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HEALTHCARE JOURNAL OF NEW ORLEANS I  MAY / JUN 2024 51 Janeiro Goffin, MD Medical Oncologist Terrebonne General | Mary Bird Perkins Cancer Center or in some instances daratumumab. People who are not candidates for stem cell trans- plantation because of age, health, or pref- erence are treated with a three-drug regi- men, such as VRd or DRd. Following initial combination therapy, two drugs are usually given for an extended time as “maintenance therapy,”typically lenalidomide in combina- tion with decadron or proteasome inhibitor or daratumumab. CAR-T therapy : This is a form of immu- notherapy that uses the person’s own im- mune system to target a specific antigen (a type of protein) found on the surface of the cancer cells. The person’s immune cells (T cells) are collected, genetically modified, and returned to the body. The modified T cells then directly target the cancer cells. Supportive care : Patients with MM are usually treated with fluids to treat kidney dysfunctions/high calcium concentrations, blood products to improve their anemia/ thrombocytopenia, antibiotics to prevent or treat infections, growth factors to improve their white blood cell count, IV immuno- globulins to help them fight infections, de- nosumab to prevent bone fractures and treat bone lesions, and plasmapheresis if blood is too thick causing neurological symptoms. Clinical trials : Progress in treating mul- tiple myeloma requires that better treat- ments be identified through clinical trials. Aclinical trial is a carefully controlled way to study the effectiveness of new treatments or new combinations of known therapies and are conducted all over the world. Patients should ask their doctor about options. n significance” (MGUS) do not require treat- ment. However, they do need long-term follow-up, as a small percentage of people withMGUS will eventually developmultiple myeloma. Once symptoms of multiple myeloma develop, treatment with one or more of the options below is recommended for almost all people. Medications : immunomodulatory drugs (Revlimid, Pomalyst); proteasome inhibitors (Kyprolis, Velcade); corticosteroids (Decad- ron); monoclonal antibodies (Darzalex; Dar- zalex Faspro); bispecific antibodies (teclis- tamab); nuclear export inhibitor (selinexor); cytotoxic chemotherapy agents (Cytoxan, doxorubicin, melphalan); BCL2 inhibitor (venetoclax). Autologous stem cell (bone marrow) transplant: This approach allows for the use of high doses of chemotherapy that would otherwise destroy the bone marrow stem cells. “Autologous”means the transplanted stem cells come from the person’s own body rather than a donor. Stem cells are collected before having chemotherapy, then returned to the body afterward to repopulate the bone marrow. People who are candidates for stem cell transplantation are often treated with a four- drug regimen such as DVRd. After this initial therapy, usually about four months, most clinicians prefer to proceed directly with stem cell transplantation rather than to de- lay this procedure until their disease pro- gresses. Following transplant, two drugs are usually given for an extended time as “main- tenance therapy,” typically lenalidomide in combination with a proteasome inhibitor, blood) and/or detection of one of the follow- ing findings: ≥ 60% plasma cells in the bone marrow; serum free light chain ratio of 100 or more, provided involved FLC level is at least 100 mg/L; or MRI showing more than one lesion, involving bone or bone marrow. Staging/risk disease The aggressiveness of MM depends upon several variables that impact disease biology. Genetic abnormalities seen in the myeloma cells are one of the strongest predictors of tumor aggressiveness. As such, all patients with newly diagnosed MM are classified based on the revised international stag- ing system as having high-, intermediate-, or standard-risk disease based on tumor genetics. • High-risk disease: Approximately 25% of people with MM have high-risk disease on cytogenetic testing. This includes patients with the following cytogenetic abnormalities: transloca- tion t (14;16), translocation t (14;20), translocation t (4;14), gain of chromo- some 1q, and deletion of chromosome 17p. This type of MM is aggressive and may shorten survival. • Standard-risk disease: All patients with MMwho lack high-risk genetic abnor- malities are considered to have stan- dard-risk MM. With modern therapy, patients with standard risk MM have an estimated median survival of 8 to 10 years. Treatment People with a related condition called “monoclonal gammopathy of undetermined

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