Melanoma and Brain Metastases

Name: Melanoma and Brain Metastases
Uploaded: 2021-10-04T12:59:02.763Z
Duration: 29 min
Description: October 3, 2021 Yale Cancer Center visit: http://www.yalecancercenter.org email: canceranswers@yale.edu call: 203-785-4095

October 04, 2021

October 3, 2021

Yale Cancer Center

visit: http://www.yalecancercenter.org

email: canceranswers@yale.edu

call: 203-785-4095

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00:00Funding for Yale Cancer Answers
00:03is provided by Smilow Cancer
00:05Hospital and AstraZeneca.
00:08Welcome to Yale Cancer Answers
00:10with host Dr Anees Chagpar.
00:12Yale Cancer Answers features the
00:14latest information on cancer care by
00:16welcoming oncologists and specialists
00:18who are on the forefront of the
00:20battle to fight cancer. This week,
00:22it's a conversation about Melanoma and
00:25brain metastases with Doctor Thuy Tran.
00:27Dr Tran is an instructor of
00:29medicine in medical oncology at
00:31the Yale School of Medicine,
00:32where Dr Chagpar is a
00:34professor of surgical oncology.
00:37Doctor Tran, maybe we can start off
00:39by you telling us a little bit
00:40about yourself and what you do.
00:42Absolutely, I am a translational
00:45researcher at Yale Cancer Center.
00:48I did my residency and fellowship
00:50in heme/onc here and I'm happy to
00:53be involved in the Melanoma team
00:55treating patients with advanced
00:57malignancies and skin cancers.
00:59I do a lot of translational research,
01:01which means that I am working at the
01:03bench but also take what we find out
01:05at the bench straight to the clinic
01:07so that we can effect real change
01:09in how we treat this disease.
01:11So tell us a little bit
01:13more about your research.
01:14I mean you work in the Melanoma team,
01:18how exactly does the translational
01:20research part fit in and what
01:22specifically are you looking at?
01:25I've been spending the past couple
01:27years really looking at innate
01:29immunity in the brain and how we
01:31can really capitalize on stimulating
01:33those cells and in conjunction with
01:35our currently available
01:37therapies to try to improve
01:39disease outcomes for our patients.
01:41So just to give you an example.
01:43One of the projects that I'm
01:45highly involved with is trying to
01:47target the blood brain barrier.
01:49The blood brain barrier
01:51has been a really understudied but
01:54very clinically relevant and highly
01:56impactful way for cancers to really
01:58gain an advantage and to metastasize
02:01and grow in the brain and so really
02:03trying to focus on the blood brain
02:06barrier and try to get these drugs
02:08into the brain has been an
02:10area of ongoing interest.
02:12Just to give you an example.
02:13So one of our currently active
02:16projects is looking at targeting Veg F,
02:19which stands for vascular
02:21endothelial growth factor.
02:22It's a subtle kind that really
02:24stimulates blood vessel development,
02:26and sometimes these tumors and the
02:28immune cells surrounding them will
02:30secrete this cytokine to help stimulate
02:33tumor growth and so how can we
02:35target this protein as well as maybe
02:38target the endothelial cells themselves to
02:40help decrease tumor growth in the brain.
02:43And so we have a couple of
02:45interesting targets,
02:45one of which is currently an active
02:48clinical trial within our Melanoma group
02:50looking at Melanoma and lung cancer
02:52patients who have brain metastases.
02:55And so this clinical trial is
02:57a phase two study looking at
02:59the combination of bevacizumab,
03:01which is our anti veg F drug
03:02to help minimize blood vessel
03:05development in combination with
03:07an immune stimulating agent,
03:09the checkpoint inhibitor pembrolizumab,
03:11which targets another pathway
03:13to help stimulate our own bodies
03:15immune system to help fight cancer.
03:18We're also going to be developing a
03:21second clinical trial of pembrolizumab
03:24or immune stimulating agent in
03:26combination with Lenvatinib,
03:28which instead of targeting the
03:29cytokine itself,
03:30targets the veg F receptors on the
03:33endothelial cells and hopefully we
03:35can get even a more dramatic immune response.
03:39So today I want to take a step back
03:41here and just kind of talk a little bit
03:43about the blood brain barrier itself.
03:46What exactly is it and how
03:50does it affect cancer cells?
