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Lecture 22 cancer notes human body stfu
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Module
The Human Body (PY4010)
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Kingston University
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Lecture 22 Cancer Mark Fisher
What is cancer
- A serious disease, resulting from a malignant growth of tumour, caused by abnormal and uncontrolled cell division
- Cancer is a disease of DNA damage
- More modern view is cancer has a problem with single transaction/ resulting in aberrant signal transduction
What are the most common cancers in the UK?
- Breast and Prostate cancer
- Lung and Colorectal cancer
Which cancers have the highest incidence of death in the UK in 2016?
- Lung and bowel cancer
What is Carcinogenesis?
- the initiation of cancer formation/ the process by which normal cells —> cancer cells
Describe the process of Carcinogenesis?
- Cancer involves a Multi-hit mechanism: 4-8 mutations needed in cancer cell —> malignant cell
Initiation —> Promotion —> Progression
- Initiation:
- Key oncogene mutates —> this gets fixed in cell
- if cells stimulated to divide then they may have a growth advantage
- if you promote growth cell might grow through to have growth advantage
- tumour cells have other features —> immotile
How does age affect cancer?
- Cancer predominantly a disease of old age
Which cancers are driven by hormones?
- Testosterone is a drive for prostate cancer as testosterone is needed for prostate to grow
- Oestrogen is a drive for breast cancer
How can drugs be used to target cancers driven by hormones?
- hormone therapy - uses medicines to block or lower the amount of hormones in the body to slow down or stop the growth of cancer
- e. drugs can prevent the binding of testosterone to its receptor
What are the causes of cancer?
- Chemicals: diet, job, lifestyle - smoking, alcohol
- Radiation - UV, gamma rays, radioactivity-radon
- Viruses: DNA - Epstein-Barr, hepatatis B, Human papilloma
- Genetic predisposition: breast cancer
- Immune suppression: EBV lymphomas-transplant patients, dont recognise viral antigens
- Co factors: enable the mutated cells to grow out, hormones oestrogen and testosterone act as co- factors. malaria-Burkitt’s lymphoma (EBV)- malaria acts as a co-factor, hormones- oestrogen (breast CA), testosterone (prostate)
Molecular genetic aspects:
- Tumours are usually clonal - derived from a single cell that out grows other cells
- Derive from cumulative changes in expression of 3 gene classes:
What are the 3 different type of changes in a tumour cell?
- Changes in (Proto)oncogenes- 50-100 known (mutate PO genes —> oncogenes)
- Tumour suppressor genes (stopping oncogenes from causing cancer)
- Metastasis suppressor genes - stops tumour from spreading
How are oncogenes and tumour suppressor genes identified?
- Human genetic linkage studies - if you have a family that carries a cancer genetic pre-disposition, you can do a human genetic linkage + study all members of family + follow inheritance of gene + isolate that gene
- Chromosome analysis- Sometimes cancers arise as the chromosomes are re-organised in the cancer + so if you can do a karyotype and isolate the cell + Display chromosomes at metaphase + can see if theres a normal display of chromosomes. You can have a translocation
- DNA transfection - Take the DNA Directly from the tumour cell and put it in a non tumour cell e: a mouse cell + convert mouse cell into a transformed cell. Identifies a set of genes
- Oncogenic retroviruses and DNA tumour viruses - Some viruses retroviruses (RNA viruses) carry oncogenes. By studying how viruses and retroviruses work in cells, you can study how the oncogene may have induced the cancer
Oncogenes
What are protoonco genes?
- codes for a protein which stimulates cell division to take place
- Regulate growth of cells
- If there was a mutation occurring to a proto-oncogene — It forms an oncogene —> this results in uncontrollable cell division.
How do oncogenes work?
- Oncogenes act dominantly - only have to change one of the protoncogenes into oncogene for cell to see the effect
- They work by short circuiting the control mechanisms that regulate the division of the cells
- When you put mutations in the protoncognees —> oncogene, you Short circuit some control mechanisms, instead of it regulating the control growth —> constitutive signal
- 1 mutation usually sufficient to subvert a signal pathway only need to change 1 protein - to subvert pathway
How do proto oncogenes give a constitutive growth signal?
