Blood Cancer Awareness Month

Transcript

00:00 --> 00:03Funding for Yale Cancer Answers is
00:03 --> 00:06provided by Smilow Cancer Hospital.
00:06 --> 00:08Welcome to Yale Cancer Answers
00:08 --> 00:10with Doctor Anees Chagpar.
00:10 --> 00:11Yale Cancer Answers features the
00:11 --> 00:13latest information on cancer
00:13 --> 00:15care by welcoming oncologists and
00:15 --> 00:17specialists who are on the forefront
00:17 --> 00:19of the battle to fight cancer.
00:19 --> 00:20This week it's a conversation about
00:20 --> 00:23the care of patients with myeloid
00:23 --> 00:25disorders with Doctor Lourdes Mendez.
00:25 --> 00:27Dr. Mendez is an assistant professor
00:27 --> 00:29of medicine and hematology at the
00:29 --> 00:31Yale School of Medicine, where Dr.
00:31 --> 00:33Chagpar is a professor of surgical oncology.
00:35 --> 00:37Dr. Mendez, maybe we can start off
00:37 --> 00:39by you telling us a little bit more
00:39 --> 00:41about yourself and what it is you do.
00:42 --> 00:47So I'm a hematologist and in the last years
00:47 --> 00:50the patients we care for has expanded
00:50 --> 00:52to include individuals who have
00:52 --> 00:55something we're calling pre disease
00:55 --> 00:58and also clonal hematopoiesis.
00:58 --> 01:02So our team includes my physician
01:02 --> 01:04colleagues who are hematologists,
01:04 --> 01:09also very dedicated Aprn's and nurses,
01:09 --> 01:11as well as an incredibly talented
01:11 --> 01:13and dedicated research team.
01:13 --> 01:15And we provide approved treatments,
01:15 --> 01:19but we're also very much involved in
01:19 --> 01:21clinical trials and investigations
01:21 --> 01:24as well as in trying to make
01:24 --> 01:27new discoveries in the lab,
01:27 --> 01:29both the wet lab as it's called
01:29 --> 01:31and in the dry lab.
01:31 --> 01:34So we work together to care for
01:34 --> 01:36existing patients and try and
01:36 --> 01:37move the needle in our field.
01:39 --> 01:41So let's get through a bit of
01:41 --> 01:43the vocabulary so you can help
01:43 --> 01:45to define some of the terms and
01:45 --> 01:47the kinds of patients you treat.
01:47 --> 01:50For example,
01:50 --> 01:52what are myeloid disorders?
01:53 --> 01:56So if we take one further step back and
01:56 --> 02:00we talk about the blood and the different
02:00 --> 02:02cell types in that are in the blood,
02:02 --> 02:04there are three main types.
02:04 --> 02:05There are white blood cells,
02:05 --> 02:07there are red blood cells,
02:07 --> 02:09and there are platelets.
02:09 --> 02:14And the white blood cell family further
02:14 --> 02:18can be subdivided into myeloid cells
02:18 --> 02:21and lymphoid cells as two subcategories.
02:21 --> 02:24And the myeloid cells,
02:24 --> 02:27I call them first responders because
02:27 --> 02:31their role is to come to the site of
02:31 --> 02:35infection or the site of an injury as
02:35 --> 02:39the first representation of the immune
02:39 --> 02:43response to that kind of insult.
02:43 --> 02:48And so these cells can become abnormal and
02:48 --> 02:50if the abnormality is profound enough,
02:50 --> 02:52they become cancerous.
02:52 --> 02:57And so then we refer to them or
02:57 --> 02:59these these conditions as myeloid
02:59 --> 03:01diseases or myeloid neoplasms,
03:01 --> 03:04they're basically myeloid cancers.
03:05 --> 03:07And then you mentioned a couple
03:07 --> 03:08of other phenomena that you've
03:08 --> 03:10started treating more recently.
03:10 --> 03:11Can you tell us a little
03:11 --> 03:12bit more about those?