03:52As we're always learning more
03:54and more about the blood brain barrier,
03:56it's not as simple as we first thought
03:58where it's just comprised of the
04:00blood vessel and death elial cells,
04:02the blood brain barrier is
04:04actually much more complicated.
04:05It's composed of not only
04:07the endothelial cells,
04:07but all these supportive cells
04:10adjacent to them,
04:11and so this includes parasites
04:13which control vasoconstriction
04:14or the ability of these blood
04:17vessels to contract and dilate.
04:19It also includes all the supportive
04:22astrocytes which have their
04:24little processes in and feet
04:26on the endothelial cells.
04:28It includes interneurons,
04:30it includes microglia,
04:32microglia are considered,
04:33sort of the innate immune cells
04:35that reside within the brain.
04:37How come the cancer cells can get
04:39into the brain but the drugs can't?
04:42You know the blood brain barrier
04:44in normal states without any
04:47pressure related to metastasis is
04:50a very intact endothelial layer,
04:52meaning that there are these specific
04:55interconnections within or
04:57between the endothelial cells
04:59that prevent any other molecules,
05:01such as drugs such as immune cells from
05:05infiltrating or getting beyond them.
05:08They typically are described
05:09as the soldiers.
05:11Remember the Roman soldiers
05:13if you ever watch one of those
05:15movies with all their Shields up
05:18so they form an impenetrable
05:20barrier to help prevent things
05:22from getting past that layer.
05:25And that's what's really
05:26caused a lot of issues.
05:28For example,
05:29in breast cancer therapy where
05:31chemotherapies that traditionally
05:33work in breast cancers can't
05:34penetrate into the brain,
05:36and so we're seeing a lot more of late
05:39relapses in the brain because these
05:41cancer effective therapies are not
05:43able to penetrate and circulate there.
05:46So why can the cancer cells get
05:48through those those Roman Shields?
05:50I mean, it sounds like that should really be,
05:53as you say, an impenetrable barrier.
05:55And yet, cancer cells can seem to
05:57sneak their way through.
05:59Cancer cells when they metastasize,
06:04they go through a very complex process,
06:08basically giving them the ability to
06:10invade through normal tissue and during
06:13that process they adopt a different shape,
06:16a different morphology.
06:17They become migratory.
06:19They get enter the bloodstream,
06:21and when they circulate,
06:23they essentially get into the brain.
06:25And either lodge at Branch points
06:28within those blood vessels in the
06:30brain and cancer cells have all
06:32sorts of different proteins and
06:34things that they up regulate or
06:37express to help them survive and
06:40proliferate during this process,
06:42and a few of those proteins include
06:45things like matrix metalloproteases
06:47where they can break apart different
06:50elements of the tumor stroma,
06:52or the tumor microenvironment,
06:54and this allows them
06:56essentially to break apart those tight
06:58junctions within this endothelial cells.
07:01Wedge themselves in between these
07:05cells and eventually be able to set up
07:08shop and grow there.
07:09So I guess just to
07:11press the point further,
07:14my question is if the tumor cells can kind
07:17of finagle their way through this barrier,
07:20either they make holes in the barrier,
07:23they kind of distort and try to get through,
07:26then are those changes to
07:29the blood brain barrier that allow
07:32the cancer cells to get through,
07:35those don't seem to be permanent enough
07:37to allow our drugs to get through.
07:39Or is there another thing at play?
07:41Are the drugs too large?
07:44Is it that they can't squish
07:46through the little spaces?
07:48Or is this more than simply
07:50a mechanical problem?
07:52I think the answer is actually a little
07:55complicated to address and we don't
07:57really at this point fully understand
07:59how our current effective therapies
08:01really penetrate to get into the brain.
08:04So one hypothesis
08:05is that actually when we give immune
08:07therapy these immune stimulating
08:09drugs that help educate our own
08:12immune system to fight the cancer,
08:14we're doing that below the
08:17neck so peripherally,
08:18so these educated immune cells can
08:21then subsequently migrate through
08:24the circulation into the brain.
08:27They have a much easier ability
08:29to transmigrate through the
08:31endothelial layer and get into
08:33the tumor to where they can have
08:36antitumor effect,
08:37the other component of this is maybe
08:40the defects that lead to
08:43forming a tumor in the brain caused
08:45vessel leakiness and vessel damage,
08:47and such that you have this
08:51chronic adima or loss of vessel
08:54integrity and that therefore
08:56allows these large monoclonal
08:59antibodies which are essentially
09:01our immune checkpoint drugs,
09:03to actually access
09:06into the tumor
09:07ecause these vessels are already so leaky.
