1234567890xyz
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Is this train of thought correct?:
- p53 promotes apoptosis
- UVB causes double strand breaks in p53
- So, p53 no longer promotes apoptosis
I am confused because in some articles, I read that after ultraviolet B irradiation, p53 protein levels increased
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HarisMalik98
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The way you've wrote it makes it seem as if you think UBV specifically targets p53. UBV, to my knowledge, doesn't specifically target p53, or any particular gene for that matter. I think there's two main things to consider:

1) UVB causes random DNA mutations due to the formation of pyrimidine dimers which, yes, may occur in the p53 gene, but can occur anywhere.
2) There are more tumour-suppression genes than just p53 (e.g. retinoblastoma, BCL2, SWI/SNF, p16 and more.....), which could also become damaged by the UVB and cause tumour growth.

Considering these points, some studies may show that in models exposed to UBV tumour growth occurs - and damage to the p53 gene also occurs. In this case, the damage to p53 is probably the main reason for the tumour growth.

However, other studies may find that in their models, tumour growth is occuring due to damage to other tumour suppressor genes. In this case, p53 may still be functional and expressed at high levels to try and counteract the pathology. They may not have determined if these genes were damaged - but since p53 is functional and expressed at high levels it's clear that mutations in other genes have been the cause. This is probably why some studies have reported this.

All in all, it depends on the angle of the study. p53 is taught as a classic tumour suppressor however there are many more - damage to p53 isn't necessarily shown in every single case associated with UBV-induced tumours.
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1234567890xyz
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(Original post by HarisMalik98)
The way you've wrote it makes it seem as if you think UBV specifically targets p53. UBV, to my knowledge, doesn't specifically target p53, or any particular gene for that matter. I think there's two main things to consider:

1) UVB causes random DNA mutations due to the formation of pyrimidine dimers which, yes, may occur in the p53 gene, but can occur anywhere.
2) There are more tumour-suppression genes than just p53 (e.g. retinoblastoma, BCL2, SWI/SNF, p16 and more.....), which could also become damaged by the UVB and cause tumour growth.

Considering these points, some studies may show that in models exposed to UBV tumour growth occurs - and damage to the p53 gene also occurs. In this case, the damage to p53 is probably the main reason for the tumour growth.

However, other studies may find that in their models, tumour growth is occuring due to damage to other tumour suppressor genes. In this case, p53 may still be functional and expressed at high levels to try and counteract the pathology. They may not have determined if these genes were damaged - but since p53 is functional and expressed at high levels it's clear that mutations in other genes have been the cause. This is probably why some studies have reported this.

All in all, it depends on the angle of the study. p53 is taught as a classic tumour suppressor however there are many more - damage to p53 isn't necessarily shown in every single case associated with UBV-induced tumours.
Legend. Thank you so much
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