Acute leukemias are clonal malignancies of hematopoietic progenitor cells characterized by uncontrolled proliferation of immature blast cells (>20% blasts in bone marrow) that crowd out normal hematopoiesis. Acute lymphoblastic leukemia (ALL) arises from lymphoid precursors (B-cell or T-cell lineage) and is the most common childhood malignancy (peak age 2-5 years). ALL blasts accumulate due to arrested differentiation and impaired apoptosis, often driven by chromosomal translocations (e.g., Philadelphia chromosome t(9;22) in adult ALL, t(12;21) TEL-AML1 in pediatric ALL). Acute myeloid leukemia (AML) originates from myeloid precursors and is more common in adults (median age 68). AML is classified by WHO criteria based on genetic abnormalities, including t(8;21), t(15;17) in acute promyelocytic leukemia (APL), and FLT3 mutations. The massive proliferation of nonfunctional blasts causes bone marrow failure: anemia (decreased RBCs), thrombocytopenia (decreased platelets), and neutropenia (decreased functional WBCs). Leukemic cells can infiltrate the CNS, liver, spleen, lymph nodes, and gingiva. Tumor lysis syndrome (TLS) occurs when rapid cell death during treatment releases intracellular contents (potassium, phosphorus, uric acid, nucleic acids), causing hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia, and acute kidney injury.