One of the major causes of prostate cancer morbidity and mortality is bone metastases. Currently, when it comes to treating prostate cancer metastases we are very limited in effective therapies that actually prolong survival.
Kirschenbaum A, etal (Departments of Urology and Medicine Division of Pulmonary Diseases Division of Endocrinology, Metabolism, and Bone Diseases, Mount Sinai School of Medicine, New York, New York) in a small study demonstrated that Prostatic Acid Phosphatase (PAP) which is a protein expressed by prostate cancer cells is strongly expressed in prostate cancer bone metastases (7/7 patients), while prostate specific antigen (PSA) is only weakly expressed.
Kirschenbaum A, etal believe that the human prostate cancer cell line VCaP secretes PAP and induces an osteoblastic reaction in bone which is very similar to that seen in human prostate cancer bone metastases. They showed that the mixing of MC3T3 mouse preosteoblast cells with VCaP cells induced MC3T3 cell growth and differentiation as measured by alkaline phosphatase secretion. They also showed that this effect is inhibited by addition of the PAP-inhibitor, l-tartrate. Taken together, these data indicate that PAP is expressed in prostate cancer bone metastases and may play a causal role in the osteoblastic phase of the disease.
Clearly, further research into the inhibition of PAP as a possible treatment to slow the development of bone metastases is both important and needed. Additional, perhaps PAP be considered as a biomarker that should be systematically monitored to better evaluate bone health in men with advanced prostate cancer.
Kirschenbaum A, Liu XH, Yao S, Leiter A, Levine AC., Ann N Y Acad Sci. 2011 Nov;1237(1):64-70. doi: 10.1111/j.1749-6632.2011.06198.
Joel T Nowak, M.A., M.S.W.