Acute Leukemias — Acute Myeloid Leukemia and Acute Lymphoblastic Leukemia
Hematology · Hematopoietic Stem Cells and Their Disorders 🎯 Practice these cards
The classic diagnostic threshold for acute leukemia is blasts ≥____% of bone marrow or blood, but ICC 2022 requires only ≥____% for genetically defined AML (except BCR::ABL1 or TP53-mutated disease, which still need the classic cutoff).
The classic diagnostic threshold for acute leukemia is blasts of 20% or more of the bone marrow or blood, but the 2022 ICC lowered this for genetically defined AML to 10% or more (creating an MDS/AML category at 10-19% blasts); AML with BCR::ABL1 or with TP53 mutation still requires at least 20% blasts.
APL is defined by t(15;17), which produces the ____ fusion; when APL is suspected, start ____ immediately without waiting for molecular confirmation.
Acute promyelocytic leukemia is defined by t(15;17)(q22;q12), which produces the PML::RARA fusion protein that blocks differentiation at the promyelocyte stage; because DIC can cause fatal intracranial or intrapulmonary hemorrhage within days, suspected APL requires starting all-trans-retinoic acid (ATRA) immediately without waiting for molecular confirmation.
The standard regimen for low-risk APL (leukocyte count ≤10,000/μL) is ATRA plus ____, which is superior to ATRA plus anthracycline chemotherapy.
For low-risk APL (leukocyte count ≤10,000/μL), the standard first-line regimen is ATRA combined with arsenic trioxide (ATO), which is superior to ATRA plus anthracycline chemotherapy, with complete remission rates approaching 100% and roughly 85% long-term survival overall.
APL differentiation syndrome, which can occur during the first three weeks of ATRA or ATO, is managed with ____ and carries about ____% mortality if unrecognized.
During the first three weeks of ATRA or ATO therapy, differentiating leukemic cells can adhere to pulmonary vascular endothelium and cause differentiation syndrome (fever, fluid retention, dyspnea, pulmonary infiltrates, pleural/pericardial effusions, hypoxemia), which is managed with glucocorticoids and carries about 10% mortality if unrecognized.
Standard AML induction "7+3" consists of continuous-infusion ____ for 7 days plus an ____ (daunorubicin or idarubicin) given on days 1-3.
Standard AML induction "7+3" delivers continuous-infusion cytarabine (100-200 mg/m²/day for 7 days) with an anthracycline (daunorubicin 60-90 mg/m² or idarubicin 12 mg/m²) on days 1-3, producing marrow aplasia lasting three to four weeks; complete response is achieved in 60% to 85% of patients younger than 60.
In the ELN 2022 risk stratification, favorable risk requires mutated ____ without ____ (or other adverse lesions).
Under ELN 2022 risk stratification, favorable risk requires mutated NPM1 without FLT3-ITD or other adverse lesions; mutated NPM1 with FLT3-ITD is intermediate risk, and FLT3-ITD confers an unfavorable outcome that merits consideration of allogeneic transplantation in first remission.
The FLT3 inhibitor ____ is added to first-line chemotherapy for FLT3-mutated AML, while ____ is the standard single-agent choice at relapse.
The FLT3 inhibitor midostaurin is added to first-line chemotherapy for FLT3-mutated AML, while gilteritinib is the standard single-agent choice at relapse.
Approved in 2023 for newly diagnosed FLT3-ITD-positive AML alongside 7+3 and consolidation, ____ carries a REMS program because of the risk of ____.
In July 2023 the FDA approved quizartinib - with standard 7+3 induction, cytarabine consolidation, and then as maintenance - for newly diagnosed FLT3-ITD-positive AML, using a REMS program because of QT-prolongation risk; in the QuANTUM-First trial, adding quizartinib improved median overall survival to 31.9 versus 15.1 months.
Mutant IDH1/IDH2 produces the oncometabolite ____, which is targeted by ivosidenib (IDH1) and ____ (IDH2).
Mutant IDH1/IDH2 enzymes produce the oncometabolite 2-hydroxyglutarate, which disrupts epigenetic regulation and blocks differentiation; this vulnerability is exploited by ivosidenib (and olutasidenib) for IDH1 and enasidenib for IDH2.
____, a BCL-2 antagonist, plus a hypomethylating agent is the standard first-line therapy for AML patients unfit for intensive induction.
Venetoclax, a BCL-2 antagonist, plus a hypomethylating agent is now the standard first-line approach for AML patients unfit for intensive induction, producing first-line response rates around 60% with a median survival of approximately 15 months.
____, the first approved menin inhibitor, is indicated for relapsed/refractory acute leukemia with ____ translocation or NPM1 mutation.
Revumenib, the first approved menin inhibitor, received accelerated FDA approval for relapsed/refractory acute leukemia with KMT2A translocation and an extended approval for relapsed/refractory NPM1-mutated AML; key class toxicities are differentiation syndrome and QTc prolongation.
CNS prophylaxis is essential in ALL: intrathecal ____, alone or with cytarabine and a glucocorticoid, plus systemic high-dose therapy has reduced CNS relapse rates to 2-5%.
CNS prophylaxis is essential in ALL because leukemic cells seed the CNS early; intrathecal methotrexate (alone or with cytarabine and a glucocorticoid) plus systemic high-dose therapy that penetrates CSF have reduced CNS relapse rates to 2-5%, with cranial radiation (18-24 Gy) reserved for selected cases.
The chemotherapy-free D-ALBA regimen for newly diagnosed Ph+ ALL combines the TKI ____ followed by the bispecific antibody ____.
In the D-ALBA trial, the chemotherapy-free regimen of dasatinib followed by blinatumomab in newly diagnosed Ph+ ALL yielded 4-year disease-free survival of 75.8% and overall survival of 80.7%, with about half of patients never receiving chemotherapy or transplantation.
____ is the one truly ALL-specific drug in the treatment backbone, with signature toxicities including pancreatitis, hypofibrinogenemia, thrombosis, and hypertriglyceridemia.
L-asparaginase is the one truly ALL-specific drug in the treatment backbone, and its unique toxicities include allergic reactions, hypofibrinogenemia (bleeding risk), thrombosis, hypertriglyceridemia, pancreatitis, and hepatotoxicity; pegylated formulations prolong asparagine depletion but do not change the risk profile.
Adult survivors of childhood leukemia with high anthracycline exposure (doxorubicin >300 mg/m²) or chest radiation should undergo screening ____ every 3-5 years to detect left ventricular dysfunction.
Adult survivors of childhood leukemia with high anthracycline exposure (such as doxorubicin exceeding 300 mg/m²) or chest radiation should have echocardiography repeated every 3-5 years to detect left ventricular dysfunction; cumulative incidence of secondary cancer after radiation therapy for childhood ALL reaches 11% at 30 years.
____ are rod-shaped cytoplasmic inclusion bodies pathognomonic of ____ differentiation, establishing AML rather than ALL.
Auer rods - rod-shaped cytoplasmic inclusion bodies formed from fused primary granules - are pathognomonic of myeloid differentiation; when seen on a peripheral smear, the diagnosis is AML, not ALL, and slender Auer rods with CD19 co-expression and increased eosinophils specifically suggest t(8;21) core-binding factor AML.
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