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- View the Talks
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1. Genetics and management of inherited cancer predisposition 1
- Prof. Joshua Schiffman
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2. Genetics and management of inherited cancer predisposition 2
- Prof. Joshua Schiffman
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3. The cytogenetics of childhood acute leukemia
- Dr. Susana C. Raimondi
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4. Chromosome translocations and cancer
- Prof. Felix Mitelman
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5. Acute myeloid leukemia: genetics, prognosis and treatments
- Prof. Stephen Nimer
-
6. Genetic abnormalities in acute lymphoblastic leukemia
- Prof. Ching Hon Pui
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7. Molecular genetics of non-Hodgkin lymphoma
- Prof. Jude Fitzgibbon
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8. Genetics of breast and ovarian cancer
- Prof. Jeffrey Weitzel
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9. The genetics and genomics of familial renal carcinoma
- Prof. Eamonn Maher
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10. Genomics of lung cancer
- Prof. Ramaswamy Govindan
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11. The genetics of glioblastoma
- Dr. Hai Yan
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12. Genetics of tumor metastasis 1
- Prof. Robert Weinberg
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13. Genetics of tumor metastasis 2
- Prof. Robert Weinberg
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14. CML: genetic paradigm of targeted therapy 1
- Prof. Michael W. Deininger
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15. CML: genetic paradigm of targeted therapy 2
- Prof. Michael W. Deininger
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16. The non-coding RNA revolution in the cancer society
- Prof. George Calin
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17. Role of molecular markers in guiding therapy in cancer
- Prof. Joe Duffy
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18. Functional cancer genomics
- Prof. Roderick Beijersbergen
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19. Pharmacogenomics in cancer therapy
- Prof. Sharon Marsh
Printable Handouts
Navigable Slide Index
- Introduction
- Talk outline
- Acute myeloid leukemia (AML)
- Cancer and the plague
- AML is a disease of the elderly
- Diagnosis of acute myeloid leukemia
- Critical milestones in understanding AML
- Cytogenetic abnormalities in AML
- AML is a complex biological disease
- IDH1/2 & TET2 mutations are mutually exclusive
- AML biology predicts response to chemotherapy
- Effects of specific mutations on survival
- Revised AML risk stratification (1)
- Revised AML risk stratification (2)
- New approaches: targeted therapies
- Leukemia fusion proteins transform stem cells
- The most common MLL partner genes in AML
- Spliceosome mutations, cytogenetic alterations
- AML and immunotherapy
- CAR-modified T cells treatment
- Summary
Topics Covered
- Introduction to acute myeloid leukemia
- Classification
- Insights into the pathogenesis
- Classes of mutations
- Treatments
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Nimer, S. (2016, January 31). Acute myeloid leukemia: genetics, prognosis and treatments [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 3, 2024, from https://doi.org/10.69645/BLGP8820.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Stephen Nimer has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Haematology
Transcript
Please wait while the transcript is being prepared...
0:00
Welcome, today's seminar
is on the genetics
of acute myeloid leukemia.
I'm Stephen Nimer.
I'm a physician scientist
and I'm the director
of the Sylvester Comprehensive
Cancer Center at the University
of Miami's Miller
School of Medicine.
0:16
Today I'd like to introduce
the disease to you, AML,
Acute Myeloid Leukemia,
talk a bit about the way
we classify this disease,
talk about our insights
into the pathogenesis
or what triggers the growth
of these abnormal cells
and then lastly,
spend some time talking about
how we treat this disease
both the conventional treatments
and some of the latest research
that's providing potential
new therapies for this disease.
0:49
So when you think
about cancer in general,
you think about a cell
that grows abnormally
and in acute myeloid leukemia,
there are two main attributes.
First, the cells don't go through
the normal differentiation process.
And second of all,
the cells proliferate
and self-renew abnormally.
So really the task is to explain
what those two properties
of AML mean.
There are three types of cells
in the peripheral blood.
There are white blood cells,
red blood cells, and platelets.
The white blood cells help us
with our immune system
and to fight infection,
the red blood cells carry oxygen,
and platelets prevent
us from bleeding.
These cells are functional.
They are what we call mature cells.
And they're all derived
from immature cells
in the bone marrow.
And so the normal immature cells
in the bone marrow
have no function,
but as they mature, they acquire
functional characteristics
and differentiate into these
three different types of cells.
So what happens in AML
is that these early cells,
which we refer to as "blast cells"
do not differentiate
into normal cells
and so they never acquire
the normal functional attributes.
Instead they accumulate
in the bone marrow,
which is where they normally live
and they spill out
into the blood stream.
But what happens is they
crowd out the normal cells
and so over time, a patient
will present with leukemia
because they have too many
of these cells in their blood
but really they present
because they have
too few normal cells.
So if you have too
few white blood cells
then you develop an infection.
And if you have too
few red blood cells,
which carry oxygen,
you can't breathe properly
and you get short of breath
and you get fatigue.
And if you don't have
enough platelets,
you develop bleeding problems,
in particular,
bleeding into your skin
or into the gums of your mouth.
And so the way patients
present is often with a fever,
with fatigue,
with bleeding problems,
and that leads to the diagnosis
of acute myelogenous
leukemia or AML.