The Expression Changes of CX3CL1 and Interlukin-6 Genes During Remission Induction Therapy in Patients With Acute Myeloid Leukemia
AbstractBackground: Acute Myeloid Leukemia syndrome (AML) is a hematologic malignancy which is due to clonal extensive proliferation of leukemic precursor cells and is rapidly fatal unless treated or response to chemotherapy. Cytogenetic findings have important role in prognosis and categorization of AML. The aim of this study was to investigate the expression changes in CX3CL1 and Interlukin-6 (IL-6) genes before and after chemotherapy as remission induction therapy in AML patients. Materials and Methods: In this study 69 patients (36 males, 33 female) with AML was selected from tertiary medical heath center. A quantitative polymerase chain reaction (PCR) was done for mRNA expression of CX3CL1 and IL-6genes before and after induction chemotherapy. To obtain expression changes in CX3CL1 and IL-6genes, we used 2-ΔΔCT method. Results: The expression of CX3CL1 and IL-6 was significantly increased after induction chemotherapy. Also, the ΔCt mean of CX3CL1 and IL-6 mRNA was not significant between AML subtype groups. Conclusion: In conclusion, as we showed that chemotherapy significantly increase the expression of CX3CL1 and IL-6 which can be used as a prognostic factor of AML.
Döhner H, Estey EH, Amadori S, Appelbaum FR, Büchner T, Burnett AK et al. Diagnosis and management of acute myeloid leukemia in adults: recommendations from an international expert panel, on behalf of the European LeukemiaNet. Blood. 2010;115(3):453-74.
Ridgway D. The first 1000 dendritic cell vaccinees. Cancer investigation. 2003;21(6):873-86.
Estey EH, editor. General approach to, and perspectives on clinical research in, older patients with newly diagnosed acute myeloid leukemia. Seminars in hematology; 2006: Elsevier.
Mavromatis B, Cheson BD. Monoclonal antibody therapy of chronic lymphocytic leukemia. Journal of clinical oncology. 2003;21(9):1874-81.
Hagenbeek A, Gadeberg O, Johnson P, Pedersen LM, Walewski J, Hellmann A et al. First clinical use of ofatumumab, a novel fully human anti-CD20 monoclonal antibody in relapsed or refractory follicular lymphoma: results of a phase 1/2 trial. Blood. 2008;111(12):5486-95.
Ibrahem L, Mahfouz R, Elhelw L, Abdsalam EM, Soliman R. Prognostic significance of DNMT3A mutations in patients with acute myeloid leukemia. Blood Cells, Molecules, and Diseases. 2015;54(1):84-9.
Li K, Lv XX, Hua F, Lin H, Sun W, Cao WB et al. Targeting acute myeloid leukemia with a proapoptotic peptide conjugated to a toll‐like receptor 2‐mediated cell‐penetrating peptide. International journal of cancer. 2014;134(3):692-702.
Nasrollahi SA, Taghibiglou C, Azizi E, Farboud ES. Cell‐penetrating peptides as a novel transdermal drug delivery system. Chemical biology & drug design. 2012;80(5):639-46.
Charo IF, Ransohoff RM. The many roles of chemokines and chemokine receptors in inflammation. New England Journal of Medicine. 2006;354(6):610-21.
Verge GM, Milligan ED, Maier SF, Watkins LR, Naeve GS, Foster AC. Fractalkine (CX3CL1) and fractalkine receptor (CX3CR1) distribution in spinal cord and dorsal root ganglia under basal and neuropathic pain conditions. European Journal of Neuroscience. 2004;20(5):1150-60.
Corcione A, Ferretti E, Pistoia V. CX3CL1/fractalkine is a novel regulator of normal and malignant human B cell function. Journal of leukocyte biology. 2012;92(1):51-8.
D'Haese JG, Demir IE, Friess H, Ceyhan GO. Fractalkine/CX3CR1: why a single chemokine-receptor duo bears a major and unique therapeutic potential. Expert opinion on therapeutic targets. 2010;14(2):207-19.
