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"Thus, we conclude that increased E2F8 expression in cancer, like that of BRCA1 and other tumor suppressors involved in homologous recombination–mediated DNA repair, such as RAD51 and FANCD2, simply reflects the high percentage of proliferating cells present in tumors."
ncbi.nlm.nih.gov/pmc/articles/P…
@DoorlessCarp @Fynnderella1 @kacdnp91 @Jikkyleaks
We really need to know if the E2f8 1.5 fold increase was just an echo or more... :S
@DoorlessCarp @Fynnderella1 @kacdnp91 @Jikkyleaks
We really need to know if the E2f8 1.5 fold increase was just an echo or more... :S
Why does chemotherapy kill cancerous but not normal cells? Most cancer biologists would answer this by stating that chemotherapy is selectively toxic to proliferating cells, and that cancer cell proliferate more than normal cells. Not exactly - there's a lot more to it.
Many normal tissues, like bone marrow and gut cells are actually more proliferative than even the most aggressive cancers. E.g. pro-myelocytes have a doubling time of around 17 hrs whilst even aggressive epithelial tumors double every 2-3 weeks or so.
So while many chemotherpeutics (e.g. #Temozolomide for GBM) show extensive myelotoxicity as a side effect, clinically useful ones are able to kill cancerous cells more efficaciously than normal ones, even if the latter proliferate faster, like pro-myelocytes.
How do they do it?
How do they do it?
