Acute myeloid leukemia (AML) with inv(3)(q21q26.2)/t(3;3)(q21;q26.2) [inv(3)/t(3;3)] is recognized as a distinctive entity in the WHO classification. Risk assignment and clinical and genetic characterization of AML with chromosome 3q abnormalities other than inv(3)/t(3;3) remain largely unresolved.Cytogenetics, molecular genetics, therapy response, and outcome analysis were performed in 6,515 newly diagnosed adult AML patients. Patients were treated on Dutch-Belgian Hemato-Oncology Cooperative Group/Swiss Group for Clinical Cancer Research (HOVON/SAKK; n = 3,501) and German-Austrian Acute Myeloid Leukemia Study Group (AMLSG; n = 3,014) protocols. EVI1 and MDS1/EVI1 expression was determined by real-time quantitative polymerase chain reaction.3q abnormalities were detected in 4.4% of AML patients (288 of 6,515). Four distinct groups were defined: A: inv(3)/t(3;3), 32%; B: balanced t(3q26), 18%; C: balanced t(3q21), 7%; and D: other 3q abnormalities, 43%. Monosomy 7 was the most common additional aberration in groups (A), 66%; (B), 31%; and (D), 37%. N-RAS mutations and dissociate EVI1 versus MDS1/EVI1 overexpression were associated with inv(3)/t(3;3). Patients with inv(3)/t(3;3) and balanced t(3q21) at diagnosis presented with higher WBC and platelet counts. In multivariable analysis, only inv(3)/t(3;3), but not t(3q26) and t(3q21), predicted reduced relapse-free survival (hazard ratio [HR], 1.99; P < .001) and overall survival (HR, 1.4; P = .006). This adverse prognostic impact of inv(3)/t(3;3) was enhanced by additional monosomy 7. Group D 3q aberrant AML also had a poor outcome related to the coexistence of complex and/or monosomal karyotypes and cryptic inv(3)/t(3;3).Various categories of 3q abnormalities in AML can be distinguished according to their clinical, hematologic, and genetic features. AML with inv(3)/t(3;3) represents a distinctive subgroup with unfavorable prognosis.
Multiple myeloma (MM) is a hematologic cancer characterized by clonal proliferation of plasma cells within the bone marrow. It is the most serious form of plasma cell dyscrasias, whose complications—hypercalcemia, renal failure, anemia, and lytic bone lesions—are severe and justify the therapeutic management. Imaging of bone lesions is a cardinal element in the diagnosis, staging, study of response to therapy, and prognostic evaluation of patients with MM. Historically, the skeletal radiographic workup (SRW), covering the entire axial skeleton, has been used to detect bone lesions. Over time, new imaging techniques that are more powerful than SRW have been evaluated. Low-dose and whole-body computed tomography (CT) supplants SRW for the detection of bone involvement, but is of limited value in assessing therapeutic response. Bone marrow MRI, initially studying the axial pelvic-spinal skeleton and more recently the whole body, is an attractive alternative. Beyond its non-irradiating character, its sensitivity for the detection of marrow damage, its capacity to evaluate the therapeutic response and its prognostic value has been demonstrated. This well-established technique has been incorporated into disease staging systems by many health systems and scientific authorities. Along with positron emission tomography (PET)-18 fluorodeoxyglucose CT, it constitutes the current imaging of choice for MM. This article illustrates the progress of the MRI technique over the past three decades and situates its role in the management of patients with MM.