09:09That's really great
09:11news on the immunotherapy front,
09:14knowing that these therapies
09:16can get into the brain,
09:18I guess the next question is, well,
09:20how come chemotherapy drugs can't do that?
09:23I mean, we give them
09:25peripherally into a vein below the neck,
09:28right into a hand,
09:29they get into a blood vessel.
09:31How come they can't follow the same
09:34kinds of path?
09:38Yeah, so our blood brain barrier
09:40through our development
09:42has upregulated a lot
09:45of drug efflux pumps and so these
09:48endothelial cells that constitute
09:50the blood brain barrier they have
09:53these specialized pumps that whenever
09:56drug does penetrate into the cells,
09:58they pump them right back out
10:00into the circulation.
10:01And so that's what limits the effectiveness
10:05of standard chemotherapy and
10:07it's really not a very good treatment
10:10option for patients with brain metastases.
10:14OK, I get all of that.
10:16So now let's talk a little
10:18bit more about this.
10:20Veg F that you were
10:21mentioning just a moment ago,
10:23this vascular endothelial
10:24growth factor is that something
10:26that is present on particular
10:29cancer cells that these
10:30therapies now are attacking?
10:33Veg F is upregulated in a lot
10:36of different cell types, and
10:38one of those being Melanoma,
10:39where we have found that circulating
10:42veg F is actually a poor prognostic
10:45marker in patients, so they
10:47say essentially they have worse
10:49outcomes when they have elevated
10:50circulating levels of this protein.
10:53So the protein is in the circulation.
10:55It's not necessarily on the
10:57tumor cells, or is it on both?
10:58It's very ubiquitously expressed.
11:02It can be expressed by the tumor cells
11:05themselves and have a local effect in that
11:08increased regulation or increased
11:11expression of VEGF can also
11:14appear as circulating levels.
11:17Tumor cells, in addition to immune cells,
11:21can also increase veg F levels too.
11:23So, for example,
11:24a specific type of immune cell
11:27which essentially gobble up a lot
11:30of tumor cells or cell debris.
11:33One of those is macrophages.
11:35So macrophages are able to secrete
11:37high levels of veg F as well.
11:40And so that makes me think that
11:43these anti VEGF therapies that you're
11:46looking at in clinical trials,
11:48they might be
11:50something not specific
11:53for particular patients that they might
11:55be more ubiquitously used rather than
11:57some of the therapies that come out
12:00where you really need to check the
12:02tumor cells to make sure that
12:05particular protein or that particular
12:06receptor is on the tumor cell.
12:08It sounds like this is something that
12:11could be used for most patients.
12:13Is that right?
12:14That's correct. So actually,
12:16even recently within the past couple
12:18weeks we've had another FDA approval
12:21for the combination of pembrolizumab
12:22and lenvatinib,
12:25being one of our veg F receptor
12:27targeting drugs in addition to other
12:30receptors that it does block as well.
12:33So that was actually just in
12:36advanced renal cell carcinoma.
12:38The combination is already
12:40been also approved in
12:41advanced endometrial cancer,
12:43and then actually Merck,
12:46the company that produces pembrolizumab
12:51is currently investigating this combination
12:55in the first line and second line
12:58setting for Melanoma patients as well.
13:01Wow, all really interesting
13:02developments which we will need
13:04to investigate more when we take
13:07a brief break for medical minute.
13:09Please stay tuned to learn
13:10more about Melanoma
13:11and brain metastases with
13:13my guest doctor Thuy Tran.
13:15Funding for Yale Cancer Answers
13:17comes from AstraZeneca, dedicated
13:19to advancing options and providing
13:21hope for people living with cancer.
13:24More information at AstraZeneca Dash us.com.
13:30The American Cancer Society
13:32estimates that more than 65,000
13:34Americans will be diagnosed with
13:36head and neck cancer this year,
13:38making up about 4% of all cancers
13:41diagnosed. When detected early,
13:43however, head and neck cancers are
13:45easily treated and highly curable.
13:47Clinical trials are currently
13:49underway at federally designated
13:51Comprehensive cancer centers such
13:53as Yale Cancer Center and at Smilow
13:55Cancer Hospital to test innovative new
13:57treatments for head and neck cancers.
