G-CSF and Stimulation of Leukemic Cells in AML
G-CSF and Stimulation of Leukemic Cells in AML
Can granulocyte colony-stimulating factor (G-CSF) stimulate leukemic cells when administered to shorten the duration of neutropenia for an acute myeloid leukemia (AML) patient in remission who is receiving consolidation chemotherapy?
AML is an adult disease with the median age of affected patients between 65 and 70 years. AML is characterized by an increased production of immature myeloid cells by the bone marrow. The normal hematopoietic process is disrupted, which results in insufficient numbers of mature myeloid cells and manifests as granulocytopenia, thrombocytopenia, or anemia. In some cases, the production of immature cells can be so great as to cause leukocytosis. The primary goals in the treatment of AML are to induce complete remission (induction) and prevent relapse (postremission therapy). Several options exist for postremission therapy: consolidation chemotherapy, autologous bone marrow transplant, or allogeneic bone marrow transplant.
Both AML itself and treatment for AML with chemotherapy cause myelosuppression. Colony-stimulating factors such as granulocyte-macrophage colony-stimulating factor (GM-CSF) and G-CSF have been studied with the aim of decreasing the duration of neutropenia following induction therapy and consolidation therapy. In general, growth factors have been shown to be of benefit by decreasing the number of neutropenic days.
The concern with using growth factors in AML is that myeloblasts express GM-CSF and G-CSF receptors on their surface. Theoretically, administration of GM-CSF or G-CSF may stimulate the production of blasts as well as mature granulocytes and macrophages. However, growth factors have been added after the induction and consolidation therapy in AML without increasing the rate of failure to induce remission, stimulating regrowth of leukemic cells, or causing early relapse.
Can granulocyte colony-stimulating factor (G-CSF) stimulate leukemic cells when administered to shorten the duration of neutropenia for an acute myeloid leukemia (AML) patient in remission who is receiving consolidation chemotherapy?
AML is an adult disease with the median age of affected patients between 65 and 70 years. AML is characterized by an increased production of immature myeloid cells by the bone marrow. The normal hematopoietic process is disrupted, which results in insufficient numbers of mature myeloid cells and manifests as granulocytopenia, thrombocytopenia, or anemia. In some cases, the production of immature cells can be so great as to cause leukocytosis. The primary goals in the treatment of AML are to induce complete remission (induction) and prevent relapse (postremission therapy). Several options exist for postremission therapy: consolidation chemotherapy, autologous bone marrow transplant, or allogeneic bone marrow transplant.
Both AML itself and treatment for AML with chemotherapy cause myelosuppression. Colony-stimulating factors such as granulocyte-macrophage colony-stimulating factor (GM-CSF) and G-CSF have been studied with the aim of decreasing the duration of neutropenia following induction therapy and consolidation therapy. In general, growth factors have been shown to be of benefit by decreasing the number of neutropenic days.
The concern with using growth factors in AML is that myeloblasts express GM-CSF and G-CSF receptors on their surface. Theoretically, administration of GM-CSF or G-CSF may stimulate the production of blasts as well as mature granulocytes and macrophages. However, growth factors have been added after the induction and consolidation therapy in AML without increasing the rate of failure to induce remission, stimulating regrowth of leukemic cells, or causing early relapse.