More research is needed to determine the effectiveness of these treatments and the optimal time to maintain each treatment. For both PC and BC, if the treatments are suc cessful then one of the preventative protocols can then be used. Discussion The protocols given for preventing and treating BC and PC are merely suggestions based on the properties of the extended E D selleck kinase inhibitor model. There are other possible alternatives that can be tried. In the case of prevention, it is possible that raising T to higher than physiological levels when using HTLD may have beneficial effects. Individuals with mutations in BRCA1 or BRCA2 may want to start a pre ventative protocol at an earlier age. A protocol for preven tion may also be applied to patients after they initially receive localized treatment, such as surgery or radiation.
Changes in lifestyle that are shown to be useful against BC and PC, such as diet and exercise, can be added to the pro tocols for prevention Inhibitors,Modulators,Libraries and treatment. BC and PC are complex diseases, and the properties of hormone receptors described in the extended E D model represent a foundation which can be built on to better understand both diseases. Bcl 2 is chosen as the main antiapoptotic protein to focus on in this model because it has been shown to be extremely powerful. It prevented apoptosis caused by calcitriol in BC and in PC. Also, bcl 2 is known to be able to prevent apoptosis caused by Fas and by Bad. Just by increasing bcl 2, using a vector of cDNA, LNCaP turned into Inhibitors,Modulators,Libraries an andro gen independent PC cell line. This is consistent with bcl 2 protecting against the apoptosis caused by ADT.
The increased chance of developing BC and PC in individuals with either the BRCA1 or BRCA2 mutation is Inhibitors,Modulators,Libraries consistent with the increased bcl 2 caused by the elimination of PRB being partly responsible for the increased incidence of cancer. Also, assuming that there is a purpose in the pat tern Inhibitors,Modulators,Libraries of which hormone receptors upregulate bcl 2 and which downregulate bcl 2, then it is possible that the same pattern may apply to other anti apoptotic proteins as well. If iAR is not functional, then apoptotic proteins will be upregulated by mAR in both BC and PC. In BC, bcl 2 will also be downregulated, helping to further increase RD, whereas, in PC, bcl 2 will be upregulated. In PC, this cre ates a situation in which the same hormone receptor Inhibitors,Modulators,Libraries exhibits one property that increases the chance of apopto sis and another that decreases the chance of apoptosis.
Ordinarily, apoptosis will occur if a sufficient quantity of androgen is present, as evidenced by the fact that T BSA resulted in a 60% reduction all targets in tumor size of LNCaP trans planted into nude mice after one month. Since mAR downregulates bcl 2 in BC, less T should be needed in order to achieve apoptosis in BC than in PC.