03:14 --> 03:17Yes, and I think I should just briefly mention
03:17 --> 03:20about leukemia before I go into the
03:20 --> 03:24more recent predisease category.
03:24 --> 03:30So leukemia refers to a growth of
03:30 --> 03:32abnormal cells in the blood and
03:32 --> 03:35it can be further divided as acute
03:35 --> 03:38leukemia and as chronic leukemia.
03:38 --> 03:42So acute leukemia is termed that
03:42 --> 03:46way because it needs really rapid
03:46 --> 03:49attention because it refers to really
03:49 --> 03:51uncontrolled production of cancer cells
03:51 --> 03:55in the bone marrow and then they
03:55 --> 03:58can also spill over into the blood.
03:58 --> 04:02Chronic leukemias are on the other end of
04:02 --> 04:05the spectrum and the term we use is indolent,
04:05 --> 04:08which refers to the fact that
04:08 --> 04:12they are kind of a slow process,
04:12 --> 04:15something that usually we address
04:15 --> 04:18over months and maybe sometimes
04:18 --> 04:21even years or can just observe.
04:21 --> 04:26And myeloid diseases can be chronic
04:26 --> 04:29myeloid neoplasms or chronic myeloid
04:29 --> 04:32leukemias or there is acute myeloid leukemia.
04:32 --> 04:36Our group actually also cares for
04:36 --> 04:38acute lymphoblastic leukemia,
04:38 --> 04:41which is that other subfamily of
04:41 --> 04:45white blood cells that I was talking
04:45 --> 04:48about within the white blood cells
04:48 --> 04:50and the as distinct from the first
04:50 --> 04:53responders which are the myeloid cells,
04:53 --> 04:54the lymphoid cells,
04:54 --> 04:57we call them the smart cells because
04:57 --> 05:00they learn and they adapt specifically
05:00 --> 05:04to infections and potentially also
05:04 --> 05:08to abnormal cells like cancer cells.
05:08 --> 05:11So that brings us to a different
05:11 --> 05:14condition that's more recently been
05:14 --> 05:18recognized that I called predisease
05:18 --> 05:20and clonal hematopoiesis.
05:20 --> 05:24And really this is a new entity that
05:24 --> 05:27was only recently codified meaning
05:27 --> 05:30made part of our classification
05:30 --> 05:33systems formally in the last year.
05:33 --> 05:37And it reflects our fields recognition
05:37 --> 05:42that there is a condition that precedes
05:42 --> 05:45myeloid neoplasms but also other blood
05:45 --> 05:49cancers called clonal hematopoiesis.
05:49 --> 05:52And it bears some of the genetic
05:52 --> 05:56fingerprint of the full blown blood cancer.
05:56 --> 05:58But it's at the very,
05:58 --> 06:00very early stages.
06:00 --> 06:04It's the first hint in some ways
06:04 --> 06:06of an abnormal cell and in the
06:06 --> 06:09overwhelming majority of people it
06:09 --> 06:12will never become a blood cancer.
06:12 --> 06:14But we do know that taken as a whole,
06:14 --> 06:17there's about an 11 fold increased
06:17 --> 06:20risk of developing a blood cancer if
06:20 --> 06:24there is this predisease condition
06:24 --> 06:26called clonal hematopoiesis.
06:26 --> 06:29The rate of developing a blood cancer
06:29 --> 06:32is very low, less than 1% a year,
06:32 --> 06:34well below that actually.
06:34 --> 06:38And so the challenge in the field
06:38 --> 06:41is to identify those individuals
06:41 --> 06:45that are at high risk of developing
06:45 --> 06:49a blood cancer down the line.
06:49 --> 06:53And we are learning about what
06:53 --> 06:57distinguishes people who have that high risk,
06:57 --> 07:01but we're very much still in the midst
07:01 --> 07:05of defining who they are and what
07:05 --> 07:08the risk factors for progression are.
07:08 --> 07:14We also know that this predisease condition
07:14 --> 07:20increases the risk of dying of mortality.
07:20 --> 07:23And surprisingly when this
07:23 --> 07:27entity was first being described,
07:27 --> 07:29it was found that it seems to
07:29 --> 07:32be due to cardiovascular disease.
