Recommendations for the assessment and management of measurable residual disease in adults with acute lymphoblastic leukemia: A consensus of North American experts
The vast majority of adults with acute lymphoblastic leukemia (ALL) achieve remission with standard chemotherapy regimens, but many of these patients ultimately relapse and die from leukemia. In these patients, relapse occurs despite achievement of morphologic remission (ie, bone marrow blasts <5%), suggesting that low levels of measurable residual disease (MRD), also called “minimal residual disease,” persist in the remission bone marrow (Figure 1). Compared with morphologic assessment alone, sensitive methods of MRD quantification can better estimate the reduction in posttreatment disease burden and provide information about the leukemia biology and treatment response of individual patients. Posttreatment MRD status is a powerful prognostic factor in all subtypes of ALL and, in many studies, supersedes historically relevant prognostic factors, including age, white blood cell count, and cytogenetics.4–7 Given the significant impact of MRD on survival outcomes in adults with ALL, many authorities suggest that MRD status can be used to inform postremission strategies, such as allogeneic hematopoietic stem cell transplantation (HSCT) in first remission. The development of novel approaches (eg, blinatumomab, inotuzumab ozogamicin, and chimeric antigen receptor [CAR] T cells) that are highly
effective in eradicating residual disease has further increased the complexity of decision-making regarding MRD.
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Acute lymphoblastic leukemia (ALL) is a cancer of the lymphoid line of blood cells characterized by the development of large numbers of immature lymphocytes. Symptoms may include feeling tired, pale skin color, fever, easy bleeding or bruising, enlarged lymph nodes, or bone pain. As an acute leukemia, ALL progresses rapidly and is typically fatal within weeks or months if left untreated.
In most cases, the cause is unknown.Genetic risk factors may include Down syndrome, Li-Fraumeni syndrome, or neurofibromatosis type 1. Environmental risk factors may include significant radiation exposure or prior chemotherapy. Evidence regarding electromagnetic fields or pesticides is unclear. Some hypothesize that an abnormal immune response to a common infection may be a trigger. The underlying mechanism involves multiple genetic mutations that results in rapid cell division. The excessive immature lymphocytes in the bone marrow interfere with the production of new red blood cells, white blood cells, and platelets. Diagnosis is typically based on blood tests and bone marrow examination.