October 10, 2024 • 43 mins
Join Dr Gavin Nimon (Orthopaedic Surgeon) for an enlightening episode with Dr. Joanna Czerwinski, a leading haematologist from Flinders Public Hospital, as she unravels the intricacies of lymphoid malignancies. Get ready to demystify the complexities of lymphocytic leukaemia and lymphoma — two formidable blood cancers that originate from lymphocytes. Dr. Czerwinski clarifies the distinctions between leukaemias, which impact the blood, and lymphomas, affecting the lymphatic system, with a deep dive into chronic lymphocytic leukaemia and acute lymphoblastic leukaemia, the latter being notably the most common cancer in children. Gain insight into how these conditions manifest in clinical practice and the critical symptoms they present, including constitutional symptoms and recurrent infections.
The conversation broadens to explore the landscape of lymphoma varieties, focusing on the nuances between diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma. We explore cutting-edge treatment protocols like R-CHOP chemotherapy and delve into the role of innovative therapies including monoclonal antibodies and Bruton tyrosine kinase inhibitors. Dr. Czerwinski sheds light on the vital role of patient immunity and the risks arising from compromised tumor surveillance, providing a thorough examination of the treatment journey and long-term care. Stay informed on the distinctions between Hodgkin's and non-Hodgkin's lymphomas, their prognosis, and the age-related occurrences that can influence outcomes.
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Dr Gavin Nimon (00:00):
Lymphoid malignancies is a topic which
encompasses lymphocyticleukaemia and lymphoma and
represents a diverse group ofblood cancers originating from
lymphocytes, a type of whiteblood cell crucial to our immune
system.
These conditions range fromslow-growing, often indolent
forms to rapidly progressivediseases.
Understanding thesemalignancies is vital for any
healthcare professional, as theycan present in various clinical
(00:20):
settings, from routinecheck-ups to emergency
admissions.
Whether you're a GP managinginitial presentations or a
medical student aiming tounderstand the fundamentals of
lymphocytic leukaemia andlymphoma, today's episode is
essential.
Today, we're here to break downthis complex area with an
interview with Dr JoannaCzerwinski, a haematologist
specialising in this area.
Welcome to Aussie Med Ed.
(00:42):
Good day and welcome to AussieMed Ed, the Australian medical
education podcast designed witha pragmatic approach to medical
conditions by interviewingspecialists in the medical field
.
I'm Gavin Nimon, an orthopaedicsurgeon based in Adelaide, and
I'm broadcasting from Kaurnaland.
I'd like to remind you thatthis podcast is available on all
podcast players and is alsoavailable as a video version on
YouTube.
I'd also like to remind youthat, if you enjoy this podcast,
(01:03):
please subscribe or leave areview or give us a thumbs up,
as I really appreciate thesupport and it helps the channel
grow.
I'd like to start the podcastby acknowledging the traditional
owners of the land on whichthis podcast is produced, the
Kaurna people, and pay myrespects to the elders, both
past, present and emerging.
Well, it's my pleasure now tointroduce Jo Czerwinski, a
(01:25):
haematologist who works atFlinders Public Hospital, who
specialises in haematologicalmalignancies and other
haematological conditions.
Jo, thanks very much for comingon.
Aussie Med Ed.
How do you go through in yourmind how you divide up these
haematological malignancies?
I used to think of them asleukaemias versus lymphomas, but
I understand you go throughlymphoid versus myeloid type
conditions as a way ofconsidering them.
Dr Joanna Czerwinski (01:46):
Thanks, Gavin, for having me.
So yes, I often divide theminto lymphoid and myeloid
conditions, becausehematological malignancies begin
from the hematologic stem cell,which is at the top end of the
rung, and these divide into twotypes of stem cells the rung,
and these divide into two typesof stem cells the lymphoid stem
(02:07):
cell and the myeloid stem cell.
From the lymphoid stem cell yougenerate B cells, t cells and
natural killer cells they're thedifferent subcategories of
lymphoid cells and from themyeloid stem cell you have the
red cells, all of the differentgranulocytes and the platelets,
and as we go through thedifferent types of malignancies,
(02:30):
I will be able to show wherethese malignancies have
generated along thosedevelopment lines.
Dr Gavin Nimon (02:37):
Excellent.
So I understand the lymphoidones were the ones we're going
to talk about today.
They're also the ones that areactually involved in development
of lymphomas as well, which isa different type of condition as
opposed to leukemias.
How do you consider leukemiasversus lymphomas and how do they
vary for the medical student?
Dr Joanna Czerwinski (02:52):
Yeah, so leukemia comes from the Latin
word of leuc, which is whitecell, and aemia, meaning in the
blood system.
So leukemias are just thecancer is in the blood system,
whereas a lymphoma is in thelymphatic system.
So you often find it in lymphnodes as well as the spleen and
the liver, which are part ofthat lymphatic.
The conditions can overlap whenit comes to the bone marrow.
Dr Gavin Nimon (03:16):
Right, and I understand.
You can't get myeloid cells inlymphomas.
It's purely from the lymphoidtype cells.
Dr Joanna Czerwinski (03:22):
That's correct, although the bone
marrow microenvironment let'scall it has both types of cells,
so you can have changes to themyeloid component with lymphoid
conditions.
Dr Gavin Nimon (03:34):
So in your experience, how often do these
conditions present in everydaypractice?
I'm curious because they seemquite rare in general practice,
but I'd like to get a sense ofwhat to look out for.
Dr Joanna Czerwinski (03:44):
From my experiences speaking with
different GPs, it seems to bethat each GP may see two or
three cases in their patientcohort, so it's not very common
from a GP perspective.
It's very common from myperspective, though.
The most common ones that we'llbe speaking about today is
chronic lymphocytic leukemia, asthat's one of the most common
(04:05):
lymphoid conditions that we see.
Dr Gavin Nimon (04:07):
Although I understand the acute lymphocytic
leukemia is actually thecommonest cancer in the young
children.
Dr Joanna Czerwinski (04:12):
So acute lymphoblastic leukemia is an
aggressive form of lymphoidcancer and it has a bimodal
development, that in childrenand that in much older adults as
well.
Dr Gavin Nimon (04:24):
Well, why don't you talk about first of all how
they may present, initially, andthen talk about how you
classify them down into thosedifferent areas?
Dr Joanna Czerwinski (04:30):
Yeah, sure .
So leukemias and lymphomas canpresent with very few symptoms
to begin with, especially ifthey're chronic versions of
disease states.
So chronic lymphocytic leukemia, for instance, can present,
incidentally, just through ablood count, where the patient
has gone to their GP just for aregular checkup.
(04:53):
But when these conditionsbecome more aggressive, they
start to present with what weterm constitutional symptoms,
and this includes dramaticweight loss where the patient is
not dieting.
It can include fevers and nightsweats, and the night sweats
are drenching where they have tochange their pajamas or their
bedsheets.
(05:14):
And it can come with severefatigue where they're
essentially bed bound or couchbound for majority of the day.
Other ways in which patientscan present is recurrent
infections which they can't getover and they need multiple
rounds of antibiotics, and theycan sometimes present with
cytopenic complications ofanemia needing transfusion
(05:37):
thrombocytopenia, where theycome out in a petechial rash or
excessive bleeding and bruising.
And, as we mentioned, rash orexcessive bleeding and bruising
and, as we mentioned, infectionswhere they have low white blood
cell counts Excellent.
Dr Gavin Nimon (05:49):
From what I can understand in my reading, the
simple blood test to see acomplete blood picture can often
pick up the diagnosis straightoff.
Dr Joanna Czerwinski (05:56):
Yeah, very often when lymphoid condition
spills out into the bloodstream,it can be seen by a simple
blood test and a blood filmanalysis.
So the laboratories will lookat a drop of blood under a
microscope and can see thenormal lymphoid cells as well as
the abnormal forms.
Dr Gavin Nimon (06:16):
Okay.
So I'm interested in how youapproach the classification once
you've got the initial findings.
What guides yourdecision-making when identifying
the specific type of lymphoidmalignancy?
Dr Joanna Czerwinski (06:25):
Hmm.
So for the lymphoid conditions,acute lymphoblastic leukemia is
sort of the prototype of acuteillness.
It usually presents within onlya couple of weeks from
development to full-blownsymptoms, and usually the acute
lymphoblastic leukemias willpresent with a pancytopenia, so
(06:46):
low red cells, low neutrophilcounts, low platelet counts, and
they may have lymphoblasts intheir circulation.
That's how the diagnosis ismade.
To further go along, obviouslythis is a bone marrow malignancy
and it is a leukemia.
So it's spilt out into theblood system.
(07:06):
So oftentimes you can get adiagnosis by complete blood
examination and flow cytometrywhich tells us the clone of that
cell.
Now to go into a bit more ofthe classification when we look
at the lymphoid stem cell andhow it generates into more
(07:27):
mature cells, we think about itas where that cell is in its
natural state.
So the lymphoid stem cell iswhere acute lymphoblastic
leukemia originates from.
It is a mutation in that stemcell.
Once the stem cell goes throughits normal development and exits
from the bone marrow, then youhave your mantle cell lymphomas
(07:51):
and some variations of chroniclymphocytic leukemia, before
that lymphoid cell then entersthe lymph node to start its
development and its training, asit were.
And in the lymph node is whereyou get a whole bunch of the
different types of lymphomas.
Now there's more than 80different types of lymphoma and
(08:12):
they're classified into B-celllymphomas and T-cell lymphomas
and they range in aggressivenessfrom indolent to more
aggressive lymphoma types.