14:00Yale Cancer Center was recently awarded
14:02grants from the National Institutes
14:05of Health to fund the Yale Head
14:07and neck Cancer Specialized program
14:10of Research Excellence or SPORE to
14:12address critical barriers to treatment
14:14of head and neck squamous cell
14:17carcinoma due to resistance to immune
14:19DNA damaging and targeted therapy.
14:22More information is available at
14:25yalecancercenter.org you're listening
14:26to Connecticut Public Radio.
14:29Welcome back to Yale Cancer Answers.
14:32This is doctor Anees Chagpar and I'm
14:34joined tonight by my guest Doctor Thuy Tran.
14:37We're talking about the care of patients
14:39with Melanoma and brain metastases,
14:42and right before the break we were
14:45talking about some of the techniques,
14:48some of the new trials that are ongoing,
14:51especially looking at use of anti
14:54veg F therapies and immunotherapy
14:56for patients with Melanoma,
14:59who had brain metastases.
15:01So I thought we'd take a step back and talk a
15:04little bit more about patients with Melanoma
15:07who have brain metastases.
15:08So I think all of us know that Melanoma
15:11is one of the deadliest skin cancers.
15:14But how common is Melanoma?
15:19Many patients get Melanoma.
15:21What proportion of them will
15:23actually develop brain metastases?
15:26Melanoma over the past couple decades
15:29it's actually the incidence
15:32that's increasing more recently about 75,000
15:35new cases are diagnosed each year and
15:38it's a malignancy that is driven by both
15:42genetic as well as environmental causes,
15:45some of which are related to non
15:49UV exposure and so really a lot of
15:52Melanoma develops as we grow older in
15:56our fifth generation or fifth decade.
15:59And so it does have a higher
16:02dominance in men,
16:03and there are certain mutations
16:06associated with it.
16:0850% of melanomas will contain
16:11a BRAF mutation that we can actually
16:14target with effective BRAF inhibiting
16:16drugs as well as MEC inhibiting drugs
16:19that also help boost that response.
16:22So just to pick up on
16:24the genetic element for a second
16:26one of the things that you said,
16:28which I found really interesting
16:30and I think our listeners will be
16:33interested to learn about as well is
16:35that there are a lot of melanomas
16:38that are not related to UV exposure.
16:40That may be genetic,
16:42so by that do you mean that we should
16:45know about our family history in terms
16:47of our risk of developing Melanoma?
16:50And when you talk about BRAF mutations,
16:53are you talking about germline
16:55mutations or are these more
16:57somatic mutations that you'll find in a tumor?
17:01The BRAF mutations are new mutations.
17:05Sometimes we actually see
17:07these mutations present but not
17:09associated with any malignancy.
17:11But when they do appear associated
17:15with advanced Melanoma,
17:16it is something that we can actually target.
17:19Now these BRAF mutations
17:20are not unique to Melanoma.
17:21They're actually present in
17:24certain types of colon cancers.
17:27And as well as lung cancers.
17:28And so the same drugs apply they're
17:31as effective in those other types
17:33of cancers as they are in Melanoma.
17:36And so some people, even if they wear
17:39sunscreen and they make sure
17:41that they're not getting a lot of
17:43UV exposure and so on and so forth.
17:45They can still get Melanoma because of
17:47these genetic mutations. Is that right?
17:49Yes, in terms of the non sun
17:52exposed related melanomas, we typically
17:55think of those as a acreal melanomas.
17:57Meaning they form between the hands,
17:59the webs of the hands and
18:01the feet on her extremities,
18:04and so these are typically places
18:05that you know aren't basking
18:06in the Sun and other places
18:10that melanomas can evolve from,
18:12is the mucosal lining of
18:16our upper oral pharanx
18:18as well as the anal rectal region.
18:21Vulvar melanomas from the reproductive tract,
18:25as well as uveal melanoma's also
18:27from the pigmented layers of the eyes.
18:29So Melanoma, in essence,
18:31is a cancer of the melanocytes.
18:34These pigmented cells and so anywhere
18:36where we have pigment there are
18:40melanocytes associated with them.
18:42When you think
18:44about these genetic mutations,
18:46now that we know more and more about them,
18:48certainly you know people who have a
18:53genetic mutation who are at increased risk,
18:56they may want to take additional precautions.
