SUMMARY: In the landmark Prostate Cancer Prevention Trial (PCPT), Finasteride (PROSCAR®) reduced the risk of Prostate Cancer development and therefore the symptoms associated with it by 33%, compared to Placebo. However, in those who did develop Prostate Cancer while on PROSCAR®, there was an increased risk of high grade tumors. After 18 years of follow up of these patients, it appears that in spite of this set back, there was no difference in the overall survival between the PROSCAR® group and the placebo group. The U.S. Preventive Services Task Force (USPSTF) has been against Prostate Cancer screening, as the consensus is that majority of the Prostate Cancers detected by screening would never become apparent in an individual’s lifetime, if this individual was not screened and therefore would never cause a problem. This long term data begs a very important question – Is it worthwhile taking PROSCAR® for Prostate Cancer prevention? Thompson IM, Goodman PJ, Tangen CM, et al. N Engl J Med 2013;369:603-610
Month: August 2013
Prostate Cancer – Is Prevention Worthwhile?
In the landmark Prostate Cancer Prevention Trial (PCPT), Finasteride (PROSCAR®) reduced the risk of Prostate Cancer development and therefore the symptoms associated with it by 33%, compared to placebo. However, in those who did develop Prostate Cancer while on PROSCAR®, there was an increased risk of more aggressive disease. After 18 years of follow up of these patients (NEJM 2013), it appears that in spite of this set back, there was no difference in the overall survival between the PROSCAR® group and the placebo group. The U.S. Preventive Services Task Force (USPSTF) has been against Prostate Cancer screening, as the consensus is that majority of the Prostate Cancers detected by screening would never become apparent in an individual’s lifetime, if this individual was not screened and therefore would never cause a problem. This long term data begs a very important question – Is it worthwhile taking PROSCAR® for Prostate Cancer prevention?
Lenalidomide plus Dexamethasone for High-Risk Smoldering Multiple Myeloma
SUMMARY: Multiple Myeloma (MM) is a clonal disorder of plasma cells in the bone marrow. It evolves from a precursor stage called Monoclonal Gammopathy of Unknown Significance (MGUS) to MM. Smoldering Multiple Myeloma (SMM) is an intermediate stage in this process of disease evolution. The risk of MGUS transforming into MM is approximately 1% per year. SMM or asymptomatic MM is a precursor to MM and is characterized by at least 10% plasma cells in the bone marrow or a M-spike of at least 3 g/dl, or both, but these patients have no evidence of active symptomatic Myeloma with associated end-organ damage such as hypercalcemia, renal insufficiency, anemia or bone lesions. Even though only 10% of patients with SMM progress to MM annually, over 50% of the SMM patients with high risk features will progress to MM in the first 2 years. The current recommendations for those with SMM are periodic monitoring and treatment intervention only when disease progresses to MM. SMM patients with high risk features include those with at least 10% plasma cells in the bone marrow, a Monoclonal component (IgG monoclonal spike of at least 3g/dL, IgA M-spike of at least 2g/dL or a urinary Bence Jones protein level of more than 1g per 24 hours) or only one of the above two criteria plus at least 95% abnormal plasma cells in the bone marrow, with a reciprocal decrease in one or two uninvolved immunoglobulins of more than 25%, compared to normal values. Identifying those who are at a high risk for progression in the SMM group, is becoming more relevant with the availability of new promising therapies. In a phase III study, 119 patients with high risk SMM were randomly assigned to receive treatment (n=57) or to be observed until progression (n=62).Treatment consisted of Lenalidomide (REVLIMID®) 25 mg given on D1-D21 and Dexamethasone (DECADRON®) 20 mg given on D1-D4 and D12-D15 of a 4 week cycle. Patients received 9 cycles of therapy followed by maintenance therapy with REVLIMID® 10 mg given on D1-D21 every four weeks for 2 years. The median follow-up time was 40 months. The primary end point was time to progression to symptomatic disease. Secondary end points included response rate, overall survival, and safety. The median time to progression was significantly longer in the treatment group compared to the observation group (hazard ratio [HR] = 0.18; P< .001). At 3 years, the survival rate was better in the treatment group than in the observation group (94% vs 80% with a 69% reduction in the risk of death. P =0.03). Treatment related toxicities were grade 2 or lower. The authors concluded that treatment intervention for patients with high risk SMM may be of value, by delaying progression to symptomatic MM and extending overall survival. It remains to be seen if treatment intervention for patients with SMM will become the standard of care. It may also be relevant to include cytogenetics in the SMM definition criteria, as treatment intervention for SMM becomes an acceptable practice. Mateos M-V, Hernandez M-T, Giraldo P, et al. N Engl J Med 2013;369:438-447