And then, once the lymphoidcell has undergone its training
and left the lymph node backinto circulation, you then have
(08:33):
other forms of chroniclymphocytic leukemia and you
also have plasma cell myelomaand other plasma cell disorders,
because the end differentiatinglymphoid cell is a plasma cell
which is capable of producingantibodies.
So, to get back to your earlierquestion about how I would
(08:54):
undergo investigations, they allstart with a CBE, they all have
a blood film and they all haveflow cytometry from peripheral
blood, because even somelymphomas they can spill out of
the lymphatic system and intothe blood where we can easily
pick them up through flowcytometry.
Dr Gavin Nimon (09:15):
What's the importance for classifying them?
If they all present with asimilar way and they all can
cause anemia and infections, whyis it so important to classify
them into these differentsubgroups?
Dr Joanna Czerwinski (09:26):
I guess because the treatment is very
different amongst the differentsubtypes of lymphoid disorders.
So how I would treat an acuteleukemia versus a chronic
leukemia, versus a B-celllymphoma versus a T-cell
lymphoma.
Dr Gavin Nimon (09:41):
And the stages between acute and chronic are
really how quickly they present.
Dr Joanna Czerwinski (09:44):
In that sense it's a crude way of
thinking about it.
Yes, so anything acute oraggressive has usually been
there for a very short period oftime before a patient presents,
whereas a chronic indolentprocess can be there for many
months to even years before apatient is aware of their
condition.
Dr Gavin Nimon (10:03):
What's the cause of the aplastic type effect
that you get from leukemias andlymphomas?
In that sense, why does thatsense?
Why does that occur?
Dr Joanna Czerwinski (10:11):
So, if we think about the bone marrow
being a production factory forred cells, white cells and
platelets, if you have an acuteleukemia event, usually the
lymphoblasts in this scenariowill crowd out the bone marrow,
leaving very little space leftover for normal cells to be
created.
So oftentimes it's because of,say, 80% of the bone marrow is
(10:37):
filled up with blasts and thatonly leaves 20% left over for
normal myeloid cells, which iswhy you get the aplastic
appearances.
Dr Gavin Nimon (10:48):
Okay.
So I'm curious about thisstaging how do you determine the
stage of condition after you'veclassified it, and what role
does that play in treatmentplanning?
Dr Joanna Czerwinski (10:56):
So the leukaemias are staged
differently for the acute andthe chronic lymphoid leukemias.
So acute leukemia, we would domolecular or genetic testing
from their bone marrow todetermine whether they're
aggressive, intermediate or lowrisk genetics and that will then
(11:18):
define whether they go aheadwith a bone marrow transplant in
their course of treatment.
For the chronic lymphocyticleukemias there is what are
called Rye and Binet stagingsystems and they are based on
how many cytopenias the patienthas, how many lymph node areas
(11:38):
are increased by palpation andwhether they have
hepatosplenomegaly.
And so most patients that I seeare actually stage zero from
those systems, meaning that theonly syndrome they have is their
lymphocytosis.
They have otherwise normalblood counts, they don't have
enlarged lymph nodes and theirliver and spleen is normal.
(12:01):
So those are the stagingsystems for the leukemias.
For the lymphomas it is by AnnArbor staging systems, which is
usually through CT guidance orPET guidance, depending on the
lymphoma type.
So stage one is one group oflymph nodes, say in the cervical
(12:23):
area.
Stage two would be two separateareas of lymph nodes but on the
same side of the diaphragm.
Stage three is that it'scrossed both sides of the
diaphragm but it's still withinthe lymph node areas.
And stage four is if it'sinvaded into other organs, such
as bone marrow, spleen and otherorgans like kidneys, for
(12:47):
instance.
So those are the stagingsystems for lymphoma and finally
, for myeloma, there is therevised international staging
system, which is based off of afew different markers like
albumin, ldh, the genetics andthe beta-2 microglobulin.
Dr Gavin Nimon (13:09):
What's the cause of these conditions?
Is it because there's such ahigh turnover of these blood
cells that they've got a greaterchance of causing malignancy or
a genetic transmutation?
Or does it all relate to acongenital cause?
Or is it some sort of exposurecause that causes them?
Dr Joanna Czerwinski (13:24):
Most of these conditions are diagnosed
above the age of 50.
So I like to think of them aswear and tear conditions where
the body has undergone, say, 60years of life and along with
that it is acquired mutations.
There are some circumstanceswhere there are inherited
disorders, so particularly wherewe mentioned acute
(13:47):
lymphoblastic leukemia inchildren.
So, particularly where wementioned acute lymphoblastic
leukemia in children, there arecertain circumstances where it's
related to a genetic mutationwhen they were born.
Dr Gavin Nimon (13:57):
Okay, I understand, Down syndrome is
actually a higher risk of it aswell.
Is that correct?
Dr Joanna Czerwinski (14:02):
Yes, absolutely so.
It is one of the causes ofinherited acute lymphoblastic
leukemia.
Dr Gavin Nimon (14:11):
So, jo, are there any other exposure causes
that can lead to theseconditions as well?
Is there anything you might seeas an adult hematologist that
can be related to this condition?
Dr Joanna Czerwinski (14:19):
Certainly, if patients have received
chemotherapy or radiotherapy forother conditions, say breast
cancer for instance, then thereis an increased risk of
developing lymphomas andleukemias in general.
The same thing goes for some ofthe immunotherapies, for
instance methotrexate, usedcommonly for rheumatoid
arthritis.
(14:39):
There is an increased incidenceof lymphomas following
methotrexate use.
In general, there is a tendencywith autoimmune and
inflammatory conditions to havea higher incidence of lymphoma
and there is also exposure risks.
Dr Gavin Nimon (14:57):
I've also read that smoking might be a factor
as well.
Is that a big factor or is thatonly a slight association?
Dr Joanna Czerwinski (15:04):
It's a slight association.
It's not as strong as, forinstance, lung cancer or head
and neck cancers.
Dr Gavin Nimon (15:10):
So, once you've got a diagnosis and you've
classified it and you've gonethrough the staging, what are
the treatment options?
If we start with, say, theacute episode, what's the sort
of thoughts that go through theprocess of actually treating
such a condition?
Dr Joanna Czerwinski (15:21):
So for acute lymphoblastic leukemia the
treatment is often many monthsof chemotherapy.
The treatment is often manymonths of chemotherapy, usually
in the hospital for majority ofthat time, as the induction
(15:42):
chemotherapies are multi-drug,multi-day therapies and they're
often quite sick in hospitalneeding to manage their febrile
neutropenias, manage theirtoxicities from their
chemotherapies.
Many of the acute lymphoblasticleukemia patients will undergo
an allogeneic stem celltransplant as part of their
therapy and that can beconsidered sort of their
consolidation treatment.
(16:03):
And some patients following anallogeneic transplant or
following their inductionchemotherapy will also have what
we call maintenance therapies.
Patients following anallogeneic transplant or
following their inductionchemotherapy will also have what
we call maintenance therapies.
So the acute lymphoblasticleukemias are very different
from the lymphoma in terms ofthe intensity of management.
If we think about diffuse largeB-cell lymphoma and follicular
(16:25):
lymphoma as the two prototypelymphomas in B-cell malignancies
, diffuse large B-cell lymphomais RCHOP gold standard and
that's the first-line therapyand that's delivered one day
every three weeks for a total ofsix rounds and most patients
will go into remission from justthat course of chemotherapy.
(16:48):
But there are some patientswhich will be resistant and will
need to undertake an autologousstem cell transplant in their
future.
Follicular lymphoma is a muchmore indolent lymphoma and not
all patients will need toundertake treatment straight
away.
And you'll often see a lot ofthis watch and wait program that
(17:11):
hematologists prescribe.
But if a follicular lymphoma isneeding treatment it is because
it is symptomatic and causingthat patient harm.
So for those indolent lymphomas, we only treat when the
lymphoma is causing an actualproblem to the patient.
Dr Gavin Nimon (17:28):
Right.
So that's different to theacute lymphoblastic leukemia
where they're more aggressivetype treatment.
In that scenario theselymphomas do they occur in
children as well, or are theymore in the adult age group?
Dr Joanna Czerwinski (17:39):
There are some Burkitt lymphomas and
follicular lymphomas that canoccur in teenagers.
Dr Gavin Nimon (17:45):
Usually they are again older populations, but
diffuse large b-cell lymphomacan occur, you know, from 30
years onwards as well so we'vegot a acute lymphocytic
leukemias occurring, the youngchildren which have a quite
aggressive treatment ofchemotherapy and I believe it
has quite a high success rate intreating, in cure.
(18:07):
They involve an induction, aconsolidation and a maintenance
type of treatment.
Is that correct?
Yep, then we have our lymphomagroup.
What age group do the lymphomasdid you say they occur in?
Dr Joanna Czerwinski (18:20):
Some types of lymphoma can occur in
teenage years, but mostlymphomas will occur above the
age of 40 or 50.
Dr Gavin Nimon (18:26):
Okay, and they're divided up into various
forms of non-Hodgkin's lymphomasor Hodgkin's lymphomas.
The ones you were mentioningbefore are non-Hodgkin's
lymphoma styles.
Is that correct?
That's right, yes, and whatdetermines the difference
between a non-Hodgkin and aHodgkin's is the presence of a
type of cell.
Is that the way it goes?
Dr Joanna Czerwinski (18:44):
So they're called Hodgkin cells or
Reed-Sternberg cells.
You may have heard that inreference in a textbook, but
they're very large cells thathave a particular histological
feature when they're looked atunder a microscope.
Dr Gavin Nimon (18:59):
Is that the one with the two nuclei, or
something?
Dr Joanna Czerwinski (19:01):
in memory they look like owl's eyes.
Dr Gavin Nimon (19:04):
So the non-Hodgkin lymphomas involve
these large type of B-celllymphomas?