18:59You know making sure that
19:00they're really getting
19:02a good dermatologic exam,
19:04and staying out of the sun,
19:05and so on and so forth.
19:07But one of the questions that I
19:09have is for some genetic mutation,
19:11for example for the RET proto oncogene,
19:15which predisposes to thyroid cancers,
19:18these are things that newborn
19:21babies have tested,
19:22whereas other mutations like
19:24BRCA for example is something
19:26that we don't generally test
19:29until you know somebody comes
19:30up to us and says,
19:31you know I have a family history of
19:34breast cancer and so should I get tested.
19:36Where does BRAF kind of
19:38fit into the grand scheme of things?
19:41It's less clear whether having
19:44a pre-existing BRAF mutation
19:46ultimately will induce cancer.
19:49A lot of the times it doesn't,
19:51and it's just something that we
19:54pick up that's not prognostic or
19:58indicative of any future malignancy.
20:01It's really something that we
20:03find later on once the cancer is
20:05developed that we can potentially
20:06target as an effective therapy.
20:08And you mentioned, BRCA mutations
20:11in a very small
20:13subset of patients can
20:16contribute to increased risk of
20:18Melanoma as well as pancreatic cancer.
20:20So really it depends on family
20:23history and it really depends
20:25on your personal history too.
20:26If you have a patient with multiple
20:29melanomas with a strong family
20:32history of multiple immediate
20:34kin with Melanoma cancers,
20:36that's when we typically
20:39flag and refer
20:41these patients to genetic counseling
20:43to see if there are indeed these
20:45generalized mutations that predispose
20:47these patients to developing Melanoma
20:50as well as other malignancies.
20:52And so it really has an
20:54impact on family members,
20:55particularly children.
20:56When we see patients in the clinic,
20:59we always counseled them about preventive
21:02measures that they can do to limit
21:06additional UV damage and sun exposure risk,
21:08but also,
21:12seeing the dermatologist regularly,
21:14making sure that they have full
21:16body skin exams and making sure
21:18that their family and their next
21:20of kin are also screened with
21:22full body skin exams as well.
21:25Sadly there isn't anything that we can
21:28do that will kind of reverse that,
21:32but certainly taking additional precautions
21:34like all of us should be in terms of
21:37avoiding sun exposure and wearing
21:38sunscreen and avoiding tanning salons and
21:40things like that are really good ideas.
21:43I wanted to take us back to the
21:46whole concept of brain metastases so
21:48we know that Melanoma, as you said,
21:52the incidence is increasing.
21:53People are getting this as they get older.
21:55But what proportion of patients with
21:58Melanoma actually will get brain metastases?
22:02So about 40% of patients with
22:04advanced Melanoma at some
22:06point get a brain metastasis.
22:08Now, as we're using a lot of
22:11better imaging modalities,
22:13mainly MRI of the brain,
22:15we're catching a lot of
22:17asymptomatic brain metastases,
22:19so these are very small
22:20metastases that are not associated with
22:22significant edema around them,
22:24and so we're able to treat
22:26these smaller metastases earlier so that
22:29they don't later become a larger issue.
22:33There's a lot of toxicity
22:36related to symptomatic brain metastases
22:38because the brain itself is,
22:40you know, encased in a very thick
22:44structural support system,
22:46which is the skull,
22:47and so there's not a lot of
22:49room for any lesions to expand
22:52or any swelling to occur,
22:53and so you have a very finite
22:56window to address growing
22:58lesions in the brain and so that's why
23:01we've come up with alternative and
23:03adjunctive therapies to help achieve
23:05local control in the brain better.
23:07And that includes not in
23:09addition to immune therapy,
23:11but also adding radiation to that
23:13plan to help boost that immune response.
23:17I want to get to the
23:19treatments and what we can do
23:21about brain metastases in a minute.
23:24But that 40% number,
23:26that seemed high to me.
23:28So is that 40% of people who present
23:31with advanced Melanoma or any Melanoma? NOTE Confidence: 0.928736929523809
23:34For example,
23:35let's suppose you were going
23:37to your dermatologist and you
23:39know they happen to find a small
23:41Melanoma on the back of your hand.
23:44Would you automatically get a brain MRI and
23:47is your risk still 40% of
23:50getting a brain metastases?
23:52No, just to correct that
23:55number really only applies to
23:57those with advanced Melanoma,
23:59so Melanoma that has metastasized
24:02to other areas of the body,
24:05typically, for staging for Melanoma
24:07we really rely on tumor thickness and
24:10whether or not it's gone to lymph nodes.
