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We hope you have enjoyed this limited-length demo
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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
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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
- Reexamining the stem-cell tumor model
- Reversibility of the program
- Epithelial cell exhibit great plasticity in vitro
- Interconvertability between SC and non-SC
- Cells can de-differentiate into stem-cell-like cells
- Chemotherapy & non-cancer SCs (CSCs)
- Desired response vs. what might happen
- Breast cancer cells ability to generate CSCs
- Basal cancer cells give rise to CSCs in vivo
- ZEB1 EMT-TF and non-CSCs-to-CSCs conversion
- Zeb1 inhibition prevents TGF-beta signaling
- ZEB1 promotor repression
- ZEB1 promotor activation
- ZEB1 promotor poised
- Model of CD44(lo)-to-CD44(hi) plasticity
- Dormant and aggressive cells in tumors
- Filopodium-like structures
- FLPs contribute to cell-matrix adhesions in 3D
- FLPs and integrin
- Abundant FLP formation in metastatic cells
- FLP formation by various breast cancer cell types
- FLP formation signal pathways
- FLP regulation and the EMT
- FLP and orthotopically-implanted cancer cells
- Mechanistic link between EMT & the CSC state
- Acknowledgments
Topics Covered
- Re-examining the stem-cell tumor model
- Interconvertibility between non-stem cells and stem cells
- The key for generating cancer stem cells (CSCs) from non-cancer stem cells
- Filopodium-like structures (FLPs) in metastatic cancer
- Mechanistic link between epithelial/mesenchymal transition (EMT) & the CSC state
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Weinberg, R. (2024, October 6). Genetics of tumor metastasis 2 [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 9, 2024, from https://doi.org/10.69645/WJMC3735.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Robert Weinberg has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Genetics of tumor metastasis 2
A selection of talks on Genetics & Epigenetics
Transcript
Please wait while the transcript is being prepared...
0:04
In the earlier lecture,
I described the fact
that one can describe
the hierarchical
organization of cells
within a carcinoma
in terms of self-renewing,
tumor-initiating
cancer stem cells,
indicated here in this
first slide with the blue cells,
which are self-renewing
stem-like cells.
And the bulk of cells in a tumor
indicated here in the gray
and the red,
which differ from one another
in that the gray and red cells
have undergone
a measure of differentiation
which takes them out
of the stem-like state
and places them in a state
where they no longer
have stem-like properties
and they no longer,
therefore, have the ability
to serve
as tumor-initiating cells.
I argued in the earlier lecture
that, in fact,
cells that have lost
this tumor initiating ability
are poor candidates
for serving as the founders
of new metastatic colonies,
because they no longer have this
tumor initiating capability.
Still, this diagram,
as pleasing as it might be,
required some
critical examination.
Among other questions
was the following one.
Given the fact
that the blue stem-like cells
can differentiate
into gray cells,
is this process,
of an arrow leading straight
down from the stem-like cells,
to the non-stem cells,
irreversible?
Or are there more complexities
that operate
in governing the interactions
and the interconversions
between, for example,
the gray cells
and the blue cells?
And this caused
Christine Chaffer
to begin to examine what happens
when one, for example,
isolates
the non stem-like cells,
transit-amplifying cells,
as they're depicted here.
What happens
when one places them
in culture
or in a living animal?
How do they behave
thereafter?
And her evidence
began to accumulate
that the diagram
that I show you here
needs to be revised.