You said there's 60 variousforms of it.
Is that correct?
Dr Joanna Czerwinski (19:11):
80 different forms across B-cell
non-Hodgkin lymphomas, and thenthere's also the T-cell
non-Hodgkin lymphomas as well.
Dr Gavin Nimon (19:20):
Right NK cells also included in this group.
Dr Joanna Czerwinski (19:23):
Yeah, they're called natural killer
cells.
They're very uncommon.
Lymphomas and leukemias, andthey predominantly present, and
leukemias, and theypredominantly present as
leukemias.
Dr Gavin Nimon (19:32):
Okay, so either B cell or T cell, predominantly
B cells, and they present in theolder age group.
If they actually get missed andare picked up late, I've read
somewhere they can present withbowel obstructions or with
respiratory distress fromcollections around the lungs.
Is that correct or is that?
A pretty rare finding nowadays.
Dr Joanna Czerwinski (19:54):
I mean, it's not rare to me but it will
be rare to the generalpopulation.
So some types of aggressivelymphomas like Burkitt's and
diffuse large B-cell lymphoma,we've been able to pick them up
as stage 1 disease, but in thebowel.
We've been able to pick them upas stage 1 disease, but in the
bowel.
And there is this theory thatif patients have pre-existing
(20:17):
Crohn's disease or ulcerativecolitis or they've had some
other immunodeficiency that itcan occur in the bowel as the
primary site.
These are still treated thesame way as if they occurred in
the lymph nodes, though there isalso presentations in the lungs
.
So superior vena cavaobstructive syndromes can often
(20:39):
present with shortness of breathand chest tightness, and the
Hodgkin lymphomas in particularcan present with mediastinal
masses With the differencebetween non-Hodgkin lymphomas in
particular can present withmediastinal masses, With the
difference between non-Hodgkin'sand Hodgkin-style lymphomas.
Dr Gavin Nimon (20:54):
is there Hodgkin-style?
Is there only one type or arethere various sub-forms of
Hodgkin's as well?
Dr Joanna Czerwinski (20:58):
There are five different forms of
Hodgkin's.
Most of them are under what wecall the classical Hodgkin
presentations and thedescription.
Differences between them is howthey appear under the
microscope from their histologysamples.
The one that's a bit differentis the nodular lymphocyte
predominant Hodgkin's lymphoma,because this is treated more
(21:22):
like your B-cell lymphomas, likeDLBCL, for instance.
Dr Gavin Nimon (21:27):
DL.
What does that stand for then?
Dr Joanna Czerwinski (21:30):
Diffuse Large B-Cell Lymphoma.
Dr Gavin Nimon (21:32):
Sorry.
And the Hodgkins?
Have they got a worse or betterprognosis than the non-Hodgkins
?
Dr Joanna Czerwinski (21:38):
Generally very good prognosis.
So especially this also has abimodal presentation in the
population.
So we can see 20-year-olds with80 year olds with them, and how
well you do and how yourprognosis is is based a bit on
your fitness.
So a young person withHodgkin's lymphoma 90% cure rate
(22:00):
with standard treatments.
Dr Gavin Nimon (22:02):
An older person with Hodgkin's because they
can't have the standardchemotherapies at their ages
they are less survived, butstill reasonable prognosis and
the actual percentage of peoplewith Hodgkin's versus
non-Hodgkin's is a significantlygreater number of non-Hodgkin's
or Hodgkin's.
Dr Joanna Czerwin (22:23):
Non-Hodgkin's is certainly much more common.
Dr Gavin Nimon (22:27):
Once the diagnosis is confirmed, how do
you start mapping out thetreatment plan?
What are the main factors thatguide your choice of treatment?
Dr Joanna Czerwinski (22:35):
So often, what can help with a referral to
a hematologist is by having thebasic complete blood
examination and fullbiochemistry with the LDH, as
well as, if there is a lump thatis easily accessible to biopsy.
A core biopsy is going to giveus a world of information,
(22:58):
because that can already startsubtyping what type of lymphoma
it is, how aggressive it is andhow soon does it need treatment.
And how soon does it needtreatment?
And often what I encourage GPsto write on their referral is
whether this patient hasconstitutional symptoms or not,
because that's going to dictatehow quickly I need to see the
(23:20):
patient as well.
There are certain other teststhat can be helpful, so flow
cytometry from peripheral blood.
But even if that's negative,that doesn't exclude the
probability of a lymphoma orleukemia.
Dr Gavin Nimon (23:36):
So flow cytometry is that where the
blood is passed through a tubeand a computer analyzes the type
of cells they are.
Or is that how it works?
Dr Joanna Czerwinski (23:43):
Yeah, roughly so.
The blood is pulled through amachine in single file and a
laser is pointed at these cellsand with all the refracting
light from it it gives off acertain cell signature.
And what we're looking for is aclone of B cells.
(24:04):
So, for instance, in chroniclymphocytic leukemia B cells
will express CD20 and CD19.
That's part of being a B cell.
And chronic lymphocyticleukemia will have another
marker called CD5, which will bepositive and CD10 will be
negative, and that begins sortof the clonality of that cell
(24:26):
and that begins sort of theclonality of that cell.
What defines a clone of a cellis whether they're expressing a
certain light chainno-transcript.
Dr Gavin Nimon (24:40):
You mentioned also getting a core biopsy.
Is that saying that a GP justtakes out a needle and puts it
into a lump, or is it done byultrasound guidance or CT
guidance?
How is it actually physicallydone?
Dr Joanna Czerwinski (24:51):
So I recommend that GPs refer off to
a radiology company for anultrasound-guided core biopsy.
Dr Gavin Nimon (24:59):
We also mentioned passing was the bone
marrow biopsies as well.
How are they actuallyphysically done?
Is that something that needs anadmission to a hospital and an
anaesthetic?
Dr Joanna Czerwinski (25:06):
So in South Australia we do them under
sedation.
So it is like a day procedure.
A patient will come in fastedand they'll have the anaesthetic
team performing the sedationand a hematology team performing
the actual bone marrow.
The procedure itself is only a15 minute procedure and involves
taking a blood sample and abone sample from the posterior
(25:31):
superior iliac spine.
Dr Gavin Nimon (25:33):
Excellent, and one question that came to mind
also is when I was doing thisreading as a surgeon, I felt
sort of left out of the process.
It doesn't sound like oftensurgery is required in these
conditions.
Dr Joanna Czerwinski (25:43):
There certainly is circumstances where
we need to involve a surgeon.
So where we mentioned Hodgkin'slymphoma before, hodgkin's
cells aren't actually not thatpopular in the actual core
biopsy specimens.
So sometimes a core biopsy willbe performed and the specimen
quality is quite good, but itstill misses out on those key
(26:06):
Reed-Sternberg cells.
So often we will refer tosurgeons to perform an
excisional lymph node biopsywhere the whole lymph node is
then sent away for analysis.
Similarly I need acardiothoracic surgeon for the
mediastinal lymph nodes ifthat's the only area of disease.
Sometimes, you know, colorectalsurgeons are needed for the
(26:26):
mediastinal lymph nodes ifthat's the only area of disease.
Sometimes, you know, colorectalsurgeons are needed for the
bowel specimens because they'vecome in with obstruction or
perforation.
And sometimes I need evenorthopedic or neurosurgeons for
the vertebral lesions that maypresent.
Dr Gavin Nimon (26:44):
Excellent, all right, so we've got our biopsies
.
We're going to talk about ourtreatment plans then, and they
obviously vary depending on allthe different classifications.
What are the main headings fortreatment options for treating
these conditions?
Dr Joanna Czerwinski (26:57):
So the stock standard would be
chemotherapy, and that's quitecommon for the aggressive forms
of cancers and usually it's aprotocol of several cycles.
Many of the protocols involvehair loss, nausea, vomiting the
usual side effects fromchemotherapy.
(27:17):
But over the last decade or sowe've developed quite a lot of
different alternative treatmentoptions.
So R-CHOP, being the sort ofprototype, involves rituximab,
which is what the R stands forand that's a monoclonal antibody
(27:41):
.
So it is actually targetingCD20, which we mentioned before,
and so any of the B-cellmalignancies that express CD20
can be targeted with rituximaband certainly for some of the
more indolent lymphomas you canuse rituximab by itself without
chemotherapy.
So chemotherapy, monoclonalantibodies.
(28:02):
There are also immunotherapiesor targeted treatments as well.
So chronic lymphocytic leukemiahas emerged as quite a popular
disease to try and avoidchemotherapy.
We know that chemotherapy works, but chemotherapy is quite a
slog for patients and haslong-term side effects.
(28:24):
So there has been quite a focusover the last decade in trying
to transform the treatmentalgorithm for patients.
So there's these targetedagents which are called Bruton,
tyrosine kinase inhibitors orBTK inhibitors, which is
actually targeting an area ofthe B-cell receptor to turn off
(28:47):
proliferation and to turn offadhesion factors.
So the three BTKs which I usequite often are ibrutinib,
acalabrutinib and zanubrutinib.
You'll notice that all of themend in nib.
(29:07):
So these three agents.
They act on CLL by releasingall of them from the lymphatic
system, from the bone marrowsystem, so that stops the
adhesion to those areas, andthen they stop proliferation, so
they make these cells inert andthe body eventually destroys
them just from it being incirculation.
(29:30):
So it's quite a commontreatment and it is being
expanded into other areas, soWaldenstrom's macroglobulinemia,
which is another form oflymphoma and mantle cell
lymphoma.
We now are able to use theseBTK inhibitors in those diseases
as well.
Dr Gavin Nimon (29:53):
Amazing, I keep getting this common theme that
keeps occurring when we talkabout cancers on these podcasts
is actually the importance ofthe patient's immunity
themselves, their naturalimmunity.
