Rockgo288
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My main question is:
Does oncogenes cause cancer as a result of activating proto oncogenes excessively?
Below are my explanation, can someone pls help me to check if it is correct?
So, oncogenes are mutations of proto-oncogenes.
How proto oncogenes stimulate cell division:
Growth factors attach to protein receptors on cell surface membrane—>cause proto oncogenes to stimulate cell division by:
Activating enzymes in cell and so activate transcriptional factors that activates the particular genes that cause DNA to replicate and the cell to divide.
When proto oncogenes mutate into oncogenes,
it becomes permanently activated and cause abnormal cell division by:
1. Activating the protein receptors on cell membrane permanently so proto oncogenes are activated permanently and cause cell divide without growth factors.
2. Coding for a growth factor that is then produced in excessive amounts so again activate proto oncogenes to cause excessive cell division.

AND SO oncogenes cause cancer as a result of the excessive activation of proto oncogenes.
PLS HELP ME thanks!!!!!!!
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randombiochemist
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That sounds like the general idea, yes.

A few points in your explanation though I would be more hesitant to call 'correct' - I'm not sure if they're just not phrased in the best way or if reflecting misunderstanding of the concept.

Proto-oncogenes code for proteins that help to regulate cell growth/division/differentiation, and are often involved in signal transduction. For example a proto-oncogene might encode a growth factor that would normally bind to particular receptors and activate a series of downstream processes, eventually leading to cell division. There are also proto-oncogenes that code for receptors themselves, and would be activated only upon receiving the correct signals (i.e. when the correct growth factor binds to it). This is all normal - stimulating progression through the cell cycle is what the protein products of these genes are supposed to do in a cell that is meant to divide, e.g. in a developing organism or stem cells.

Oncogenes are proto-oncogenes that have been mutated or upregulated. They still code for the same growth factor or receptor as the original protein. But these proteins may be present in more ('excessive') copies or have become constitutively active (when a receptor activates downstream pathways even when it doesn't receive the go-ahead signal from a growth factor). This leads to body cells dividing when they shouldn't, which can give rise to tumours.

If what I've just typed above sounds like what you already know, then your understanding was correct to begin with
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Rockgo288
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(Original post by randombiochemist)
That sounds like the general idea, yes.

A few points in your explanation though I would be more hesitant to call 'correct' - I'm not sure if they're just not phrased in the best way or if reflecting misunderstanding of the concept.

Proto-oncogenes code for proteins that help to regulate cell growth/division/differentiation, and are often involved in signal transduction. For example a proto-oncogene might encode a growth factor that would normally bind to particular receptors and activate a series of downstream processes, eventually leading to cell division. There are also proto-oncogenes that code for receptors themselves, and would be activated only upon receiving the correct signals (i.e. when the correct growth factor binds to it). This is all normal - stimulating progression through the cell cycle is what the protein products of these genes are supposed to do in a cell that is meant to divide, e.g. in a developing organism or stem cells.

Oncogenes are proto-oncogenes that have been mutated or upregulated. They still code for the same growth factor or receptor as the original protein. But these proteins may be present in more ('excessive') copies or have become constitutively active (when a receptor activates downstream pathways even when it doesn't receive the go-ahead signal from a growth factor). This leads to body cells dividing when they shouldn't, which can give rise to tumours.

If what I've just typed above sounds like what you already know, then your understanding was correct to begin with
ok, so proto oncogenes aren’t stimulated by growth factors binding to proteins receptors but proto oncogenes actually code for protein receptors and growth factors which stimulate cell division.
When proto oncogenes are mutated, oncogenes is resulted and it cause abnormal cell division because of coding for:
1. permanently activated protein receptors
2. excessive growth factors

Another question arise then, my book just say “oncogenes cause cancer as a result of the activation of proto oncogenes”. Does it mean that oncogenes acts like a permanently activated proto oncogene and so code for excessive growth factor or permanently activated receptors?
And also, another question, the whole chapter is talking about how gene expression leads to cancer. I know that like the tumor suppressor gene, methylation of it will turn it off, so cause cancer.
But for oncogenes, isn’t mutation the reason that it leads to cancer? Where does the gene expression part comes in?
Thanks!!!
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Asklepios
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(Original post by Rockgo288)
ok, so proto oncogenes aren’t stimulated by growth factors binding to proteins receptors but proto oncogenes actually code for protein receptors and growth factors which stimulate cell division.
When proto oncogenes are mutated, oncogenes is resulted and it cause abnormal cell division because of coding for:
1. permanently activated protein receptors
2. excessive growth factors

Another question arise then, my book just say “oncogenes cause cancer as a result of the activation of proto oncogenes”. Does it mean that oncogenes acts like a permanently activated proto oncogene and so code for excessive growth factor or permanently activated receptors?
And also, another question, the whole chapter is talking about how gene expression leads to cancer. I know that like the tumor suppressor gene, methylation of it will turn it off, so cause cancer.
But for oncogenes, isn’t mutation the reason that it leads to cancer? Where does the gene expression part comes in?
Thanks!!!
Yes those are all examples of proteins that could be encoded by oncogenes. Transcription factors would be another example - really any gene thats protein product acts to increase cell proliferation could be oncogene.

Gene expression tends to be dysregulated in cancer. You're correct that this could be by methylation, but either increased or decreased expression can conceivably result from mutation of regulatory genes. Or even from copy number increases. The classic example of an overexpressed protein would be oestrogen receptor (ER) in breast cancer.
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Rockgo288
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(Original post by Asklepios)
Yes those are all examples of proteins that could be encoded by oncogenes. Transcription factors would be another example - really any gene thats protein product acts to increase cell proliferation could be oncogene.

Gene expression tends to be dysregulated in cancer. You're correct that this could be by methylation, but either increased or decreased expression can conceivably result from mutation of regulatory genes. Or even from copy number increases. The classic example of an overexpressed protein would be oestrogen receptor (ER) in breast cancer.
thanks!!!
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