07:32 --> 07:36And the increased risk of clonal
07:36 --> 07:38hematopoiesis on cardiovascular
07:38 --> 07:41disease is on the order of other
07:41 --> 07:44very well established risk factors
07:44 --> 07:46for cardiovascular disease.
07:46 --> 07:48So this has become a part of
07:48 --> 07:49our counseling when
07:49 --> 07:52someone is found to have clonal
07:52 --> 07:55hematopoiesis about the need to
07:55 --> 07:57assess for other existing risk
07:57 --> 07:59factors and to optimize management
07:59 --> 08:02of those other risk factors.
08:04 --> 08:06So that all sounds really exciting that
08:06 --> 08:09you find this precancer as it were.
08:09 --> 08:11And we know that in a number
08:11 --> 08:12of other malignancies,
08:12 --> 08:15for example breast cancer, skin cancer,
08:15 --> 08:17colon cancer, cervical cancer,
08:17 --> 08:20we have these preinvasive kind of
08:20 --> 08:22diseases that we can screen for
08:22 --> 08:25often times we find them early
08:25 --> 08:28and that allows us to treat them.
08:28 --> 08:31So in the case of clonal hematopoiesis,
08:31 --> 08:33I guess the same question applies.
08:33 --> 08:35I mean how do we know who gets it?
08:35 --> 08:38Can we screen for it?
08:38 --> 08:40And is there anything that we can do
08:40 --> 08:42that can stop it from progressing
08:42 --> 08:44to full blown myeloid leukemia?
08:45 --> 08:48So those are exactly the questions
08:48 --> 08:53of the moment for this condition.
08:53 --> 08:56And the simple answer is that we
08:56 --> 08:59do not screen for this condition
08:59 --> 09:03because we don't have any proven
09:03 --> 09:05or validated interventions and
09:05 --> 09:08in fact we're still defining who
09:08 --> 09:12would need an intervention at all.
09:12 --> 09:16So currently this is really
09:16 --> 09:19found incidentally as a part
09:19 --> 09:21of other genetic testing.
09:21 --> 09:24For example, if someone has one, you know,
09:24 --> 09:28a solid tumor as you were mentioning
09:28 --> 09:31and underwent genetic testing for that.
09:31 --> 09:33And there's different kinds,
09:33 --> 09:35some that would be more directed
09:35 --> 09:36at characterizing the genetics
09:36 --> 09:38of the solid tumor.
09:38 --> 09:39Whereas other people get
09:39 --> 09:41referred if they have a,
09:41 --> 09:42for example,
09:42 --> 09:45a family history of breast cancer or
09:45 --> 09:48ovarian cancer to genetic counseling.
09:48 --> 09:50And then there's genetic testing
09:50 --> 09:53to see if there's an inherited
09:53 --> 09:56risk for developing cancer.
09:56 --> 10:00And in the course of such genetic testing,
10:00 --> 10:03there can be the incidental
10:03 --> 10:07finding of a genetic mutation that
10:07 --> 10:10best fits with this condition,
10:10 --> 10:13this predisease, clonal hematopoiesis.
10:13 --> 10:17But we don't screen for it.
10:19 --> 10:24If someone has unexplained low blood counts,
10:24 --> 10:29then we do increasingly send a
10:29 --> 10:33panel of genetic testing that has a
10:33 --> 10:38capacity to identify this condition.
10:38 --> 10:40But if someone does not have low blood
10:40 --> 10:42counts, if the blood counts are normal,
10:42 --> 10:47we don't send off such testing to
10:47 --> 10:49screen for clonal hematopoiesis.
10:49 --> 10:52And here I should specify the clonal
10:52 --> 10:55hematopoiesis itself can be further
10:55 --> 10:58subdivided into those cases where
10:58 --> 11:01there is a blood count abnormality,
11:01 --> 11:05like low red blood cells called anemia,
11:05 --> 11:08low white blood cells called leukopenia
11:08 --> 11:11or low platelets thrombocytopenia,
11:11 --> 11:14and that's called secus.