Dr Joanna Czerwinski (30:01):
It is certainly something that I
discuss, with all of my newdiagnoses of any form of cancer,
with my patients.
Lymphoid malignancies are aparticular kettle of fish that
we need to discuss.
So it doesn't make a differencewhether it's a B-cell
malignancy or a T-cellmalignancy.
There is damage to the immunesystem talking to itself.
(30:25):
So B cells and T cells thenormal approach to infection to
foreign bodies is the B cellwill present antigens to the T
cell and the T cell will thendestroy those antigens and
associated pathogens.
(30:47):
And this is a broken systemwhen you've got a malignancy
from either the B cell or the Tcell side.
So one thing that I often talkto with patients is that,
regardless of their lymphoidmalignancy, they are now
considered immunocompromised andthere are three things that I
can do for that patient.
(31:08):
I can test their immunoglobulinlevels and if the
immunoglobulin G level is low,there is replacement available
in the form of intravenous orsubcutaneous immunoglobulins.
There is the system of needingto have easy access to
antibiotics and antiviralsbecause they're more likely to
(31:31):
suffer with infections at a moresevere degree than a patient
with a normal immune system, andthere is vaccinations.
So we do not give any livevaccines because there is a
great risk that the patient willactually develop the disease
that the vaccination wasintended for.
But I tell all of my patientsto be up to date with the
(31:55):
influenza vaccine, covid vaccine, the latest shingles vaccine,
which is called shingrix, andthen the pneumococcal or
pneumovax vaccine.
So that's one part of theimmune system that is in a way
broken.
The other part of the immunesystem that is also broken is
(32:15):
what's called tumor surveillance, so that same B cell presenting
antigen to T cells thatpresents tumor antigens as well
in the normal healthy individualand that system is again broken
.
So any patient with any ofthese lymphoid malignancies has
an increased risk of a secondmalignancy occurring.
(32:37):
So I tell patients you know, beup to date with your age,
appropriate malignancy screening.
So that's bowel cancer,prostate cancer, breast cancer,
cervical cancer, and must notforget about skin cancers.
Dr Gavin Nimon (32:53):
You talked about the use of chemotherapy as well
, but then chemotherapy can alsobe associated with the cause of
leukemias and lymphomas as well.
So can the actual drugs you useto treat the leukemias cause a
cancer too, in that sense?
Dr Joanna Czerwinski (33:05):
Yeah, absolutely so.
Once a patient has undergonechemotherapy, and regardless of
if they've achieved a cure orremission, I do tell them that
it is important to keep up todate with their normal
malignancy checks, but also tohave a blood test every year
just a complete bloodexamination and biochemistry
(33:29):
because we have found somepatients have had chemotherapy
and it's damaged their bonemarrow in other ways, and so we
can often see myelodysplasticsyndrome and acute myeloid
leukemia developing as a resultof prior chemotherapy.
Dr Gavin Nimon (33:46):
Well, actually we mentioned targeted therapy
and use of monoclonal antibodies.
Is that like a tablet you canjust get over the counter, or is
it specifically produced forone individual patient and they
have to have a genetic testingto actually produce it?
How do these medications work?
Dr Joanna Czerwinski (33:59):
So the monoclonal antibodies are
infusions and so long as thepatient has a CD20 malignancy we
can apply for it.
It is dosed based on their bodysurface area, so their height
and weight are taken intoaccount For the targeted
treatments like the BTKinhibitors that I mentioned.
(34:21):
That is an authority scriptthat only a hematologist can
apply for, but it is the samedosing regardless of the patient
indication and regardless ofthe patient weight.
Dr Gavin Nimon (34:35):
So the immune therapy, then the actual targets
, are actually a common form oftherapy.
It's not.
I always had this idea that youmight take the patient's blood,
work out what the immuneresponse would be and target
that particular individual.
Dr Joanna Czerwinski (34:49):
I would hope.
I would hope that that will bethe case in the future, where we
have more tailored approachesto patients.
At the moment, we're using thegenetic tests predominantly to
give us the risk profile of thepatient.
So if they're high risk, I knowthat they may not respond to
chemotherapies and I would morelikely use the targeted
(35:10):
treatments or immunotherapyapproach.
And similarly, if they're lowrisk, that gives me prognostic
information and tells me that itcould be a while away before
this patient needs treatment,and that's a good thing.
Dr Gavin Nimon (35:25):
Jo, when we're talking to a lot of other
physicians about the treatmentof different malignancies or
even just conditions in general,another common thing that comes
up is the use ofmultidisciplinary teams involved
with treatment of patients.
Jo, do you tend to use an MDTas a part of your process, or is
it more of an individualisedtype approach?
Dr Joanna Czerwinski (35:43):
No, absolutely.
We definitely utilisemultidisciplinary teams.
For Flinders, we do have anestablished lymphoma MDT, and so
in these groups we have severalhematologists.
We have the radiationoncologists who can provide
their input in whether radiationcan be delivered safely in this
(36:06):
patient.
We've got the anatomicalpathologists which are
presenting the histologyspecimens, and we have the
radiologists who present the CTscan and PET scan and MRI
findings.
So with all this informationtogether we can establish a
treatment plan that is agreed toby the consensus group.
(36:28):
We also have other types ofMDTs where we involve our allied
health colleagues, becauseoftentimes having a cancer
diagnosis is very stressful fora patient and involves financial
and legal matters as well ashow is this patient going to be
cared for?
Do they need additional OT orPT input?
(36:52):
And we also involve palliativecare, as that can be.
One of the treatment options issupportive cares.
We also involve our infectiousdiseases colleagues in a weekly
meeting because many times,especially in the hospital
setting, our patients have comein with infectious complications
(37:14):
.
Dr Gavin Nimon (37:15):
So it really is quite an extensive group we've
got there.
When others were reading aboutCLL as well, almost it sounded a
bit like prostate cancer, inthat it's actually a lot of.
It can be quite indolent andlongstanding and that generally
there'll be a large number ofproportions of the community
might have it without evenknowing it and might not even
have symptoms of it.
Is that the way of thinkingabout CLL?
It can be as low as grade asthat.
Dr Joanna Czerwinski (37:36):
More than 90% of my patients are found
incidentally and they go on toLymphoma Australia and the
various private Facebook groupsand they find that you know,
neighbors, friends they have CLLas well.
It's only 10% of my patientsthat need treatment and those
(37:57):
10% usually need second andthird-line treatments some way
down the line.
Usually need second and thirdline treatments some way down
the line.
But if a patient has had CLLfor a decade, that bodes well
that they will never requiretreatment.
Dr Gavin Nimon (38:13):
Obviously, we mentioned the ALL definitely
requires treatment, and thelymphomas almost invariably
would require treatment as well.
Would that not be the case?
Dr Joanna Czerwinski (38:22):
Most of the lymphomas will require
treatment at some point.
For some of the subtypes thatare indolent, like the
follicular lymphoma, marginalzone lymphoma is usually
indolent as well.
Many of them can undergo watchand wait, and that could be the
case for a few years, before thelymphoma progresses enough that
(38:42):
it requires treatment at thatstage.
Dr Gavin Nimon (38:45):
So, jo, where do you think things are heading
for the future?
Obviously it's been a lot ofadvances.
Will AI have a lot of inputinto this area down the track,
and is there other areas or newadvances coming out, new
medications or new approaches?
Dr Joanna Czerwinski (38:57):
Certainly there's a lot of work in the
genetic side of things, wherethe more information we are
gleaning from a patient'sgenomic status, the more we can
tailor our approach.
So, for instance, in CLL thereare the BTK inhibitors that I
mentioned.
There are also another class ofdrug called the BCL inhibitors,
(39:20):
like venetoclax, and which oneyou start off with may be
differentiated by what geneticstatus that patient has, and
certainly you can developresistances to those protein
markers and you would not wantto treat a patient with a BCL2
inhibitor if they've got a BCL2mutation, if they've got a BCL2
(39:41):
mutation.
The other side of things, wherethe future holds, there's a lot
of input and research into CAR-Ttherapies, which is chimeric
antigen receptor T celltherapies, and this is in a way
a form of a transplant, whereyou take a patient's T cells,
(40:03):
you send it away for engineeringand manufacturing to make that
T cell smarter and target thelymphoma or the leukemia, and
then you re-infuse the T cellsback into the patient and so
you're retraining the immunesystem to target that tumor and
kill it.
The other form of treatmentthat is emerging quite strongly
(40:27):
is bite therapies, which arebispecific T-cell engagers and
again you're harnessing theT-cells to target the B-cell
malignancies.
Now, these technologies thatI've both mentioned are against
B-cell malignancies.
We don't have that kind oftechnology against T-cells as
(40:48):
yet, but that is something forthe future with further research
.
Dr Gavin Nimon (40:54):
Brilliant.
Well, it's been fantastichearing about this area.
It's actually massive.
In preparation for this podcasttoday, you might have heard me
mention my reading.
I have had to do a lot ofreading as a general orthopedic
surgeon.
I didn't know much about it andit's great hearing about these
different areas and the greattreatment you're offering these
(41:14):
patients.
So thank you very much, joe,for coming on.
Aussie med ed been brilliant.
I'd like to get you back atsome stage to talk about the
myeloid dysplasias andlignancies, and it it's great to
have you here today.
So thank you very much.
Dr Joanna Czerwinski (41:25):
Thank you for having me and looking
forward to the future.
Dr Gavin Nimon (41:28):
Brilliant Well.
Thank you very much, Dr JoCzerwinski.
Thank you very much for comingon.
A specialist haematologist atthe Flinders Public Hospital.
