is
a very good case to say howmuch we advanced in development of new drugs.
(37:42):
Very rare condition but driven by thisgenetic abnormality which makes them bed protein
method at FGFR. So far youwould die within a year ear and a
half. Now, we in Augustthis year got approval of FGFR inhibitor pay
me gutt a name, and thatwas one of the presentations that ash longer
follow up on patients. In majorityof patients ninety plus percent, you eliminate
(38:06):
disease. You don't take the drug. It's not going to go away right,
or you'll stop taking drug, itwill come back and your life is
short. So there are different reasonswhy I am not that what it in
MPN that people would be not takingpills. So basically, you're dealing with
a group of very motivated patients,patients that really want to improve their health
(38:28):
related quality of life and make surethat these therapies, if these therapies can
eliminate the disease or cure them,at least can help in controlling disease so
that they can continue living exactly exactly. The annual meeting of the American Society
of Hermatology is being held over manydays. In addition to what you're focusing
on, are there other interesting studieswe need to pay attention to. Well,
(38:52):
I'm focused one hundred percent on mildprolivative neopolisms, and one of the
major points on several medic presentation wasthat we should perhaps find a middle ground
between controlling the signs and symptoms,how you feel, how bigger splin is
or how is your anemia and completeemission, which would be eliminational disease,
and look at the other benefits,which we call a molecular response decreasing the
(39:16):
number of cells, decreasing, perhapsnot eliminating, decreasing number of cells that
patients are affected by, which transfersto benefits of fewer progressions some patients progress
them also decreasing progression to acutukemia orfrom ATMPV to malifibrosis. So progression free
survival is being built as an endpointfor some therapies through modification of the mutational
(39:43):
profile or a number of cells affectiveat different mutations. So kind of stepwise
advance from just how you feel towhat's your molecular response? Can we prevent
progression to maybe with the antibody eliminationof the disease. And in each step,
in each part of the patient's journey, you're looking at how these developments
may contribute to improving their health relatedquality of life. Right, that's priority
(40:07):
to number one. And then youwant to have a longevity. My goal
is to get the people to feelgood and live longer. And with that,
thank you so much, doctor forstaff Sack for joining me today in
the angusime Brave. I think we'velearned a lot about the disease and treatment
options, as well as really goodnews in improving treatment outcomes. Absolutely,
(40:29):
we are making strikes. This isenhancing our ability to tackle the problem with
the disease biology so much so thatthere will be a number of new therapists
with the next five years. Sothank you very much for having on the
program today. In this episode ofthe angusin Brave, I spoke with doctor
(40:52):
Christopher Here. Doctor Here is aboard certified medical oncologist with primary expertise in
the translational andical development of immune therapiesincluding, and let me emphasize this not
limited to PDL one inhibitors, therapeuticcancer vaccines, immune suppressor modulators, adoptive
ndcase cells, and many other therapeutics. As the chief medical officer of our
(41:15):
selics, he is responsible for medicaloversight, clinical strategy, medical affairs,
and regulatory strategy for the company's pipeline. For more information about the company and
what they are developing, go totheir website at wwwar slix dot com.
That is aar ce llx dot com. And I also spoke with doctor certain
(41:37):
for staff Sec. Doctor for staffSec is a medical oncologist and professor in
the Department of Leukemia at the Universityof Texas MD Anderson Cancer Center and we
spoke about some of the developments ina treatment of miloprolibative neoplasms. For more
information about this group of diseases,go to the website of the Leukemia and
(41:58):
Lymphoma Society at LLS dot org.Another great resource about this group of diseases
with additional disease information, educational information, helpful of resources and tips, and
community activities, as well as opportunitiesfor patients and caregivers to share their stories
and spread awareness. Go to thewebsite Voice of MPN dot com. That
(42:21):
is Voices of MPN dot com.And if you are a US based healthcare
professional treating patients diagnosed with MILO proliferiveneoplasms or MPN, take some time to
explore the insights and the expertise fromexperts at mpnconnect dot com. For more
information about the studies presented in thisprogram, please go to our online journal
(42:45):
Oncoisine at oncoisine dot com. I'mPeter Hoffland and this is the youngessin Brave.
For us here at the oncsin Brave, we want to thank you,
our listeners, sponsors, and advertisersfor your ongoing support. Your support makes
it possible that you can hear thisprogram via PRX Public Radio Exchange and in
the United Kingdom and mainland Europe viaUK Health Radio. And you can also
(43:07):
download our program via podcast and streamingmedia including iTunes, Spotify, Audible,
Stitcher, SoundCloud, and nearly anywhereyou can find the podcast. For more
information about supporting the On Cuisine Brief, visit our website on Cuisine at on
cuisine dot com. If you're livingin the United States and want to receive
our newsletter, text the word cancerto six six eight six six, that
(43:30):
is six six eight six six,and we will make sure that you'll receive
our newsletter, which includes an overviewof the latest news in oncology and tematology.
Thank you all, and thank youfor listening, and join us again
for our next episode. I'm PeterHoffland and this is the Youngusine Brief.
(43:58):
The Ongazine Brief global medical educational servicefrom the publishers of on Gazine and ADC
Review, the Journal of Antibody DrugConjugates. Support for the Ongazine Brief comes
from our commercial underwriters and advertisers andthe listeners to this station. For more
information about advertising, underwriting and sponsoringoptions, visit on Gazine at www dot
(44:20):
Oncazine, dot com, Forward Slashpodcasts. The on Gazine Brief contains health
and medicine related information and is providedfor educational and entertainment purposes only. The
content in this program is not intendedas a substitute for professional medical or health
advice, and does not replace yourdoctor's advice and guidance. Your doctor is
the best person to answer questions aboutyour personal health. If you hear something
(44:43):
in this program that doesn't agree withwhat your doctor has told you, ask
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