24:12When it's gone to the lymph nodes,
24:14that makes you a stage three Melanoma
24:17and at the initial visit we usually
24:19scan the brain to just make
24:21sure that it isn't a stage four
24:23Melanoma that we aren't catching,
24:25and under diagnosing what would
24:28have been metastatic disease.
24:30So that 40% really reflects those with
24:33advanced disease that spread beyond
24:36the lymph nodes to other distant sites.
24:39Got it and so if you do have a brain
24:42met it could be asymptomatic.
24:45It could be picked up on an MRI or it
24:48could be symptomatic at presentation.
24:50Tell us a little bit more about how exactly
24:55you treat these patients?
25:00So if you presented with symptoms are
25:04you likely to resolve those symptoms?
25:06How good are our treatments?
25:10The treatments themselves over the past
25:13five years have just magically improved.
25:16Not only do we have better systemic therapies
25:19that we know are effective in the brain,
25:22but we also are better at timing in terms
25:25of when to go in and resect symptomatic
25:29brain metastases or radiate them in
25:32conjunction with her systemic therapies.
25:35So, for example,
25:36if a patient presents to the emergency room
25:40with nausea, vomiting,
25:41some dizziness and balance issues,
25:44they get a brain scan in the emergency room
25:47are found to have new lesions in the brain,
25:50if those lesions are large and associated
25:53with significant edema, and that is
25:55what's contributing to the symptoms,
25:57oftentimes we have to get our
26:00neurosurgery colleagues involved to
26:02rapidly address that lesion and
26:04the most rapid way is via surgery.
26:07You know, it's a morbid procedure,
26:08but the outcomes are typically
26:10very good and people have
26:12a very fast recovery.
26:13If, for example,
26:15the lesion is amenable to what we
26:19call stereotactic radiosurgery,
26:21which is very high radiation but
26:24very focused radiation to try to
26:26spare the normal surrounding brain
26:28tissue and therefore limit the side
26:31effects of radiation in the brain,
26:33that itself is also a very effective therapy.
26:36It's considered definitive, however,
26:38it can only really be treated
26:41for lesions that are less than 3 centimeters,
26:44if you have a lesion greater
26:46than 3 centimeters,
26:46surgery is the best option.
26:49If you have multiple lesions,
26:51basically multiple small lesions,
26:53too many to be individually treated
26:56with what we call stereotactic
26:59radiosurgery or gamma knife,
27:01then the next option is whole
27:04brain radiation which used to be very
27:07neurotoxic long term because these patients
27:10would develop cognitive decline later on.
27:13Memory issues very similar to dementia.
27:17Nowadays we have additional options
27:19where we can spare the hippocampus.
27:21This learning and memory center
27:23in our brain and so we can try to
27:26avoid some of these late chronic
27:29sequella of radiation therapy.
27:31Other options are to actually use some
27:33of the drugs that have been known to be
27:36effective in treating Alzheimer's patients
27:38while they get whole brain radiation to try
27:41to have a neuroprotective effect to spare
27:44the normal brain from receiving
27:46some of the detrimental long
27:49term side effects of radiation.
27:51I mean it sounds like there's
27:53a lot of potential for
27:55therapies for brain metastases,
27:57but just in our last 30 seconds.
28:00So if you have a brain
28:02metastasis and it's been treated,
28:04what's your overall prognosis?
28:06So we're finding with the combination
28:09of radiation and immune therapies,
28:11prognosis can be actually very good.
28:14Before it was three to six months
28:16for anyone with brain metastases.
28:18Now we're talking years out.
28:21If you have a tumor that
28:23responds to these treatments,
28:24and so the overall survival,
28:26the prognosis is much more bright
28:28than what it was ten years ago.
28:31Doctor Thuy Tran is an instructor
28:33of medicine in medical oncology
28:35at the Yale School of Medicine.
28:37If you have questions,
28:38the address is cancer answers at
28:41yale.edu and past editions of the
28:43program are available in audio and
28:46written form at yalecancercenter.org.
28:47We hope you'll join us next week to
28:50learn more about the fight against
28:52cancer here on Connecticut Public
28:54radio funding for Yale Cancer
28:55Answers is provided by Smilow
28:57Cancer Hospital and AstraZeneca.