11:14 --> 11:18It's a very long name clonal cytopenia
11:18 --> 11:20of undetermined significance and if
11:20 --> 11:21it's incidentally found in someone
11:21 --> 11:23who has low normal blood counts,
11:23 --> 11:26then it's called CHIP, clonal
11:26 --> 11:28hematopoiesis of indeterminate potential.
11:28 --> 11:31So the goal in the field is of course
11:31 --> 11:35for those individuals that seem to
11:35 --> 11:40have high risk features to ultimately
11:40 --> 11:43develop effective interventions to
11:43 --> 11:46halt the progression to cancer.
11:46 --> 11:49But we're still very much at
11:49 --> 11:52the beginning of that effort.
11:52 --> 11:55It's a very exciting effort however,
11:55 --> 11:55because
11:58 --> 12:00this condition can develop
12:00 --> 12:02into something called MDS,
12:02 --> 12:04myelodysplastic syndrome or
12:04 --> 12:07even acute myeloid leukemia.
12:07 --> 12:12And these conditions can have
12:12 --> 12:14really outcomes that are
12:14 --> 12:16not what we would want five
12:16 --> 12:18year survival rates in the case
12:18 --> 12:21of a ML that on average are 30%.
12:21 --> 12:24And so it would be very desirable
12:24 --> 12:29to be able to cut that off at
12:29 --> 12:32the pass so to speak and that's
12:32 --> 12:36really a major hope in our field.
12:38 --> 12:40So for patients who have
12:40 --> 12:41this premalignant condition,
12:41 --> 12:44we don't screen for them because there
12:44 --> 12:46isn't an intervention that can prevent
12:46 --> 12:49it from becoming an invasive cancer.
12:49 --> 12:51But is there any merit to
12:51 --> 12:52following these patients?
12:52 --> 12:54So let's suppose they incidentally
12:54 --> 12:56were found to have a genetic
12:56 --> 12:58mutation on another panel.
12:58 --> 13:00And so we know that they're at
13:00 --> 13:03increased risk of getting clonal
13:03 --> 13:05hematopoiesis and subsequently
13:05 --> 13:07developing fullblown myeloid leukemia,
13:07 --> 13:08let's say.
13:08 --> 13:12Is there any value to following these
13:12 --> 13:15patients more more frequently to try to
13:15 --> 13:18discover the leukemia when it develops?
13:18 --> 13:21If it develops at an earlier stage,
13:21 --> 13:23maybe we can treat it more effectively,
13:23 --> 13:25particularly given the fact that
13:25 --> 13:27this condition is associated
13:27 --> 13:29with such a poor prognosis?
13:31 --> 13:34That's an excellent question and
13:34 --> 13:37the short answer is that we are
13:37 --> 13:39following some of these individuals
13:39 --> 13:42in clonal hematopoiesis or sometimes
13:42 --> 13:44they're called chip clinics now.
13:44 --> 13:49And that is as you're kind
13:49 --> 13:52of alluding to, to track
13:52 --> 13:55how things change or don't change.
13:55 --> 13:58The complication is that in most
13:58 --> 14:00patients, probably more than 90%,
14:00 --> 14:02what we're detecting we think
14:02 --> 14:04is an age-related phenomenon.
14:04 --> 14:06It's the blood system changing
14:06 --> 14:09as people age because this is a
14:09 --> 14:11a fairly frequent condition
14:11 --> 14:14in older individuals and a rare
14:14 --> 14:16condition in young individuals,
14:16 --> 14:19let's say less than 40
14:19 --> 14:21compared to 70 or older.
14:21 --> 14:23And so we are starting,
14:23 --> 14:25to follow these
14:25 --> 14:28patients as I mentioned and particularly
14:28 --> 14:31those who have low blood counts,
14:31 --> 14:33but it's not because we're ready
14:33 --> 14:36to offer them an intervention.
