There is a wide range of therapies options in multiple myeloma treatment. Many recent research studies on multiple myeloma and its drugs are published in “Hematology” and “Current Research in Oncology” journals. For example, there are many new drugs being studied as treatment options for multiple myeloma, such as bortezomib, ixabepilone and others. The advent of the next-generation therapies such as immunotherapy, bortezomib, lenalidomide, and carfilzomib as treatment options has dramatically improved multiple myeloma patient's survival and progression-free survival.
Multiple myeloma is a blood cancer that almost always begins with a nondiagnostic bone marrow biopsy. Treatment typically entails systemic anticancer therapy, most prominently bortezomib and lenalidomide. More than half of the patients receiving bortezomib and lenalidomide ultimately succumb to those drugs. Survival is often improved when patients are managed by a myeloma specialist. Patient groups that require attention are those whose disease is highly progressive, has relapsed after initial bortezomib and lenalidomide treatments, or whose disease has progressed after either bortezomib-based and lenalidomide and dexamethasone-based treatments.
The risk of development of multiple myeloma is increased in individuals who have antibodies present against hepatitis C virus, in individuals with a single family member with multiple myeloma, in individuals who are first-degree relatives of a person with multiple myeloma, and in individuals of black or Hispanic ethnicity in the United States. Further studies are needed to identify the genetic susceptibility and the etiological factors for this disease, and to determine the usefulness of screening individuals for hepatitis C virus antibody status, genetic testing of family members, and surveillance of risk factors to identify individuals who are at increased risk for multiple myeloma.
In a patient with symptomatic MM, the most common signs are appetite loss, weight loss, thrombocytosis, and anemia. More than 60% of patients have evidence of osteolysis. Other features of the disease in the skeleton may include lytic bone lesions, pathologic fractures, and pathologic fractures from bone pain or pain originating from metastases. Pain arising from iliopsoas and adhesions can also cause bone pain. Osteoexcitability, as evidenced by pathologic fractures from trauma, is less common in the skeleton compared with the soft tissues of the skull and maxillofacial area.
This is the first estimate of the number of cases of MM in the United States that was determined from Medicare claim data. The number and age distributions of people with MM in the United States are similar to the global burden of disease.
MM can be cured, but patients with multiple relapses or who are amyloidosis negative will be very likely to relapse. In the early stages, as with other B-cell malignancies, remission is achievable with good induction regimens, frequently combined with peripheral stem cell mobilization and a consolidation chemotherapy regimen.
Survival and progression-free survival are not predictive of progression-free survival as a endpoint in IMiD-treated MM. Patients are unlikely to benefit from IMiD therapy if they have detectable myeloma plasma cells or disease that is in the symptomatic stage.
In the present population-based study of 1045 MM patients, [myeloma-free survival, clinical stage, and treatment were the most significant prognostic factors that were significantly associated with risk of death] (http://www.european-medicine.info/content.cfm?tid=638). All of these were significant prognostic factors for overall survival, irrespective of age or disease duration.
The primary spread of MM is, at present, through hematogenous spread from bone lesions (osseous), which is likely due to the blood-testis barrier disrupting normal hematopoiesis to cause spread throughout the blood stream via the lymphatic drainage system. There is also evidence that MM in bone marrow may be able to escape hematogenous barriers and spread via the bloodstream. While the precise mechanisms of MM spreading remain unclear, current research efforts aim at developing novel and effective treatments to impede these processes.
Despite the dramatic differences between different studies in the use of TBI in patients with MM, few patients are left with disease-free disease following TBI therapy. Most patients will relapse following this treatment. TBI is a powerful antineoplastic therapy that provides the best survival for patients following initial treatment with myeloma medications. However, TBI therapies are accompanied by a high rate of late toxicity, most notably marrow failure. New approaches to treat this side effect are necessary to improve the benefit of TBI therapy.
[A prospective study] involving over 4000 individuals aged 40 years and aged 65 years and over with a newly established diagnosis of multiple myeloma showed that [some people] with symptomatic multiple myeloma at the time of diagnosis had a 2·5 times greater chance of developing [myeloma] after 20 years of follow-up, as compared with the general population. [A 2008 prospective study] found [a 5 years survival rate of 5·8% for patients with symptomatic multiple myeloma; and a 12 years survival rate of 12·5% for those with newly diagnosed, asymptomatic disease.
The prevalence of MM in families with MM is similar to the prevalence of MM in patients with MM. A possible clue that the familial occurrence of MM is hereditary is a report by some of the first families in which a parent (father) with MM had spawned at least two affected sons within a relatively short period.