I'd like to remind you that allthe information presented today
is just one opinion and thatthere are numerous ways of
treating all medical conditions.
Therefore, you should alwaysseek advice from your health
professionals in the area inwhich you live.
Also, if you have any concernsabout the information raised
today, please speak to your GPor seek assistance from health
(41:50):
organisations such as Lifelinein Australia.
Thank you very much forlistening to our podcast today.
I'd like to remind you that theinformation provided is just
general advice and may varydepending on the region in which
you are practising or beingtreated.
If you have any concerns orquestions about what we've
discussed, you should seekadvice from your general
practitioner.
I'd like to thank you very muchfor listening to our podcast
and please subscribe to thepodcast for the next episode.
(42:12):
Until then, please stay safe.
Lymphoid malignancies is a topic which
encompasses lymphocyticleukaemia and lymphoma and
represents a diverse group ofblood cancers originating from
lymphocytes, a type of whiteblood cell crucial to our immune
system.
These conditions range fromslow-growing, often indolent
forms to rapidly progressivediseases.
Understanding thesemalignancies is vital for any
healthcare professional, as theycan present in various clinical
(00:20):
settings, from routinecheck-ups to emergency
admissions.
Whether you're a GP managinginitial presentations or a
medical student aiming tounderstand the fundamentals of
lymphocytic leukaemia andlymphoma, today's episode is
essential.
Today, we're here to break downthis complex area with an
interview with Dr JoannaCzerwinski, a haematologist
specialising in this area.
Welcome to Aussie Med Ed.
(00:42):
Good day and welcome to AussieMed Ed, the Australian medical
education podcast designed witha pragmatic approach to medical
conditions by interviewingspecialists in the medical field
.
I'm Gavin Nimon, an orthopaedicsurgeon based in Adelaide, and
I'm broadcasting from Kaurnaland.
I'd like to remind you thatthis podcast is available on all
podcast players and is alsoavailable as a video version on
YouTube.
I'd also like to remind youthat, if you enjoy this podcast,
(01:03):
please subscribe or leave areview or give us a thumbs up,
as I really appreciate thesupport and it helps the channel
grow.
I'd like to start the podcastby acknowledging the traditional
owners of the land on whichthis podcast is produced, the
Kaurna people, and pay myrespects to the elders, both
past, present and emerging.
Well, it's my pleasure now tointroduce Jo Czerwinski, a
(01:25):
haematologist who works atFlinders Public Hospital, who
specialises in haematologicalmalignancies and other
haematological conditions.
Jo, thanks very much for comingon.
Aussie Med Ed.
How do you go through in yourmind how you divide up these
haematological malignancies?
I used to think of them asleukaemias versus lymphomas, but
I understand you go throughlymphoid versus myeloid type
conditions as a way ofconsidering them.
Dr Joanna Czerwinski (01:46):
Thanks, Gavin, for having me.
So yes, I often divide theminto lymphoid and myeloid
conditions, becausehematological malignancies begin
from the hematologic stem cell,which is at the top end of the
rung, and these divide into twotypes of stem cells the rung,
and these divide into two typesof stem cells the lymphoid stem
(02:07):
cell and the myeloid stem cell.
From the lymphoid stem cell yougenerate B cells, t cells and
natural killer cells they're thedifferent subcategories of
lymphoid cells and from themyeloid stem cell you have the
red cells, all of the differentgranulocytes and the platelets,
and as we go through thedifferent types of malignancies,
(02:30):
I will be able to show wherethese malignancies have
generated along thosedevelopment lines.
Dr Gavin Nimon (02:37):
Excellent.
So I understand the lymphoidones were the ones we're going
to talk about today.
They're also the ones that areactually involved in development
of lymphomas as well, which isa different type of condition as
opposed to leukemias.
How do you consider leukemiasversus lymphomas and how do they
vary for the medical student?
Dr Joanna Czerwinski (02:52):
Yeah, so leukemia comes from the Latin
word of leuc, which is whitecell, and aemia, meaning in the
blood system.
So leukemias are just thecancer is in the blood system,
whereas a lymphoma is in thelymphatic system.
So you often find it in lymphnodes as well as the spleen and
the liver, which are part ofthat lymphatic.
The conditions can overlap whenit comes to the bone marrow.
Dr Gavin Nimon (03:16):
Right, and I understand.
You can't get myeloid cells inlymphomas.
It's purely from the lymphoidtype cells.
Dr Joanna Czerwinski (03:22):
That's correct, although the bone
marrow microenvironment let'scall it has both types of cells,
so you can have changes to themyeloid component with lymphoid
conditions.
Dr Gavin Nimon (03:34):
So in your experience, how often do these
conditions present in everydaypractice?
I'm curious because they seemquite rare in general practice,
but I'd like to get a sense ofwhat to look out for.
Dr Joanna Czerwinski (03:44):
From my experiences speaking with
different GPs, it seems to bethat each GP may see two or
three cases in their patientcohort, so it's not very common
from a GP perspective.
It's very common from myperspective, though.
The most common ones that we'llbe speaking about today is
chronic lymphocytic leukemia, asthat's one of the most common
(04:05):
lymphoid conditions that we see.
Dr Gavin Nimon (04:07):
Although I understand the acute lymphocytic
leukemia is actually thecommonest cancer in the young
children.
Dr Joanna Czerwinski (04:12):
So acute lymphoblastic leukemia is an
aggressive form of lymphoidcancer and it has a bimodal
development, that in childrenand that in much older adults as
well.
Dr Gavin Nimon (04:24):
Well, why don't you talk about first of all how
they may present, initially, andthen talk about how you
classify them down into thosedifferent areas?
Dr Joanna Czerwinski (04:30):
Yeah, sure .
So leukemias and lymphomas canpresent with very few symptoms
to begin with, especially ifthey're chronic versions of
disease states.
So chronic lymphocytic leukemia, for instance, can present,
incidentally, just through ablood count, where the patient
has gone to their GP just for aregular checkup.
(04:53):
But when these conditionsbecome more aggressive, they
start to present with what weterm constitutional symptoms,
and this includes dramaticweight loss where the patient is
not dieting.
It can include fevers and nightsweats, and the night sweats
are drenching where they have tochange their pajamas or their
bedsheets.
(05:14):
And it can come with severefatigue where they're
essentially bed bound or couchbound for majority of the day.
Other ways in which patientscan present is recurrent
infections which they can't getover and they need multiple
rounds of antibiotics, and theycan sometimes present with
cytopenic complications ofanemia needing transfusion
(05:37):
thrombocytopenia, where theycome out in a petechial rash or
excessive bleeding and bruising.
And, as we mentioned, rash orexcessive bleeding and bruising
and, as we mentioned, infectionswhere they have low white blood
cell counts Excellent.
Dr Gavin Nimon (05:49):
From what I can understand in my reading, the
simple blood test to see acomplete blood picture can often
pick up the diagnosis straightoff.
Dr Joanna Czerwinski (05:56):
Yeah, very often when lymphoid condition
spills out into the bloodstream,it can be seen by a simple
blood test and a blood filmanalysis.
So the laboratories will lookat a drop of blood under a
microscope and can see thenormal lymphoid cells as well as
the abnormal forms.
Dr Gavin Nimon (06:16):
Okay.
So I'm interested in how youapproach the classification once
you've got the initial findings.
What guides yourdecision-making when identifying
the specific type of lymphoidmalignancy?
Dr Joanna Czerwinski (06:25):
Hmm.
So for the lymphoid conditions,acute lymphoblastic leukemia is
sort of the prototype of acuteillness.
It usually presents within onlya couple of weeks from
development to full-blownsymptoms, and usually the acute
lymphoblastic leukemias willpresent with a pancytopenia, so
(06:46):
low red cells, low neutrophilcounts, low platelet counts, and
they may have lymphoblasts intheir circulation.
That's how the diagnosis ismade.
To further go along, obviouslythis is a bone marrow malignancy
and it is a leukemia.
So it's spilt out into theblood system.
(07:06):
So oftentimes you can get adiagnosis by complete blood
examination and flow cytometrywhich tells us the clone of that
cell.
Now to go into a bit more ofthe classification when we look
at the lymphoid stem cell andhow it generates into more
(07:27):
mature cells, we think about itas where that cell is in its
natural state.
So the lymphoid stem cell iswhere acute lymphoblastic
leukemia originates from.
It is a mutation in that stemcell.
Once the stem cell goes throughits normal development and exits
from the bone marrow, then youhave your mantle cell lymphomas
(07:51):
and some variations of chroniclymphocytic leukemia, before
that lymphoid cell then entersthe lymph node to start its
development and its training, asit were.
And in the lymph node is whereyou get a whole bunch of the
different types of lymphomas.
Now there's more than 80different types of lymphoma and
(08:12):
they're classified into B-celllymphomas and T-cell lymphomas
and they range in aggressivenessfrom indolent to more
aggressive lymphoma types.
And then, once the lymphoidcell has undergone its training
and left the lymph node backinto circulation, you then have
(08:33):
other forms of chroniclymphocytic leukemia and you
also have plasma cell myelomaand other plasma cell disorders,
because the end differentiatinglymphoid cell is a plasma cell
which is capable of producingantibodies.
So, to get back to your earlierquestion about how I would
(08:54):
undergo investigations, they allstart with a CBE, they all have
a blood film and they all haveflow cytometry from peripheral
blood, because even somelymphomas they can spill out of
the lymphatic system and intothe blood where we can easily
pick them up through flowcytometry.
Dr Gavin Nimon (09:15):
What's the importance for classifying them?
If they all present with asimilar way and they all can
cause anemia and infections, whyis it so important to classify
them into these differentsubgroups?
Dr Joanna Czerwinski (09:26):
I guess because the treatment is very
different amongst the differentsubtypes of lymphoid disorders.