14:36 --> 14:41Although clinical trials for
14:41 --> 14:45the combination of low blood
14:45 --> 14:48counts and this finding
14:48 --> 14:49of a genetic fingerprint
14:52 --> 14:56that overlaps with the net genetic
14:56 --> 14:58fingerprint of myeloid cancers.
14:58 --> 15:01When those two things coincide and seek us,
15:01 --> 15:03then there are clinical trials
15:03 --> 15:05and interventions that are under
15:05 --> 15:07development for these patients.
15:07 --> 15:10So we have a clonal hematopoiesis clinic
15:10 --> 15:13here at Yale where we're doing just that.
15:13 --> 15:14We're following these patients
15:14 --> 15:18and the goal will be to offer a
15:18 --> 15:20subset of them clinical trials as
15:20 --> 15:23a part of the effort to learn and
15:23 --> 15:25to change the disease course.
15:27 --> 15:29Terrific. Well, we're going to take
15:29 --> 15:31a short break for a medical minute,
15:31 --> 15:33but after the break, I'd like to learn
15:33 --> 15:35more about the research that's been
15:35 --> 15:37going on to potentially help these
15:37 --> 15:39patients with myeloid disorders,
15:39 --> 15:41particularly in honor of
15:41 --> 15:43Blood Cancer Awareness month.
15:43 --> 15:44Please stay tuned to learn
15:44 --> 15:46more with my guest Dr.
15:46 --> 15:47Lourdes Mendez.
15:48 --> 15:50Funding for Yale Cancer Answers
15:50 --> 15:52comes from Smilow Cancer Hospital,
15:52 --> 15:54where their hematology program
15:54 --> 15:56offers diagnosis and treatment of
15:56 --> 15:58blood cancers including lymphoma,
15:58 --> 16:00leukemia, and myeloma.
16:00 --> 16:03More at smilowcancerhospital.org or
16:03 --> 16:05e-mail Cancer Answers at Yale dot Edu.
16:08 --> 16:09Breast cancer is one of the
16:09 --> 16:11most common cancers in women.
16:11 --> 16:12In Connecticut alone,
16:12 --> 16:15approximately 3500 women will be
16:15 --> 16:17diagnosed with breast cancer this year.
16:17 --> 16:19But there is hope thanks
16:19 --> 16:20to earlier detection,
16:20 --> 16:20noninvasive treatments,
16:20 --> 16:23and the development of novel therapies.
16:23 --> 16:25To fight breast cancer,
16:25 --> 16:27women should schedule a baseline
16:27 --> 16:29mammogram beginning at age 40 or
16:29 --> 16:30earlier if they have risk factors
16:30 --> 16:32associated with the disease.
16:32 --> 16:34With screening, early detection,
16:34 --> 16:36and a healthy lifestyle,
16:36 --> 16:38breast cancer can be defeated.
16:38 --> 16:40Clinical trials are currently
16:40 --> 16:42underway at federally designated
16:42 --> 16:44comprehensive cancer centers such
16:44 --> 16:46as Yale Cancer Center and Smilow
16:46 --> 16:48Cancer Hospital to make innovative
16:48 --> 16:50new treatments available to patients.
16:50 --> 16:52Digital breast homosynthesis or 3D
16:52 --> 16:55mammography is also transforming breast
16:55 --> 16:57cancer screening by significantly
16:57 --> 16:59reducing unnecessary procedures
16:59 --> 17:01while picking up more cancers.
17:01 --> 17:04More information is available
17:04 --> 17:05at yalecancercenter.org.
17:05 --> 17:08You're listening to Connecticut Public Radio.
17:08 --> 17:09Welcome
17:09 --> 17:10back to Yale Cancer Answers.
17:10 --> 17:12This is Doctor Anees Chagpar and
17:12 --> 17:14I'm joined tonight by my guest,
17:14 --> 17:15Doctor Lourdes Mendez.
17:15 --> 17:18We're discussing the care of patients
17:18 --> 17:20with myeloid disorders in honor
17:20 --> 17:22of Blood Cancer Awareness Month.
