Prostate cancer is the most frequently diagnosed cancer and the second leading cause of cancer-related deaths among men in the United States. If detected at early stages the prognosis is quite favorable; however, aggressive forms of metastatic prostate cancer spread primarily to the skeleton.
Bone tumors cause great pain, promote fractures and ultimately represent the main cause of morbidity, with a 70 percent incidence documented by autopsies, according to Gabriela Loots, an LLNL biomedical scientists and an associate adjunct professor at UC Merced.
It has been hypothesized that the bone microenvironment serves as a rich “soil” by secreting factors that promote survival and propagation of cancer cells; in turn, tumors secrete factors that alter the bone microenvironment to promote metastatic colonization. Development of new therapies for the prevention and treatment of prostate cancer bone metastasis depends on understanding the dynamic reciprocal interactions between prostate cancer cells and the bone microenvironment.
Yet in a study led by Aimy Sebastian, a graduate student in the School of Natural Sciences at UC Merced who is conducting her Ph.D thesis work under Loots, identified the secreted bone protein Sclerostin (SOST), as a key molecule dysregulated as a result of prostate cancer-bone microenvironment interactions.
Scientists from Lawrence Livermore National Laboratory in collaboration with researchers from University of California campuses at Merced and Davis have found that a secreted protein predominantly expressed in bone inhibits prostate cancer metastasis to bone.
The connection between Prostate cancer and bone cancer is something that can’t be overlooked ..