|1.||Fuks, Zvi: 1 article (01/2009)|
|2.||Marquez, Victor E: 1 article (01/2009)|
|3.||Kolesnick, Richard: 1 article (01/2009)|
|4.||Kang, Ji-Hye: 1 article (01/2009)|
|5.||Haimovitz-Friedman, Adriana: 1 article (01/2009)|
|6.||Rotenberg, Susan A: 1 article (01/2009)|
|7.||Truman, Jean-Philip: 1 article (01/2009)|
|8.||Lerman, Gabriel: 1 article (01/2009)|
01/01/2009 - "Using the LNCaP orthotopic prostate model it is shown that treatment with TPA or DAG-lactone induces significant reduction in tumor ATM levels coupled with tumor growth delay. "
01/01/2009 - "Furthermore, while fractionated radiation alone produces significant tumor growth delay, pretreatment with TPA or DAG-lactone significantly potentiates tumor cure. "
|2.||Prostatic Neoplasms (Prostate Cancer)
01/01/2009 - "We previously demonstrated that treatment of human androgen-responsive prostate cancer cell lines LNCaP and CWR22-Rv1 with 12-O-tetradecanoylphorbol 13-acetate (TPA), a known protein kinase C (PKC) activator, decreases ATM protein levels, thus de-repressing the enzyme ceramide synthase (CS) and promoting apoptosis as well as radio-sensitizing these cells.(1) Here we show that PKCalpha mediates the TPA effect on ATM expression, since ATM suppression and apoptosis induced by either TPA or diacylglycerol-lactone (DAG-lactone), both inducing PKCalpha activation,(2) are abrogated in LNCaP cells following transfection of a kinase-dead PKCalpha mutant (KD-PKCalpha). "
|1.||Protein Kinase C
|4.||ataxia telangiectasia mutated protein