Abstract
Minimal (or measurable) residual (MRD) disease provides a biomarker of response quality for which there is robust validation in the context of modern intensive treatment for younger patients with Acute Myeloid Leukemia (AML). Nevertheless, it remains a relatively unexplored area in older patients with AML. The lack of progress in this field can be attributed to two main reasons. First, physicians have a general reluctance to submitting older adults to intensive chemotherapy due to their frailty and to the unfavourable biological disease profile predicting a poor outcome following conventional chemotherapy. Second, with the increasing use of low-intensity therapies (i.e., hypomethylating agents) differing from conventional drugs in mechanism of action and dynamics of response, there has been concomitant skepticism that these schedules can produce deep hematological responses. Furthermore, age dependent differences in disease biology also contribute to uncertainty on the prognostic/predictive impact in older adults of certain genetic abnormalities including those validated for MRD monitoring in younger patients. This review examines the evidence for the role of MRD as a prognosticator in older AML, together with the possible pitfalls of MRD evaluation in older age.
Highlights
Incidence of acute myeloid leukemia (AML) is highest among older adults, with a median age of 67 years at presentation [1]
The aim of this review is to explore the clinical evidence supporting the role and value of MRD monitoring in older patients with Acute Myeloid Leukemia (AML)
Older patients with AML are less likely to be enrolled in studies involving intensive therapy [5]
Summary
Incidence of acute myeloid leukemia (AML) is highest among older adults, with a median age of 67 years at presentation [1]. The general outcome of AML in older adults (e.g., ≥60 years old) is poor as compared to younger patients, with less of 20% of patients becoming long-term survivors. Several reasons explain such a disappointing clinical outcome. AML is often unfavourable due to the higher incidence of poor-risk karyotypes and the lower frequency of good-risk molecular features [3]. Older patients are more likely to have comorbidities, which complicate the treatment decision-making process and exaggerate the side-effects of therapy [4]
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