I guess this might be a weird question, but it seems to me that, when it comes to tumor suppression, all roads go through Rb. Are there any tumors that don't involve disruption of Rb in some way?
Http://www.aacrmeetingabstracts.org/cgi/content/abstract/2006/1/844-b
http://www.nature.com/oncsis/journal/v1/n7/full/oncsis201216a.html
RB1 protein is inactivated in many of cervical cancer cell lines infected with HPV16 that expresses E6 and E7 oncoprotein, leading to a defect in G1 checkpoint of cell cycle. On the other hand, RB1 protein remains as the wild-type in many breast cancer cell lines including MCF7, T47D and ZR75. So try these breast cancer cell lines (although I do not know about the condition of other RB family proteins like p107 and p130.) Good luck!
RB as has been discovered in 1971 relation to Knudson hypothesis of two "hits" genetic events explained that RB disruption occuring in retinoblastoma as condition sine quanon. The tumor suppressor activity has been related to block entry into S phase by inhibiting E2F transcriptional program due to RB preferential binding. However, RB is not essential for controling cell cycle. RB loss, by mutation or deletion, can occur in several tumors, predominantly in small cell lung cancer (80%0, less in non-small cell lung cancer (20-30%). For the cancer cell growth, mutually exclusive NK4A loss has been observed in 15 % and 58 % respectively. In cervical cancer caused by HPV the HPV E7 oncoprotein targeted RB to become inactivated. In HPV E7 negative cervical cancer the RB loss was caused by somatic mutation.
Other tumors or cell lines with defective RB have been reported e.g. osteosarcoma and bladder cancer.
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