So how I would treat an acuteleukemia versus a chronic
leukemia, versus a B-celllymphoma versus a T-cell
lymphoma.
Dr Gavin Nimon (09:41):
And the stages between acute and chronic are
really how quickly they present.
Dr Joanna Czerwinski (09:44):
In that sense it's a crude way of
thinking about it.
Yes, so anything acute oraggressive has usually been
there for a very short period oftime before a patient presents,
whereas a chronic indolentprocess can be there for many
months to even years before apatient is aware of their
condition.
Dr Gavin Nimon (10:03):
What's the cause of the aplastic type effect
that you get from leukemias andlymphomas?
In that sense, why does thatsense?
Why does that occur?
Dr Joanna Czerwinski (10:11):
So, if we think about the bone marrow
being a production factory forred cells, white cells and
platelets, if you have an acuteleukemia event, usually the
lymphoblasts in this scenariowill crowd out the bone marrow,
leaving very little space leftover for normal cells to be
created.
So oftentimes it's because of,say, 80% of the bone marrow is
(10:37):
filled up with blasts and thatonly leaves 20% left over for
normal myeloid cells, which iswhy you get the aplastic
appearances.
Dr Gavin Nimon (10:48):
Okay.
So I'm curious about thisstaging how do you determine the
stage of condition after you'veclassified it, and what role
does that play in treatmentplanning?
Dr Joanna Czerwinski (10:56):
So the leukaemias are staged
differently for the acute andthe chronic lymphoid leukemias.
So acute leukemia, we would domolecular or genetic testing
from their bone marrow todetermine whether they're
aggressive, intermediate or lowrisk genetics and that will then
(11:18):
define whether they go aheadwith a bone marrow transplant in
their course of treatment.
For the chronic lymphocyticleukemias there is what are
called Rye and Binet stagingsystems and they are based on
how many cytopenias the patienthas, how many lymph node areas
(11:38):
are increased by palpation andwhether they have
hepatosplenomegaly.
And so most patients that I seeare actually stage zero from
those systems, meaning that theonly syndrome they have is their
lymphocytosis.
They have otherwise normalblood counts, they don't have
enlarged lymph nodes and theirliver and spleen is normal.
(12:01):
So those are the stagingsystems for the leukemias.
For the lymphomas it is by AnnArbor staging systems, which is
usually through CT guidance orPET guidance, depending on the
lymphoma type.
So stage one is one group oflymph nodes, say in the cervical
(12:23):
area.
Stage two would be two separateareas of lymph nodes but on the
same side of the diaphragm.
Stage three is that it'scrossed both sides of the
diaphragm but it's still withinthe lymph node areas.
And stage four is if it'sinvaded into other organs, such
as bone marrow, spleen and otherorgans like kidneys, for
(12:47):
instance.
So those are the stagingsystems for lymphoma and finally
, for myeloma, there is therevised international staging
system, which is based off of afew different markers like
albumin, ldh, the genetics andthe beta-2 microglobulin.
Dr Gavin Nimon (13:09):
What's the cause of these conditions?
Is it because there's such ahigh turnover of these blood
cells that they've got a greaterchance of causing malignancy or
a genetic transmutation?
Or does it all relate to acongenital cause?
Or is it some sort of exposurecause that causes them?
Dr Joanna Czerwinski (13:24):
Most of these conditions are diagnosed
above the age of 50.
So I like to think of them aswear and tear conditions where
the body has undergone, say, 60years of life and along with
that it is acquired mutations.
There are some circumstanceswhere there are inherited
disorders, so particularly wherewe mentioned acute
(13:47):
lymphoblastic leukemia inchildren.
So, particularly where wementioned acute lymphoblastic
leukemia in children, there arecertain circumstances where it's
related to a genetic mutationwhen they were born.
Dr Gavin Nimon (13:57):
Okay, I understand, Down syndrome is
actually a higher risk of it aswell.
Is that correct?
Dr Joanna Czerwinski (14:02):
Yes, absolutely so.
It is one of the causes ofinherited acute lymphoblastic
leukemia.
Dr Gavin Nimon (14:11):
So, jo, are there any other exposure causes
that can lead to theseconditions as well?
Is there anything you might seeas an adult hematologist that
can be related to this condition?
Dr Joanna Czerwinski (14:19):
Certainly, if patients have received
chemotherapy or radiotherapy forother conditions, say breast
cancer for instance, then thereis an increased risk of
developing lymphomas andleukemias in general.
The same thing goes for some ofthe immunotherapies, for
instance methotrexate, usedcommonly for rheumatoid
arthritis.
(14:39):
There is an increased incidenceof lymphomas following
methotrexate use.
In general, there is a tendencywith autoimmune and
inflammatory conditions to havea higher incidence of lymphoma
and there is also exposure risks.
Dr Gavin Nimon (14:57):
I've also read that smoking might be a factor
as well.
Is that a big factor or is thatonly a slight association?
Dr Joanna Czerwinski (15:04):
It's a slight association.
It's not as strong as, forinstance, lung cancer or head
and neck cancers.
Dr Gavin Nimon (15:10):
So, once you've got a diagnosis and you've
classified it and you've gonethrough the staging, what are
the treatment options?
If we start with, say, theacute episode, what's the sort
of thoughts that go through theprocess of actually treating
such a condition?
Dr Joanna Czerwinski (15:21):
So for acute lymphoblastic leukemia the
treatment is often many monthsof chemotherapy.
The treatment is often manymonths of chemotherapy, usually
in the hospital for majority ofthat time, as the induction
(15:42):
chemotherapies are multi-drug,multi-day therapies and they're
often quite sick in hospitalneeding to manage their febrile
neutropenias, manage theirtoxicities from their
chemotherapies.
Many of the acute lymphoblasticleukemia patients will undergo
an allogeneic stem celltransplant as part of their
therapy and that can beconsidered sort of their
consolidation treatment.
(16:03):
And some patients following anallogeneic transplant or
following their inductionchemotherapy will also have what
we call maintenance therapies.
Patients following anallogeneic transplant or
following their inductionchemotherapy will also have what
we call maintenance therapies.
So the acute lymphoblasticleukemias are very different
from the lymphoma in terms ofthe intensity of management.
If we think about diffuse largeB-cell lymphoma and follicular
(16:25):
lymphoma as the two prototypelymphomas in B-cell malignancies
, diffuse large B-cell lymphomais RCHOP gold standard and
that's the first-line therapyand that's delivered one day
every three weeks for a total ofsix rounds and most patients
will go into remission from justthat course of chemotherapy.
(16:48):
But there are some patientswhich will be resistant and will
need to undertake an autologousstem cell transplant in their
future.
Follicular lymphoma is a muchmore indolent lymphoma and not
all patients will need toundertake treatment straight
away.
And you'll often see a lot ofthis watch and wait program that
(17:11):
hematologists prescribe.
But if a follicular lymphoma isneeding treatment it is because
it is symptomatic and causingthat patient harm.
So for those indolent lymphomas, we only treat when the
lymphoma is causing an actualproblem to the patient.
Dr Gavin Nimon (17:28):
Right.
So that's different to theacute lymphoblastic leukemia
where they're more aggressivetype treatment.
In that scenario theselymphomas do they occur in
children as well, or are theymore in the adult age group?
Dr Joanna Czerwinski (17:39):
There are some Burkitt lymphomas and
follicular lymphomas that canoccur in teenagers.
Dr Gavin Nimon (17:45):
Usually they are again older populations, but
diffuse large b-cell lymphomacan occur, you know, from 30
years onwards as well so we'vegot a acute lymphocytic
leukemias occurring, the youngchildren which have a quite
aggressive treatment ofchemotherapy and I believe it
has quite a high success rate intreating, in cure.
(18:07):
They involve an induction, aconsolidation and a maintenance
type of treatment.
Is that correct?
Yep, then we have our lymphomagroup.
What age group do the lymphomasdid you say they occur in?
Dr Joanna Czerwinski (18:20):
Some types of lymphoma can occur in
teenage years, but mostlymphomas will occur above the
age of 40 or 50.
Dr Gavin Nimon (18:26):
Okay, and they're divided up into various
forms of non-Hodgkin's lymphomasor Hodgkin's lymphomas.
The ones you were mentioningbefore are non-Hodgkin's
lymphoma styles.
Is that correct?
That's right, yes, and whatdetermines the difference
between a non-Hodgkin and aHodgkin's is the presence of a
type of cell.
Is that the way it goes?
Dr Joanna Czerwinski (18:44):
So they're called Hodgkin cells or
Reed-Sternberg cells.
You may have heard that inreference in a textbook, but
they're very large cells thathave a particular histological
feature when they're looked atunder a microscope.
Dr Gavin Nimon (18:59):
Is that the one with the two nuclei, or
something?
Dr Joanna Czerwinski (19:01):
in memory they look like owl's eyes.
Dr Gavin Nimon (19:04):
So the non-Hodgkin lymphomas involve
these large type of B-celllymphomas?
You said there's 60 variousforms of it.
Is that correct?
Dr Joanna Czerwinski (19:11):
80 different forms across B-cell
non-Hodgkin lymphomas, and thenthere's also the T-cell
non-Hodgkin lymphomas as well.
Dr Gavin Nimon (19:20):
Right NK cells also included in this group.
Dr Joanna Czerwinski (19:23):
Yeah, they're called natural killer
cells.
They're very uncommon.
Lymphomas and leukemias, andthey predominantly present, and
leukemias, and theypredominantly present as
leukemias.
Dr Gavin Nimon (19:32):
Okay, so either B cell or T cell, predominantly
B cells, and they present in theolder age group.
