Ghoulfriend
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Hello y'all

I was checking the spec and it said I needed to understand the role of (proto)oncogenes and tumour suppressor genes in the prevention, treatment, and cure of cancer.

I understand how they naturally work and assume this is the 'prevention' aspect but have no clue on the other two ? Please help !
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macpatgh-Sheldon
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Hi,

When we humans [hopefully being slightly smarter [sorry US terminology! ] than other animals] use drugs to treat disease, and the mechanisms of drug action that we use attempt to nullify the pathological processes without [ideally] damaging our own cells.

Drugs currently widely used to treat cancer will, as above, kill neoplastic (cancer) cells and not [ideally] normal cells; however, some normal cells will be adversely affected [e.g. people lose hair when on chemotherapeutic agents - these drugs mainly affect dividing cells].

Now that we are in the era of gene therapy, drugs are currently being developed to modify genes that predispose individuals to certain diseases. Although still under heavy research activity, drugs are beginning to appear on the market (I mean as prescription drugs, NOT in ghettos in San Francisco ) that attempt to prevent or treat cancer by modifying the very genes that increase susceptibility to neoplastic disease. You might know that although smoking causes cancer [anyone who refutes this is either stupid or a smoker], not all smokers get lung cancer [or bladder cancer, also caused by smoking]; those who develop cancer might have a genetic predisposition, and cigarette tar + chemicals spark it off.

So to keep it simple [as YOU MUST in biology and medicine], we are making drugs that will reduce the effects of oncogenes and increase the expression of tumour suppressor genes. (For A* at A level: a drug called imatinib [and others] prolongs lifespan in patients with one type of leukaemia [cancer of white blood cells] by inhibiting protein kinase [one example is tyrosine kinase [you might have come across the amino acid tyrosine]]; this ultimately inhibits the transcription (DNA ----> mRNA) of a proto-oncogene.

Thanks!
M
M (specialist biology tutor)
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Jpw1097
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(Original post by Ghoulfriend)
Hello y'all

I was checking the spec and it said I needed to understand the role of (proto)oncogenes and tumour suppressor genes in the prevention, treatment, and cure of cancer.

I understand how they naturally work and assume this is the 'prevention' aspect but have no clue on the other two ? Please help !
Since you have said you understand how (proto)oncogenes and tumour suppressor genes work in the prevention of cancer, I am assuming you are aware of a few examples such as HER2 (in breast cancer), oestrogen receptors (also in breast cancer), various oncogenes in the Ras signalling pathway, as well as p53, BRCA1, BRCA2 and things like that?

A good example to highlight the roles of oncogenes and TSGs in the treatment of cancer is breast cancer. In breast cancer, HER2 is overexpressed and therefore is a target for treatment - the treatment of which is herceptin (trastuzumab), a monoclonal antibody that binds to the HER2 receptor. Also, the oestrogen receptor is usually overexpressed in breast cancer, and therefore is susceptible to tamoxifen - a molecule which inhibits the activity of the oestrogen receptor. Many cancers have mutations in cell surface receptors (e.g. EGFR) which can be targetted by small molecules.

Just as macpatgh-Sheldon has said, chronic myeloid leukaemia is characterised by the philadelphia chromosome - a chromosome formed by the fusion of chromosomes 22 and 9, causing two genes, BCR and ABL to fuse together, forming the BCR-ABL fusion protein which produces the Bcr-Abl protein that is responsible for causing the leukaemia. Bcr-Abl is an enzyme that is constitutively (always) active - more specifically it is a tyrosine kinase. This enzyme can be targetted and inhibited by a class of enzymes known as tyrosine kinase inhibitors (one of these is imatinib).
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Ghoulfriend
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(Original post by Jpw1097)
Since you have said you understand how (proto)oncogenes and tumour suppressor genes work in the prevention of cancer, I am assuming you are aware of a few examples such as HER2 (in breast cancer), oestrogen receptors (also in breast cancer), various oncogenes in the Ras signalling pathway, as well as p53, BRCA1, BRCA2 and things like that?

A good example to highlight the roles of oncogenes and TSGs in the treatment of cancer is breast cancer. In breast cancer, HER2 is overexpressed and therefore is a target for treatment - the treatment of which is herceptin (trastuzumab), a monoclonal antibody that binds to the HER2 receptor. Also, the oestrogen receptor is usually overexpressed in breast cancer, and therefore is susceptible to tamoxifen - a molecule which inhibits the activity of the oestrogen receptor. Many cancers have mutations in cell surface receptors (e.g. EGFR) which can be targetted by small molecules.

Just as macpatgh-Sheldon has said, chronic myeloid leukaemia is characterised by the philadelphia chromosome - a chromosome formed by the fusion of chromosomes 22 and 9, causing two genes, BCR and ABL to fuse together, forming the BCR-ABL fusion protein which produces the Bcr-Abl protein that is responsible for causing the leukaemia. Bcr-Abl is an enzyme that is constitutively (always) active - more specifically it is a tyrosine kinase. This enzyme can be targetted and inhibited by a class of enzymes known as tyrosine kinase inhibitors (one of these is imatinib).
I'll be quite honest - I only have the basics as I missed U6 due to ill health and they wont accept me to repeat or send resources so its all being self taught from what I can gather from the spec etc
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Ghoulfriend
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Just for clarification - are y'all students or teachers in the UK or is this just general advanced knowledge on the subject ?
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macpatgh-Sheldon
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As far as I remember, @jpw1097 is now a 2nd year (or is it 3rd year? - time flies!) medical student, and I am a former medical student; do various things now, including lecturing, medical editing, training doctors on medical software and teaching A level biology.
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Jpw1097
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(Original post by macpatgh-Sheldon)
As far as I remember, @jpw1097 is now a 2nd year (or is it 3rd year? - time flies!) medical student, and I am a former medical student; do various things now, including lecturing, medical editing, training doctors on medical software and teaching A level biology.
3rd year now

Sounds very interesting!
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