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Printable Handouts
Navigable Slide Index
- Introduction
- Multi-step metastasis model: EMT is not a one-way street
- Circulating breast tumor cells exhibit EMT features
- Skin-specific inducible Twist1 mouse model
- Experimental design
- Twist1 induces rapid conversion from papillomas to invasive cell carcinomas
- Twist1 induces loss of E-cadherin
- Twist1 induces basement membrane breakdown
- Transient activation of Twist1 promotes distant metastasis
- Topical induction of Twist1 reverses EMT in metastases
- Reversible EMT promotes tumor metastasis
- Recording EMT by lineage tracing during metastasis
- Epithelial-mesenchymal plasticity in tumor metastasis
- Part II: Metastasis organotropism
- I. Blood circulation route affects seeding efficiency in distant organs
- II. “Seed and soil” hypothesis
- Selection of highly metastatic variants to various organs
- Bone metastasis gene signature
- Part III: targeting metastasis
- Metastasis dormancy
- Design the right clinical trials for metastasis prevention (1)
- Design the right clinical trials for metastasis prevention (2)
- Targeting osteoclasts via the RANKL/RANK pathway
- Denosumab clinical trial
- Conclusion
- Thank you for listening
Topics Covered
- Molecular regulation of EMT
- Adherens junction
- E-cadherins
- Epithelial-Mesenchymal Plasticity
- Metastasis dormancy
- Metastasis organ tropism
- Targeting tumor metastasis
Links
Series:
- The Molecular Basis of Cancer
- Periodic Reports: Advances in Clinical Interventions and Research Platforms
Categories:
Therapeutic Areas:
Talk Citation
Yang, J. (2023, April 30). The molecular basis of cancer metastasis: multi-step metastasis process and anti-metastasis therapeutic development [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved October 8, 2024, from https://doi.org/10.69645/XJGQ4289.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Jing Yang has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
The molecular basis of cancer metastasis: multi-step metastasis process and anti-metastasis therapeutic development
Published on April 30, 2023
26 min
Other Talks in the Series: The Molecular Basis of Cancer
Other Talks in the Series: Periodic Reports: Advances in Clinical Interventions and Research Platforms
Transcript
Please wait while the transcript is being prepared...
0:05
One major concept
I would like to
discuss is this multi-step
metastasis model.
In there the EMT program
is actually not a
one-way street.
The reason I say that
is because we all know
that when the patient
developed distant metastasis,
the distant metastasis
actually present
many of the same features
of the primary tumor.
What I mean is, if you
have a breast cancer,
the distant metastasis also is
a breast tumor and
may still express ER,
or still express HER2 and still
maintain a relative
epithilioid morphology.
There are a lot of
debate in the field.
If the distant
metastasis do not look
like a sarcoma does not look
like a mesenchymal tumor,
how can EMT program play a role?
I think that brought up to
this very important concept that
EMT is not a one-way street.
Tumor cells actually
appear on this program to
allow the invasion and
intravasation, the extravasation.
By that distant site,
we think this program
probably needs to be
turned off to allow
this migrated cell to
actually now stay in
a distant site to
start to regrow and
colonize the distance site.
In the next few slides,
I would like to show you
some of the evidence from
animal models to show the
importance of this plasticity.
1:30
But before I go on,
I want to show you the
evidence why we think
EMT plasticity exists
in human cancer.
I think the best
place to look at
this plasticity in human patient
is in circulating tumor cells.
This is the early
study from Ming Hu,
the isolated
circulating tumor cells
from breast cancer patients.
You can see there's 17
patients than they stained for
either epithelial or
mesenchymal markers defined
the circulating cell
either they're E
or EM or M.
As you can see here in the
majority of the patient,
there are highly
enriched sub population
of the cell that present
a mesenchymal signature.
And this has been reported
not only in breast cancer,
but also in many type of
human eye carcinomas.
So what this suggests is
that the enrichment of this
more mesenchymal
phenotype, this is a much
higher than present
in a primary tumor.
Usually the more
mesenchymal cell cannot be,
go over 10 percent.
Is that turning on this
program probably gave
this tumor cell the
advantage to be able to
enter the circulation
to become CTC.
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