If they actually get missed andare picked up late, I've read
somewhere they can present withbowel obstructions or with
respiratory distress fromcollections around the lungs.
Is that correct or is that?
A pretty rare finding nowadays.
Dr Joanna Czerwinski (19:54):
I mean, it's not rare to me but it will
be rare to the generalpopulation.
So some types of aggressivelymphomas like Burkitt's and
diffuse large B-cell lymphoma,we've been able to pick them up
as stage 1 disease, but in thebowel.
We've been able to pick them upas stage 1 disease, but in the
bowel.
And there is this theory thatif patients have pre-existing
(20:17):
Crohn's disease or ulcerativecolitis or they've had some
other immunodeficiency that itcan occur in the bowel as the
primary site.
These are still treated thesame way as if they occurred in
the lymph nodes, though there isalso presentations in the lungs
.
So superior vena cavaobstructive syndromes can often
(20:39):
present with shortness of breathand chest tightness, and the
Hodgkin lymphomas in particularcan present with mediastinal
masses With the differencebetween non-Hodgkin lymphomas in
particular can present withmediastinal masses, With the
difference between non-Hodgkin'sand Hodgkin-style lymphomas.
Dr Gavin Nimon (20:54):
is there Hodgkin-style?
Is there only one type or arethere various sub-forms of
Hodgkin's as well?
Dr Joanna Czerwinski (20:58):
There are five different forms of
Hodgkin's.
Most of them are under what wecall the classical Hodgkin
presentations and thedescription.
Differences between them is howthey appear under the
microscope from their histologysamples.
The one that's a bit differentis the nodular lymphocyte
predominant Hodgkin's lymphoma,because this is treated more
(21:22):
like your B-cell lymphomas, likeDLBCL, for instance.
Dr Gavin Nimon (21:27):
DL.
What does that stand for then?
Dr Joanna Czerwinski (21:30):
Diffuse Large B-Cell Lymphoma.
Dr Gavin Nimon (21:32):
Sorry.
And the Hodgkins?
Have they got a worse or betterprognosis than the non-Hodgkins
?
Dr Joanna Czerwinski (21:38):
Generally very good prognosis.
So especially this also has abimodal presentation in the
population.
So we can see 20-year-olds with80 year olds with them, and how
well you do and how yourprognosis is is based a bit on
your fitness.
So a young person withHodgkin's lymphoma 90% cure rate
(22:00):
with standard treatments.
Dr Gavin Nimon (22:02):
An older person with Hodgkin's because they
can't have the standardchemotherapies at their ages
they are less survived, butstill reasonable prognosis and
the actual percentage of peoplewith Hodgkin's versus
non-Hodgkin's is a significantlygreater number of non-Hodgkin's
or Hodgkin's.
Dr Joanna Czerwin (22:23):
Non-Hodgkin's is certainly much more common.
Dr Gavin Nimon (22:27):
Once the diagnosis is confirmed, how do
you start mapping out thetreatment plan?
What are the main factors thatguide your choice of treatment?
Dr Joanna Czerwinski (22:35):
So often, what can help with a referral to
a hematologist is by having thebasic complete blood
examination and fullbiochemistry with the LDH, as
well as, if there is a lump thatis easily accessible to biopsy.
A core biopsy is going to giveus a world of information,
(22:58):
because that can already startsubtyping what type of lymphoma
it is, how aggressive it is andhow soon does it need treatment.
And how soon does it needtreatment?
And often what I encourage GPsto write on their referral is
whether this patient hasconstitutional symptoms or not,
because that's going to dictatehow quickly I need to see the
(23:20):
patient as well.
There are certain other teststhat can be helpful, so flow
cytometry from peripheral blood.
But even if that's negative,that doesn't exclude the
probability of a lymphoma orleukemia.
Dr Gavin Nimon (23:36):
So flow cytometry is that where the
blood is passed through a tubeand a computer analyzes the type
of cells they are.
Or is that how it works?
Dr Joanna Czerwinski (23:43):
Yeah, roughly so.
The blood is pulled through amachine in single file and a
laser is pointed at these cellsand with all the refracting
light from it it gives off acertain cell signature.
And what we're looking for is aclone of B cells.
(24:04):
So, for instance, in chroniclymphocytic leukemia B cells
will express CD20 and CD19.
That's part of being a B cell.
And chronic lymphocyticleukemia will have another
marker called CD5, which will bepositive and CD10 will be
negative, and that begins sortof the clonality of that cell
(24:26):
and that begins sort of theclonality of that cell.
What defines a clone of a cellis whether they're expressing a
certain light chainno-transcript.
Dr Gavin Nimon (24:40):
You mentioned also getting a core biopsy.
Is that saying that a GP justtakes out a needle and puts it
into a lump, or is it done byultrasound guidance or CT
guidance?
How is it actually physicallydone?
Dr Joanna Czerwinski (24:51):
So I recommend that GPs refer off to
a radiology company for anultrasound-guided core biopsy.
Dr Gavin Nimon (24:59):
We also mentioned passing was the bone
marrow biopsies as well.
How are they actuallyphysically done?
Is that something that needs anadmission to a hospital and an
anaesthetic?
Dr Joanna Czerwinski (25:06):
So in South Australia we do them under
sedation.
So it is like a day procedure.
A patient will come in fastedand they'll have the anaesthetic
team performing the sedationand a hematology team performing
the actual bone marrow.
The procedure itself is only a15 minute procedure and involves
taking a blood sample and abone sample from the posterior
(25:31):
superior iliac spine.
Dr Gavin Nimon (25:33):
Excellent, and one question that came to mind
also is when I was doing thisreading as a surgeon, I felt
sort of left out of the process.
It doesn't sound like oftensurgery is required in these
conditions.
Dr Joanna Czerwinski (25:43):
There certainly is circumstances where
we need to involve a surgeon.
So where we mentioned Hodgkin'slymphoma before, hodgkin's
cells aren't actually not thatpopular in the actual core
biopsy specimens.
So sometimes a core biopsy willbe performed and the specimen
quality is quite good, but itstill misses out on those key
(26:06):
Reed-Sternberg cells.
So often we will refer tosurgeons to perform an
excisional lymph node biopsywhere the whole lymph node is
then sent away for analysis.
Similarly I need acardiothoracic surgeon for the
mediastinal lymph nodes ifthat's the only area of disease.
Sometimes, you know, colorectalsurgeons are needed for the
(26:26):
mediastinal lymph nodes ifthat's the only area of disease.
Sometimes, you know, colorectalsurgeons are needed for the
bowel specimens because they'vecome in with obstruction or
perforation.
And sometimes I need evenorthopedic or neurosurgeons for
the vertebral lesions that maypresent.
Dr Gavin Nimon (26:44):
Excellent, all right, so we've got our biopsies
.
We're going to talk about ourtreatment plans then, and they
obviously vary depending on allthe different classifications.
What are the main headings fortreatment options for treating
these conditions?
Dr Joanna Czerwinski (26:57):
So the stock standard would be
chemotherapy, and that's quitecommon for the aggressive forms
of cancers and usually it's aprotocol of several cycles.
Many of the protocols involvehair loss, nausea, vomiting the
usual side effects fromchemotherapy.
(27:17):
But over the last decade or sowe've developed quite a lot of
different alternative treatmentoptions.
So R-CHOP, being the sort ofprototype, involves rituximab,
which is what the R stands forand that's a monoclonal antibody
(27:41):
.
So it is actually targetingCD20, which we mentioned before,
and so any of the B-cellmalignancies that express CD20
can be targeted with rituximaband certainly for some of the
more indolent lymphomas you canuse rituximab by itself without
chemotherapy.
So chemotherapy, monoclonalantibodies.
(28:02):
There are also immunotherapiesor targeted treatments as well.
So chronic lymphocytic leukemiahas emerged as quite a popular
disease to try and avoidchemotherapy.
We know that chemotherapy works, but chemotherapy is quite a
slog for patients and haslong-term side effects.
(28:24):
So there has been quite a focusover the last decade in trying
to transform the treatmentalgorithm for patients.
So there's these targetedagents which are called Bruton,
tyrosine kinase inhibitors orBTK inhibitors, which is
actually targeting an area ofthe B-cell receptor to turn off
(28:47):
proliferation and to turn offadhesion factors.
So the three BTKs which I usequite often are ibrutinib,
acalabrutinib and zanubrutinib.
You'll notice that all of themend in nib.
(29:07):
So these three agents.
They act on CLL by releasingall of them from the lymphatic
system, from the bone marrowsystem, so that stops the
adhesion to those areas, andthen they stop proliferation, so
they make these cells inert andthe body eventually destroys
them just from it being incirculation.
(29:30):
So it's quite a commontreatment and it is being
expanded into other areas, soWaldenstrom's macroglobulinemia,
which is another form oflymphoma and mantle cell
lymphoma.
We now are able to use theseBTK inhibitors in those diseases
as well.
Dr Gavin Nimon (29:53):
Amazing, I keep getting this common theme that
keeps occurring when we talkabout cancers on these podcasts
is actually the importance ofthe patient's immunity
themselves, their naturalimmunity.
Dr Joanna Czerwinski (30:01):
It is certainly something that I
discuss, with all of my newdiagnoses of any form of cancer,
with my patients.
Lymphoid malignancies are aparticular kettle of fish that
we need to discuss.
So it doesn't make a differencewhether it's a B-cell
malignancy or a T-cellmalignancy.
There is damage to the immunesystem talking to itself.
(30:25):
So B cells and T cells thenormal approach to infection to
foreign bodies is the B cellwill present antigens to the T
cell and the T cell will thendestroy those antigens and
associated pathogens.
(30:47):
And this is a broken systemwhen you've got a malignancy
from either the B cell or the Tcell side.
