Mechanisms of bone resorption and skeletal protection in solid tumor metastases and use of denosumab as a potent drug Doi: https://doi.org/10.55522/jhpo.V2I5.0047

Abstract

Cancer that spreads to bones is actually a common and serious problem in patients with advanced tumors, especially from breast, prostate, and lung cancers. This bone spread definitely happens frequently and causes major complications. Tumor cells in bone tissue disturb normal bone repair process and further increase bone breakdown activity. This leads to bone problems like fractures, spinal cord pressure, and severe pain in the bone itself. The main cause of bone disease from tumors actually involves three key proteins - RANK, RANKL, and OPG - which definitely control how bone-breaking cells grow and work. As per research findings, too much RANKL protein at the tumor-bone area increases bone-eating cell activity, which causes bone damage and helps tumors grow. Regarding this process, the bone destruction and cancer spread happen together. Denosumab is a human antibody that blocks RANKL protein, which further stops bone breakdown cells from forming. This treatment itself targets the specific pathway that controls bone destruction. Basically, Denosumab works better than old bisphosphonates because you can inject it under the skin, it starts working fast, and it's the same safe option for patients with kidney problems. Also, clinical trials have further shown that the treatment itself reduces bone complications and improves life quality in patients with bone cancer spread from solid tumors. Basically, this review explains how cancer damages bones by focusing on the same RANK/RANKL/OPG pathway that controls bone breakdown. We are seeing studies that look at how stopping RANKL can help treat patients, what happens when doctors use Denosumab medicine, and what new bone treatments we can add to cancer care in future only.