17:22 --> 17:23And right before the break,
17:23 --> 17:24Doctor Mendez,
17:24 --> 17:27you were telling us about this
17:27 --> 17:29phenomenon of clonal hematopoiesis
17:29 --> 17:33and how this is a a novel kind
17:33 --> 17:37of discovery of what is
17:37 --> 17:39essentially a premalignancy,
17:39 --> 17:45a predisease that leads to myeloid leukemias.
17:45 --> 17:47So a couple of questions.
17:47 --> 17:49Given the fact that we're still
17:49 --> 17:50learning about this disease,
17:50 --> 17:53can you shed some light on some
17:53 --> 17:55of the research that's going on
17:55 --> 17:58into it and and perhaps into
17:58 --> 17:59myeloid leukemias as well?
18:01 --> 18:04Absolutely. So in terms of
18:04 --> 18:06the research in this space,
18:06 --> 18:09it's of great interest to kind
18:09 --> 18:13of define what is the natural
18:13 --> 18:14history of this condition.
18:14 --> 18:15So what happened,
18:15 --> 18:18meaning what happens over time,
18:18 --> 18:20when does this start and
18:20 --> 18:22how long is it present?
18:22 --> 18:26Before maybe we can detect it,
18:26 --> 18:31or before it becomes a blood cancer,
18:31 --> 18:35a myeloid neoplasm, for example?
18:35 --> 18:38And one of the things that has
18:38 --> 18:42been reported by scientists who are
18:42 --> 18:44studying clonal hematopoiesis is
18:44 --> 18:48that the best estimations are that
18:48 --> 18:51in probably the majority of cases,
18:51 --> 18:55this condition is present for decades,
18:55 --> 18:59maybe 30 years before it's actually detected.
18:59 --> 19:03Which is really, I think in my mind,
19:03 --> 19:08startling to think that the roots
19:08 --> 19:11of a cancer could go back so far.
19:11 --> 19:12But again,
19:12 --> 19:16I think it's worth reiterating
19:16 --> 19:20that this is a pre disease.
19:20 --> 19:23Maybe that's one of the best ways to call it,
19:23 --> 19:26because in some ways it and in most
19:26 --> 19:29people it's probably a reflection of
19:29 --> 19:34aging more than a condition that has
19:34 --> 19:37any significant pre malignant potential.
19:37 --> 19:40So even though I spoke about the fact
19:40 --> 19:43that there's an elevenfold increased
19:43 --> 19:46risk of a hematologic malignancy,
19:46 --> 19:50I also mentioned that probably
19:50 --> 19:53in 90% of individuals this
19:53 --> 19:56is not going to
19:58 --> 20:01lead to a significant risk of
20:01 --> 20:04a blood cancer and that the
20:05 --> 20:06risk of developing a blood cancer,
20:06 --> 20:09the annual risk, is under 1%.
20:09 --> 20:10That's taken as a whole.
20:10 --> 20:14So really
20:14 --> 20:16maybe one of the main challenges is
20:16 --> 20:19separating out the high risk from
20:19 --> 20:22the low risk individuals and so
20:22 --> 20:26there's a lot of effort to understand,
20:26 --> 20:30to have to collect groups of these cases
20:30 --> 20:35across academic institutions and to
20:35 --> 20:38to understand what types of mutations,
20:38 --> 20:41how much of that mutation,
20:41 --> 20:46what kind of other traits and
20:46 --> 20:48in the blood count, for example.
20:48 --> 20:52How do these things fit together to
20:52 --> 20:55associate either with a very low risk
20:55 --> 20:58situation or a higher risk situation?
20:58 --> 21:02So some of the efforts in terms
21:02 --> 21:04of potential interventions for
21:04 --> 21:06those individuals who are higher
21:06 --> 21:08risk are using designer drugs,
21:08 --> 21:12which we also call targeted drugs which are
21:12 --> 21:15already in use for example in leukemia.
21:15 --> 21:18So in CML,
21:18 --> 21:22we use a class of medications called IDH
21:22 --> 21:26inhibitors that target IDH mutations.
