Registration for a live webinar on 'Precision medicine treatment for anticancer drug resistance' 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
- Learning outcomes
- Part 1: Oncogenes
- Oncogenes (1)
- Oncogenes (2)
- Retrovirus promoter insertion: Oncogene activation
- Oncogene activation: Point mutation
- Oncogene activation: Amplification & truncation
- Oncogene activation: Inappropriate regulation
- Oncoproteins include growth signalling pathway proteins
- Tumour suppressor genes (TSGs)
- Retinoblastoma
- Cell cycle, G1/S checkpoint and Rb
- Rb controls G1/S checkpoint
- Deregulation of the pRb pathway
- p53 response to DNA damage
- p53 “guardian of the genome”
- The p53 pathway
- Deregulation of pathways
- Cancers and age UK
- Genetic instability
- DNA mismatch repair – MMR
- DNA nucleotide excision repair
- DNA strand break repair
- Fanconi anaemia DNA crosslink repair
- Chromosome translocations: Philadelphia chromosome Ph+
- Copy number alterations and structural chromosomal alterations (aneuploidy)
- Different mutation levels in different cancers
- Cell death
- Apoptosis pathways
- Breast cancer: Invasion and lymphatic metastasis
- Cancer diagnosis
- Invasion
- Tumour angiogenesis
- Invasion and metastasis
- Metastatic spread is not random
- Colorectal cancer: Haematogenous metastasis
- Summary: Cancer hallmarks
- Summary: Clonal evolution of tumours
- Summary
Topics Covered
- Oncogenes
- Tumour suppressor genes (TSGs)
- Retinoblastoma
- p53 “guardian of the genome”
- Genetic instability
- DNA and chromosome alterations
- Cell death and apoptosis
- Cancer diagnosis
- Invasion and metastasis
- Hallmarks of cancer
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Arends, M. (2024, November 28). Pathogenesis of neoplasia [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 26, 2024, from https://doi.org/10.69645/LSPL4010.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Mark Arends has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Transcript
Please wait while the transcript is being prepared...
0:00
Hello. My name is Mark Arends.
I'm the Professor
of Pathology at
the University of Edinburgh and
today, I'm giving a lecture on
the pathogenesis of neoplasia.
0:13
The learning outcomes
for this lecture are to
learn about what are
the genetic changes
driving tumour progression.
Focusing on both oncogenes and
tumour suppressor genes as
the two major classes
of genetic changes.
Followed by, how does
genetic instability occur and
the role of abnormalities of
DNA repair, and then how do
cancers invade and metastasise?
0:42
Starting with oncogenes,
we can start with the
question, what genes
are targeted for
mutation in cancer?
These are the genes that
regulate cell proliferation,
cell death and the signalling
within cells, to and from
cells, and the matrix.
These genes are involved
in monitoring and
maintaining genetic stability
and genomic integrity.
They're also genes
involved in regulating and
maintaining tissue
architecture including
cell movement and cell adhesion.
In cancer, the two major classes
of gene that are altered
are firstly, the oncogenes
and secondly, the tumour
suppressor genes.
1:25
What are oncogenes?
Oncogenes are
essentially a class of
normal genes and if one of
the alleles is mutated,
they are said to act in
a dominant or positive
gain-of-function fashion in
contributing to the
development of a tumour.
Typically, mutations
affect only one allele
of the pair of alleles
of an oncogene.
And as I mentioned, these are
not special cancer genes,
but these are normal genes
that have a normal role in
growth control and they can
be activated in several ways.