Hormonal therapy for neoplasia commonly involves use of glucocorticoids. Direct antitumor effects are related to their lympholytic properties; glucocorticoids can inhibit mitosis, RNA synthesis, and protein synthesis in sensitive lymphocytes. Glucocorticoids are considered cell-cycle nonspecific and are often used in chemotherapeutic protocols after induction by another agent. Unfortunately, resistance to a given glucocorticoid may develop rapidly and typically extends to other glucocorticoids. Toxic effects of glucocorticoid therapy can include peptic ulceration, glucose intolerance, polydipsia and polyuria, immunosuppression, pancreatitis, osteopenia, hypokalemia, cataracts, and muscle wasting. Prednisone and prednisolone are commonly used to treat lymphoreticular neoplasms in combination with other drugs. Because they readily enter the CSF, dexamethasone, prednisone, and prednisolone are especially useful in treatment of leukemias and lymphomas of the CNS.
Indirect benefits of glucocorticoid therapy in cancer include symptomatic improvements in appetite and attitude, suppression of noninfectious fevers, management of hypercalcemia of malignancy (after a definitive diagnosis has been made), and relief of edema associated with spinal cord and brain tumors. However, evidence from several sources suggests that treatment of certain lymphomas with prednisone may increase resistance of neoplastic cells to subsequent cycles of antineoplastic chemotherapy through induction of MDR-1–related P-glycoprotein expression.