21:26 --> 21:32And so this is going to be a forthcoming
21:32 --> 21:35strategy that's going to be tested in
21:35 --> 21:38patients who have high
21:38 --> 21:40risk clonal hematopoiesis.
21:40 --> 21:43There's also another mutation
21:43 --> 21:47in both clonal hematopoiesis and
21:47 --> 21:49myeloid cancer is called TET 2,
21:49 --> 21:52and it has a cofactor,
21:52 --> 21:54vitamin C And so there's another
21:54 --> 21:57clinical trial that's going to test high
21:57 --> 22:01doses of vitamin C and when I last checked,
22:01 --> 22:04there's also going to be a clinical
22:04 --> 22:08trial even checking whether
22:08 --> 22:12something like metformin may have
22:12 --> 22:15some potential to change the natural
22:15 --> 22:17progression of this condition.
22:17 --> 22:19So there are lots of things being
22:19 --> 22:22planned and underway and lots of
22:22 --> 22:24collaborations that we are also
22:24 --> 22:28participating in to do 2 things kind
22:28 --> 22:30of simultaneously, to continue to
22:30 --> 22:34learn about the basic biology and the,
22:34 --> 22:35as I was saying,
22:35 --> 22:37natural history of these conditions.
22:37 --> 22:40And also at the same time based as
22:40 --> 22:44we learn things in real time to
22:44 --> 22:46pull from even existing therapies
22:46 --> 22:48and see if for people who are who
22:48 --> 22:50are at high risk,
22:50 --> 22:52we can start to have them benefit
22:52 --> 22:54from what we already know.
22:56 --> 22:58So that sounds really exciting.
22:58 --> 23:00The other thing that
23:00 --> 23:01we often think about is,
23:01 --> 23:03you know when you were talking about
23:03 --> 23:05this being a genetic condition,
23:05 --> 23:10so you can find mutations very
23:10 --> 23:12often these days we hear about
23:12 --> 23:14things like CRISPR and gene editing.
23:14 --> 23:17Can you talk a little bit more about
23:17 --> 23:19what exactly those are and if they
23:19 --> 23:21have any role to play in this space?
23:22 --> 23:25I'm glad you bring up the point
23:25 --> 23:27about mutations and genetics.
23:27 --> 23:32So it I think it's worth spending a few
23:32 --> 23:35seconds to distinguish inherited genetic
23:35 --> 23:39changes or mutations or variants from
23:39 --> 23:43acquired during someone's lifetime.
23:45 --> 23:48The condition I've been talking about,
23:48 --> 23:50I'm referring to mutations
23:50 --> 23:53that occurred during a person's
23:53 --> 23:56lifetime and not changes that were
23:56 --> 23:59inherited from someone's parents.
23:59 --> 24:01So just to make that distinction,
24:01 --> 24:04we do have information,
24:04 --> 24:05increasing information in
24:05 --> 24:08myeloid diseases as a whole,
24:08 --> 24:12that there are people who are born
24:12 --> 24:14with a susceptibility to myeloid
24:14 --> 24:18diseases and really to blood cancers.
24:18 --> 24:21So that field is really gaining
24:21 --> 24:24more and more momentum and we
24:24 --> 24:27now know that also true of
24:27 --> 24:31clonal hematopoesis where there are
24:31 --> 24:37places in our genome in our DNA that
24:37 --> 24:40are associated with an increased
24:40 --> 24:43risk for clonal hematopoesis.
24:43 --> 24:48And then to your question about these
24:48 --> 24:52technologies that were first
24:52 --> 24:57used in the laboratory to change
24:57 --> 25:01genes like you were referring to
25:01 --> 25:04CRISPR editing tools that are now
25:04 --> 25:06commonly used in experiments.
25:06 --> 25:11So these to my knowledge are not
25:11 --> 25:14part of the kind of first
25:16 --> 25:18round of intervention so to speak
25:18 --> 25:20or clinical trials that are
25:20 --> 25:22planned for clonal hematopoiesis.
25:22 --> 25:25But they are being applied
25:25 --> 25:29in other blood diseases.
