Registration for a live webinar on 'Chronic inflammation, immune cell trafficking and anti-trafficking agents' is now open.
See webinar detailsWe noted you are experiencing viewing problems
-
Check with your IT department that JWPlatform, JWPlayer and Amazon AWS & CloudFront are not being blocked by your network. The relevant domains are *.jwplatform.com, *.jwpsrv.com, *.jwpcdn.com, jwpltx.com, jwpsrv.a.ssl.fastly.net, *.amazonaws.com and *.cloudfront.net. The relevant ports are 80 and 443.
-
Check the following talk links to see which ones work correctly:
Auto Mode
HTTP Progressive Download Send us your results from the above test links at access@hstalks.com and we will contact you with further advice on troubleshooting your viewing problems. -
No luck yet? More tips for troubleshooting viewing issues
-
Contact HST Support access@hstalks.com
-
Please review our troubleshooting guide for tips and advice on resolving your viewing problems.
-
For additional help, please don't hesitate to contact HST support access@hstalks.com
We hope you have enjoyed this limited-length demo
This is a limited length demo talk; you may
login or
review methods of
obtaining more access.
Printable Handouts
Navigable Slide Index
- Introduction
- Lecture outline
- Multi-step metastasis model
- Part I: EMT and cellular plasticity
- Epithelial cells are connected by various cell junctions
- How do carcinoma cells invade?
- Local invasion – collective invasion
- Local invasion – invasive ductal carcinoma
- Mammary terminal endbud invades stroma
- Local invasion – single cell invasion
- Local invasion – Cajal's drawings
- Local invasion – invasive lobular carcinoma
- Gastrulation
- Neural crest development
- Epithelial-Mesenchymal Transition (EMT)
- Epithelial-mesenchymal plasticity
- How is this program regulated?
- Adherens junction
- Suppression of E-cadherin during EMT
- CDH1 germline mutations in hereditary diffuse gastric cancers (1)
- CDH1 germline mutations in hereditary diffuse gastric cancers (2)
- Loss of cell adhesion in invasive lobular carcinoma
- Cell scattering and invasiveness induced by HGF
- Transcription regulation of EMT
- Snail represses E-cadherin transcription through E-boxes
- Snail in gastrulation
- Snail in neural crest development
- EMT in Drosophila mesoderm formation
- Twist is a potent inducer of EMT
- Twist is essential for breast tumors to metastasize
- EMT: molecular markers summary
- Invadopodia: specialized structures for matrix degradation
- Twist-induced invadopodia is functional in ECM degradation
- Transcription regulation of EMT: main families
- Transcription regulation of EMT: cancer associations
Topics Covered
- Multi-step metastasis model
- Epithelial derived carcinoma
- Collective invasion
- Drosophila gastrulation
- Xenopus neural crest formation
- Epithelial-mesenchymal transition (EMT)
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: molecular mechanisms of epithelial-mesenchymal transition in tumor metastasis [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved June 10, 2023, from https://hstalks.com/bs/5286/.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: molecular mechanisms of epithelial-mesenchymal transition in tumor metastasis
Published on April 30, 2023
30 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
0:00
Hello everyone.
Today, my lecture's
title is the molecular
basis of cancer metastasis.
Let's first introduce myself.
My name is Jing Yang, I'm
a professor at University
of California,
San Diego, department
pharmacology and pediatrics.
My lab is the Moores
Cancer Center at UCSD.
0:22
First-ever like to introduce you
the outline of the lecture.
I will first discuss
the multi-step process
of tumor metastasis.
Then they will spend
a significant amount
of time to discuss
this epithelial
mesenchymal transition
and cellular
plasticity metastasis.
Then we will talk about the
organ topic metastasis and
how this regulation in
tropism is regulated.
In the end, I will have
a brief discussion
on how to develop
therapeutics to prevent or
inhibit develop of metastasis.
0:59
As you all know that although
there's a lot of work had
been done trying to understand
the molecular basis of
primary tumor formation.
But what's really killing
cancer patients is
actually metastasis.
Metastasis is a
multi-step process where
a primary tumor cells
that initially located in
this primary site become
locally invasive,
invaded through the
basement membrane
and then made it to
the nearby tissue and
some of the tumor cells are able
to intravasate into
the circulation,
enter the blood and
lymphatic circulation.
After surviving in
the circulation,
they extravasated
from the circulation
into the distant organs
and at a decent organ,
some of the tumor cells are able
to either adapt themselves to
this new microenvironment
or they actually
modify this environment
to make it much more
friendly against to themselves
that allow them to re-grow
formed the secondary
growth that are
eventually life-threatening
to the patients.
Major research effort in
the metastasis research is
trying to understand what are
the molecular and cellular
programs that are activated to
allow the stationary
epithelial cell
the ability to migrate,
to invade and to actually
eventually spread into
a distance sites.
Hide