MedStudentt
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Does anyone know any good sites that explain the molecular biology underpining oncogenes especially TP53 and Rb? Specifically in relation to HPV virus and cervical cancer as I'm having a hard time getting my head around it all.

If not, would anyone be able to explain the effects of oncogene E7 on Rb as what I have so far is that Rb binds to E2F transcription factors which are involved in key protein synthesis processes so that E2F can no longer bind to DNA so cannot upregaulate expressions of these key genes. But when Rb is phosphorylated at the restriction point by E7, E2F is released and can go on to interact with transcription activating proteins and expressions of genes required for the cell cycle.

But if E2F can still go on to express the genes required for the cell cycle, how does this lead to cervical cancer? shouldn't it be blocked the entire cell cycle ?

idk, i'm just really confused! Thankful to anyone who can lend a helping hand to this confused med student haha :')
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Asklepios
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(Original post by MedStudentt)
Does anyone know any good sites that explain the molecular biology underpining oncogenes especially TP53 and Rb? Specifically in relation to HPV virus and cervical cancer as I'm having a hard time getting my head around it all.

If not, would anyone be able to explain the effects of oncogene E7 on Rb as what I have so far is that Rb binds to E2F transcription factors which are involved in key protein synthesis processes so that E2F can no longer bind to DNA so cannot upregaulate expressions of these key genes. But when Rb is phosphorylated at the restriction point by E7, E2F is released and can go on to interact with transcription activating proteins and expressions of genes required for the cell cycle.

But if E2F can still go on to express the genes required for the cell cycle, how does this lead to cervical cancer? shouldn't it be blocked the entire cell cycle ?

idk, i'm just really confused! Thankful to anyone who can lend a helping hand to this confused med student haha :'
First of all, both p53 and RB are tumour-suppresor genes rather than oncogenes. I.e. they normally "put the brakes" on cell proliferation, but when mutated they no longer function so cells divide excessively (ie forming a cancer).

You are right about how RB and E2F control the cell cycle. Specifically, E2F is a transcription factor that switches on genes that mediate progression from G1 to S phase. So the more E2F activity you have, the more your cells will proliferate.

Now remember I said RB puts the breaks on cell proliferation. The mechanism of this is by binding E2F and stopping it from doing its job, so these genes are switched off.

In normal cell regulation, the activity of RB is controlled by phosphorylation. So for example, a growth factor could bind to a receptor on a cell, which will trigger a cascade of kinase enzymes to phosphorylate various proteins. This inactivates RB so the brakes are taken off.

Cancer results when the brakes are permanently taken off (even in the absence of growth factors). This could be due to a mutation in the gene encoding RB. Alternatively, the E7 protein produced by the HPV virus degrades RB (we think through the ubiquitin pathway). No RB = no brakes = cancer.
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