- under normal conditions, cell wont grow until signals from outside
- growth factor bound e PDFT
- GF’s bind to receptors in membrane —> receptors change chape + communicate singlal to nucleus
- communicating that growth factor is bound to cell membrane + it is okay for nucleus to kick in the cell cycle —> get a goth response
- if there isn't a high level of growth factors —> cell wont grow
- if mutation in receptor —> changes shape as if it has a GF bound —> signalling nucleus to grow constantly ebbed though GF is not found —> short circuiting the pathway + Telling the cell to grow
- RAS protein - molecular switch on inside of plasma membrane - when receptors are binding the EGF or PDF —> RAS protein changes shape —> send signal to nucleus —> stimulates transcription factor to join
Apoptosis:
What is Apoptosis?
All cells programmed to self destruct unless otherwise
sufficiency in growth signals
inactivate growth inhibitory signals
evade apoptosis
sustained angiogenesis
invasion + Spread
How are cancers diagnosed and treated?
- surgery, radiotherapy
- chemotherapy - inhibit tumour cell growth
- Hormone therapy
- Block oncogenic activity
- Stimulate tumour suppressors
- Tweek immune system Block metastasis - angiogenesis -required for metastasis
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Lecture 22 cancer notes human body stfu
Module: The Human Body (PY4010)
171 Documents
Students shared 171 documents in this course
University: Kingston University
Was this document helpful?
Lecture 22
Cancer
Mark Fisher
What is cancer
• A serious disease, resulting from a malignant growth of tumour, caused by abnormal and uncontrolled
cell division
• Cancer is a disease of DNA damage
• More modern view is cancer has a problem with single transaction/ resulting in aberrant signal
transduction
What are the most common cancers in the UK?
• Breast and Prostate cancer
• Lung and Colorectal cancer
Which cancers have the highest incidence of death in the UK in 2016?
- Lung and bowel cancer
What is Carcinogenesis?
• the initiation of cancer formation/ the process by which normal cells —> cancer cells
Describe the process of Carcinogenesis?
• Cancer involves a Multi-hit mechanism: 4-8 mutations needed in cancer cell —> malignant cell
Initiation —> Promotion —> Progression
1. Initiation:
• Key oncogene mutates —> this gets fixed in cell
• if cells stimulated to divide then they may have a growth advantage
• if you promote growth cell might grow through to have growth advantage
• tumour cells have other features —> immotile
How does age affect cancer?
• Cancer predominantly a disease of old age
Which cancers are driven by hormones?
• Testosterone is a drive for prostate cancer as testosterone is needed for prostate to grow
• Oestrogen is a drive for breast cancer
How can drugs be used to target cancers driven by hormones?
• hormone therapy - uses medicines to block or lower the amount of hormones in the body to slow down
or stop the growth of cancer
• e.g. drugs can prevent the binding of testosterone to its receptor
What are the causes of cancer?
1. Chemicals: diet, job, lifestyle - smoking, alcohol
2. Radiation - UV, gamma rays, radioactivity-radon
3. Viruses: DNA - Epstein-Barr, hepatatis B, Human papilloma
4. Genetic predisposition: breast cancer
5. Immune suppression: EBV lymphomas-transplant patients, dont recognise viral antigens
6. Co factors: enable the mutated cells to grow out, hormones oestrogen and testosterone act as co-
factors. malaria-Burkitt’s lymphoma (EBV)- malaria acts as a co-factor, hormones- oestrogen (breast
CA), testosterone (prostate)
Molecular genetic aspects:
• Tumours are usually clonal - derived from a single cell that out grows other cells
• Derive from cumulative changes in expression of 3 gene classes:
What are the 3 different type of changes in a tumour cell?
• Changes in (Proto)oncogenes- 50-100 known (mutate PO genes —> oncogenes)
• Tumour suppressor genes (stopping oncogenes from causing cancer)
• Metastasis suppressor genes - stops tumour from spreading