25:29 --> 25:33And it it is very tantalizing to
25:33 --> 25:37imagine that at some point they could
25:37 --> 25:41be applied as a precision tool to fix
25:41 --> 25:45this acquired genetic abnormality and
25:45 --> 25:49stop progression to a blood cancer.
25:53 --> 25:57When we think about the
25:57 --> 26:00preconditions clonal hematopoiesis,
26:00 --> 26:02one of the nice things that you
26:02 --> 26:05were mentioning is that
26:05 --> 26:08trying to think about therapies that
26:08 --> 26:11are relatively non-toxic that can
26:11 --> 26:16potentially slow or even prevent
26:16 --> 26:19progression to fullblown leukemias.
26:19 --> 26:22Can you talk a little bit about some
26:22 --> 26:24of the research and work that's been
26:24 --> 26:27going on in terms of leukemias themselves?
26:27 --> 26:30I mean are we making any progress
26:30 --> 26:33on the research front in terms of
26:33 --> 26:35more targeted therapies for these
26:35 --> 26:38kinds of leukemias whether that's
26:38 --> 26:40with the precision drugs
26:40 --> 26:43that you were talking about or
26:43 --> 26:45even things like immunotherapies.
26:46 --> 26:51So thank you for the question because
26:51 --> 26:53as I mentioned at the very beginning,
26:53 --> 26:55this is a time of a lot of
26:55 --> 26:58optimism in our field for myeloid
26:58 --> 27:00diseases and for acute leukemias.
27:00 --> 27:04Our toolbox has really increased in the
27:04 --> 27:08last several years and it's becoming
27:08 --> 27:12more complex in a good way in terms
27:12 --> 27:14of decisions as to how to approach
27:14 --> 27:16the treatment of these conditions.
27:18 --> 27:20We are seeing improvements and
27:20 --> 27:22outcomes for patients as a result
27:22 --> 27:25of these of this increased toolbox
27:25 --> 27:30and that really those gains are
27:30 --> 27:34on years of of research on the
27:34 --> 27:37molecular biology of these conditions.
27:37 --> 27:42And to give an example of something
27:42 --> 27:46that's exciting in the other
27:46 --> 27:48type of acute leukemia and acute
27:48 --> 27:51lymphoblastic leukemia in a subtype
27:51 --> 27:53called pH positive BALL,
27:53 --> 27:56there's a lot of discussion about
27:56 --> 27:59the potential of chemotherapy free
27:59 --> 28:01treatment now and that's
28:01 --> 28:04one thing that we're very excited
28:04 --> 28:06about is the potential to spare
28:06 --> 28:09our patients the side effects
28:09 --> 28:10of traditional chemotherapy.
28:10 --> 28:13But we're also very involved as
28:13 --> 28:17a field and in Yale in testing
28:17 --> 28:19ways to modulate the immune system
28:19 --> 28:22against myeloid diseases and against
28:22 --> 28:24acute leukemia in particular.
28:24 --> 28:29And so that's a cause for a lot
28:29 --> 28:31of optimism and excitement.
28:32 --> 28:33Dr. Lourdes Mendez
28:33 --> 28:35is an assistant professor of
28:35 --> 28:37medicine and hematology at
28:37 --> 28:38the Yale School of Medicine.
28:38 --> 28:40If you have questions,
28:40 --> 28:42the address is canceranswers@yale.edu,
28:42 --> 28:45and past editions of the program
28:45 --> 28:47are available in audio and written
28:47 --> 28:48form at yalecancercenter.org.
28:48 --> 28:51We hope you'll join us next week to
28:51 --> 28:53learn more about the fight against
28:53 --> 28:54cancer here on Connecticut Public Radio.
28:54 --> 28:57Funding for Yale Cancer Answers is
28:57 --> 29:00provided by Smilow Cancer Hospital.

Information

Blood Cancer Awareness Month with guests Dr. Lourdes Mendez September 10, 2023 Yale Cancer Center visit: http://www.yalecancercenter.org email: canceranswers@yale.edu call: 203-785-4095