Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds a tumor-associated surface antigen on malignant hematologic cells independent of MHC. Antigen engagement triggers CD3ζ signaling with costimulatory domains (e.g., CD28 or 4-1BB), leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing, with potential in vivo expansion and persistence for ongoing antitumor activity.