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Background and objectives: Acute myeloid leukemia (AML) is a heterogeneous malignancy caused by various pathological mechanisms. Chemokines are involved in the initiation, progression, migration, survival, treatment and complications of AML. CXCL1 has an indirect effect on the progression of cancer and CXCL10 produced by leukemia cells attracts natural killer cells toward tumor sites to eradicate cancer cells. The present study investigated effects of chemotherapy on serum levels of CXCL1 and CXCL10 in patients with AML.
Methods: Throughout this case-control study, blood samples were collected from AML patients with M4/M5 subtype (n=25) before and after the first stage of a chemotherapy regimen (7+3). Serum levels of the chemokines were determined using commercial ELISA kits. Data were analyzed using two-sample and paired T-test in SPSS 22 software.
Results: The level of CXCL10 was high in patients but decreased following chemotherapy. After the chemotherapy the patients attained partial remission. However, the level of CXCL1 did not change in the patients.

Conclusion: Although chemotherapy could decrease CXCL10 levels and induce partial remission, CXCL1 levels does not change in AML patients with M4/M5 subtype. Based on the results, the employment of CXCL1 and CXCL10 inhibitors in the chemotherapy regimen could prevent relapse in the later stages or even reduce the duration of treatment.

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Background and objectives: Acute myeloid leukemia (AML) is a malignancy that involves the bone marrow and peripheral blood. Some chemokines play a role in the progression, migration and tumor initiation and are therefore associated with poor prognosis. CCL2 promotes tumor growth and is associated with poor prognosis in AML patients. We investigated effects of chemotherapy on serum level of CCL2 in AML patients.
Methods: Throughout this case-control study, blood samples were collected from 25 healthy individuals and 25 AML (M4 and M5) patients before and after the first stage of the current chemotherapy regimen (7+3). Serum level of CCL2 was measured using commercial ELISA kits. Data were analyzed in SPSS 22 using the two-sample t-test and paired t-test.
Results: Before chemotherapy, serum level of CCL2 was significantly higher in the patients than in the healthy controls. Following chemotherapy, the serum level of CCL2 reduced significantly to a level comparable to that of the healthy controls.
Conclusion: The current chemotherapy (7+3) can effectively inhibit CCL2 in AML patients.