So one thing that I often talkto with patients is that,
regardless of their lymphoidmalignancy, they are now
considered immunocompromised andthere are three things that I
can do for that patient.
(31:08):
I can test their immunoglobulinlevels and if the
immunoglobulin G level is low,there is replacement available
in the form of intravenous orsubcutaneous immunoglobulins.
There is the system of needingto have easy access to
antibiotics and antiviralsbecause they're more likely to
(31:31):
suffer with infections at a moresevere degree than a patient
with a normal immune system, andthere is vaccinations.
So we do not give any livevaccines because there is a
great risk that the patient willactually develop the disease
that the vaccination wasintended for.
But I tell all of my patientsto be up to date with the
(31:55):
influenza vaccine, covid vaccine, the latest shingles vaccine,
which is called shingrix, andthen the pneumococcal or
pneumovax vaccine.
So that's one part of theimmune system that is in a way
broken.
The other part of the immunesystem that is also broken is
(32:15):
what's called tumor surveillance, so that same B cell presenting
antigen to T cells thatpresents tumor antigens as well
in the normal healthy individualand that system is again broken
.
So any patient with any ofthese lymphoid malignancies has
an increased risk of a secondmalignancy occurring.
(32:37):
So I tell patients you know, beup to date with your age,
appropriate malignancy screening.
So that's bowel cancer,prostate cancer, breast cancer,
cervical cancer, and must notforget about skin cancers.
Dr Gavin Nimon (32:53):
You talked about the use of chemotherapy as well
, but then chemotherapy can alsobe associated with the cause of
leukemias and lymphomas as well.
So can the actual drugs you useto treat the leukemias cause a
cancer too, in that sense?
Dr Joanna Czerwinski (33:05):
Yeah, absolutely so.
Once a patient has undergonechemotherapy, and regardless of
if they've achieved a cure orremission, I do tell them that
it is important to keep up todate with their normal
malignancy checks, but also tohave a blood test every year
just a complete bloodexamination and biochemistry
(33:29):
because we have found somepatients have had chemotherapy
and it's damaged their bonemarrow in other ways, and so we
can often see myelodysplasticsyndrome and acute myeloid
leukemia developing as a resultof prior chemotherapy.
Dr Gavin Nimon (33:46):
Well, actually we mentioned targeted therapy
and use of monoclonal antibodies.
Is that like a tablet you canjust get over the counter, or is
it specifically produced forone individual patient and they
have to have a genetic testingto actually produce it?
How do these medications work?
Dr Joanna Czerwinski (33:59):
So the monoclonal antibodies are
infusions and so long as thepatient has a CD20 malignancy we
can apply for it.
It is dosed based on their bodysurface area, so their height
and weight are taken intoaccount For the targeted
treatments like the BTKinhibitors that I mentioned.
(34:21):
That is an authority scriptthat only a hematologist can
apply for, but it is the samedosing regardless of the patient
indication and regardless ofthe patient weight.
Dr Gavin Nimon (34:35):
So the immune therapy, then the actual targets
, are actually a common form oftherapy.
It's not.
I always had this idea that youmight take the patient's blood,
work out what the immuneresponse would be and target
that particular individual.
Dr Joanna Czerwinski (34:49):
I would hope.
I would hope that that will bethe case in the future, where we
have more tailored approachesto patients.
At the moment, we're using thegenetic tests predominantly to
give us the risk profile of thepatient.
So if they're high risk, I knowthat they may not respond to
chemotherapies and I would morelikely use the targeted
(35:10):
treatments or immunotherapyapproach.
And similarly, if they're lowrisk, that gives me prognostic
information and tells me that itcould be a while away before
this patient needs treatment,and that's a good thing.
Dr Gavin Nimon (35:25):
Jo, when we're talking to a lot of other
physicians about the treatmentof different malignancies or
even just conditions in general,another common thing that comes
up is the use ofmultidisciplinary teams involved
with treatment of patients.
Jo, do you tend to use an MDTas a part of your process, or is
it more of an individualisedtype approach?
Dr Joanna Czerwinski (35:43):
No, absolutely.
We definitely utilisemultidisciplinary teams.
For Flinders, we do have anestablished lymphoma MDT, and so
in these groups we have severalhematologists.
We have the radiationoncologists who can provide
their input in whether radiationcan be delivered safely in this
(36:06):
patient.
We've got the anatomicalpathologists which are
presenting the histologyspecimens, and we have the
radiologists who present the CTscan and PET scan and MRI
findings.
So with all this informationtogether we can establish a
treatment plan that is agreed toby the consensus group.
(36:28):
We also have other types ofMDTs where we involve our allied
health colleagues, becauseoftentimes having a cancer
diagnosis is very stressful fora patient and involves financial
and legal matters as well ashow is this patient going to be
cared for?
Do they need additional OT orPT input?
(36:52):
And we also involve palliativecare, as that can be.
One of the treatment options issupportive cares.
We also involve our infectiousdiseases colleagues in a weekly
meeting because many times,especially in the hospital
setting, our patients have comein with infectious complications
(37:14):
.
Dr Gavin Nimon (37:15):
So it really is quite an extensive group we've
got there.
When others were reading aboutCLL as well, almost it sounded a
bit like prostate cancer, inthat it's actually a lot of.
It can be quite indolent andlongstanding and that generally
there'll be a large number ofproportions of the community
might have it without evenknowing it and might not even
have symptoms of it.
Is that the way of thinkingabout CLL?
It can be as low as grade asthat.
Dr Joanna Czerwinski (37:36):
More than 90% of my patients are found
incidentally and they go on toLymphoma Australia and the
various private Facebook groupsand they find that you know,
neighbors, friends they have CLLas well.
It's only 10% of my patientsthat need treatment and those
(37:57):
10% usually need second andthird-line treatments some way
down the line.
Usually need second and thirdline treatments some way down
the line.
But if a patient has had CLLfor a decade, that bodes well
that they will never requiretreatment.
Dr Gavin Nimon (38:13):
Obviously, we mentioned the ALL definitely
requires treatment, and thelymphomas almost invariably
would require treatment as well.
Would that not be the case?
Dr Joanna Czerwinski (38:22):
Most of the lymphomas will require
treatment at some point.
For some of the subtypes thatare indolent, like the
follicular lymphoma, marginalzone lymphoma is usually
indolent as well.
Many of them can undergo watchand wait, and that could be the
case for a few years, before thelymphoma progresses enough that
(38:42):
it requires treatment at thatstage.
Dr Gavin Nimon (38:45):
So, jo, where do you think things are heading
for the future?
Obviously it's been a lot ofadvances.
Will AI have a lot of inputinto this area down the track,
and is there other areas or newadvances coming out, new
medications or new approaches?
Dr Joanna Czerwinski (38:57):
Certainly there's a lot of work in the
genetic side of things, wherethe more information we are
gleaning from a patient'sgenomic status, the more we can
tailor our approach.
So, for instance, in CLL thereare the BTK inhibitors that I
mentioned.
There are also another class ofdrug called the BCL inhibitors,
(39:20):
like venetoclax, and which oneyou start off with may be
differentiated by what geneticstatus that patient has, and
certainly you can developresistances to those protein
markers and you would not wantto treat a patient with a BCL2
inhibitor if they've got a BCL2mutation, if they've got a BCL2
(39:41):
mutation.
The other side of things, wherethe future holds, there's a lot
of input and research into CAR-Ttherapies, which is chimeric
antigen receptor T celltherapies, and this is in a way
a form of a transplant, whereyou take a patient's T cells,
(40:03):
you send it away for engineeringand manufacturing to make that
T cell smarter and target thelymphoma or the leukemia, and
then you re-infuse the T cellsback into the patient and so
you're retraining the immunesystem to target that tumor and
kill it.
The other form of treatmentthat is emerging quite strongly
(40:27):
is bite therapies, which arebispecific T-cell engagers and
again you're harnessing theT-cells to target the B-cell
malignancies.
Now, these technologies thatI've both mentioned are against
B-cell malignancies.
We don't have that kind oftechnology against T-cells as
(40:48):
yet, but that is something forthe future with further research
.
Dr Gavin Nimon (40:54):
Brilliant.
Well, it's been fantastichearing about this area.
It's actually massive.
In preparation for this podcasttoday, you might have heard me
mention my reading.
I have had to do a lot ofreading as a general orthopedic
surgeon.
I didn't know much about it andit's great hearing about these
different areas and the greattreatment you're offering these
(41:14):
patients.
So thank you very much, joe,for coming on.
Aussie med ed been brilliant.
I'd like to get you back atsome stage to talk about the
myeloid dysplasias andlignancies, and it it's great to
have you here today.
So thank you very much.
Dr Joanna Czerwinski (41:25):
Thank you for having me and looking
forward to the future.
Dr Gavin Nimon (41:28):
Brilliant Well.
Thank you very much, Dr JoCzerwinski.
Thank you very much for comingon.
A specialist haematologist atthe Flinders Public Hospital.
I'd like to remind you that allthe information presented today
is just one opinion and thatthere are numerous ways of
treating all medical conditions.
Therefore, you should alwaysseek advice from your health
professionals in the area inwhich you live.
Also, if you have any concernsabout the information raised
today, please speak to your GPor seek assistance from health
(41:50):
organisations such as Lifelinein Australia.
Thank you very much forlistening to our podcast today.
I'd like to remind you that theinformation provided is just
general advice and may varydepending on the region in which
you are practising or beingtreated.
If you have any concerns orquestions about what we've
discussed, you should seekadvice from your general
practitioner.
I'd like to thank you very muchfor listening to our podcast
and please subscribe to thepodcast for the next episode.
(42:12):
Until then, please stay safe.
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