ROLE OF DEXAMETHASONE IN THE TREATMENT OF HUMORAL HYPERCALCEMIA OF MALIGNANCY (HHM) USING JAR HUMAN CHORIOCARCINOMA CANCER CELL LINE AS A MODEL

Tumors cause multiple effects on the skeleton and on calcium homeostasis, but they do so in specific patterns which are becoming better defined as the mediators responsible become more fully characterized. Approximately 1,000,000 people die each year in Western Europe and the United States from these three malignancies bone, lung, and breast and the majority of these have bone metastases. Bone is the third commonest site of metastatic disease in tumors of all types and the second most common in breast and prostate cancers. PTH-rP produced by tumor cells of various forms is a killer in at least 15% of the 1,000, 000 cases reported in U.S. and Western Europe a significant number that is hard to ignore. The sole aim of this research is to establish whether dexamethazone inhibit the action of PTH-rP in-vitro and therefore providing a possible remedy for the ailing HHM. Here JAR human choriocarcinoma cells was used with PTH-rP with and without Dexamethasone also, DNA and thymidine incorporation proliferation assays were carried out to determine the extent of stimulation by PTH-rP or inhibition by dexamethasone. The stimulation aggravates HHM, while the inhibition is assumed to alleviate the sufferings of patients with HHM. Dexamethasone was found to inhibit the stimulated cell proliferation by PTH-rP in JAR human choriocarcinoma cells. Thus, the experiment may act as a spring board for alleviating the sufferings and possible treatment of patients with Humoral Hypercalcaemia of Malignancy (HHM