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The **graft-versus-tumor effect** (**GvT**) is an immunological phenomenon observed after allogeneic hematopoietic stem cell transplantation. It occurs when immune effector cells from a donor—primarily T lymphocytes and sometimes natural killer (NK) cells—recognize and destroy residual malignant tumor cells in the transplant recipient. This beneficial anti-tumor response is most commonly seen in hematologic cancers such as leukemias, lymphomas, and multiple myeloma but may also play a role in some solid tumors. The mechanism involves donor-derived T cells recognizing alloantigens or minor histocompatibility antigens on the surface of cancerous host cells. Dendritic cells are important for presenting these antigens and optimizing the anti-tumor response. The same principle underlies both **graft-versus-host disease** (GVHD)—where normal host tissues are attacked—and the desired GvT activity against cancerous tissue. Separating these two effects remains a major therapeutic challenge because strategies that reduce GVHD often also diminish the beneficial GvT activity. Enhancement of this effect has been attempted with cytokines like interleukin 2 or adoptive transfer of NK/T-cell subsets but carries risks such as increased infection rates or exacerbation of GVHD. The biology underlying selective targeting of tumors without harming normal tissues is not fully understood, making precise manipulation difficult at present[1][2][3][5][6]. **Note:** The "graft-versus-tumor effect" is not a molecule or receptor but rather an immunological process/phenomenon involving multiple cellular players; thus it does *not* fit standard definitions for molecular drug targets like receptors or enzymes.
Donor T cell-mediated cytotoxicity against recipient tumor cells[1][3][5][7] Natural killer cell-mediated cytotoxicity[2] Alloantigen and tumor-specific antigen recognition by donor immune cells[1][3]
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