Sugiyama H, Inoue K, Ogawa H, Yamagami T, Soma T, Miyake S et al. The expression of IL-6 and its related genes in acute leukemia. Leukemia & lymphoma. 1996;21(1-2):49-52.
Park J, Tadlock L, Gores GJ, Patel T. Inhibition of interleukin 6-mediated mitogen‐activated protein kinase activation attenuates growth of a cholangiocarcinoma cell line. Hepatology. 1999;30(5):1128-33.
Heinrich PC, Behrmann I, Serge H, Hermanns HM, Müller-Newen G, Schaper F. Principles of interleukin (IL)-6-type cytokine signalling and its regulation. Biochemical journal. 2003;374(1):1-20.
Iravani Saadi M, Arandi N, Yaghobi R, Azarpira N, Geramizadeh B, Ramzi M. Aberrant Expression of the miR-181b/miR-222 after Hematopoietic Stem Cell Transplantation in Patients with Acute Myeloid Leukemia. Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion. 2019;35(3):446-50. doi:10.1007/s12288-018-01066-6.
SAADI MI, Arandi N, Yaghobi R, Azarpira N, Geramizadeh B, Ramzi M. Up-Regulation of the miR-92a and miR-181a in Patients with Acute Myeloid Leukemia and their Inhibition with Locked Nucleic acid (LNA)-antimiRNA; Introducing c-Kit as a New Target Gene. International Journal of Hematology and Oncology.28(3):001-9.
Saadi MI, Beigi MAB, Ghavipishe M, Tahamtan M, Geramizadeh B, Zare A et al. The circulating level of interleukins 6 and 18 in ischemic and idiopathic dilated cardiomyopathy. Journal of cardiovascular and thoracic research. 2019;11(2):132.
Ramzi M, Saadi MI, Yaghobi R, Arandi N. Dysregulated Expression of CD28 and CTLA-4 Molecules in Patients with Acute Myeloid Leukemia and Possible Association with Development of Graft versus Host Disease after Hematopoietic Stem Cell Transplantation. Int J Organ Transplant Med (IJOTM). 2019;10(2).
Saadi MI, Ramzi M, Hosseinzadeh M, Ebrahimi N, Owjfard M, Abdolyousefi EN et al. Expression Levels of Il-6 and Il-18 in Acute Myeloid Leukemia and Its Relation with Response to Therapy and Acute GvHD After Bone Marrow Transplantation. Indian Journal of Surgical Oncology. 2021. doi:10.1007/s13193-021-01358-w.
Saadi MI, Bozorgi H, Ramzi M, Noshadi E, Akbari A, Haghighinejad ZK et al. Characterization of MiR-92b, 1275 and 551 in Patients with Acute Myeloid Leukemia and their association with acute Graft versus Ho Disease after Hematopoietic Stem cell Transplantation.
Middleton PG, Taylor PR, Jackson G, Proctor SJ, Dickinson AM. Cytokine gene polymorphisms associating with severe acute graft-versus-host disease in HLA-identical sibling transplants. Blood. 1998;92(10):3943-8.
Johnston L. Acute graft-versus-host disease: differing risk with differing graft sources and conditioning intensity. Best Practice & Research Clinical Haematology. 2008;21(2):177-92.
Baron F, Labopin M, Niederwieser D, Vigouroux S, Cornelissen J, Malm C et al. Impact of graft-versus-host disease after reduced-intensity conditioning allogeneic stem cell transplantation for acute myeloid leukemia: a report from the Acute Leukemia Working Party of the European group for blood and marrow transplantation. Leukemia. 2012;26(12):2462.
Brissot E, Bossard C, Malard F, Braudeau Cc, Chevallier P, Guillaume T et al. Involvement of the CX3CL1 (fractalkine)/CX3CR1 pathway in the pathogenesis of acute graft‐versus‐host disease. Journal of leukocyte biology. 2015;97(2):227-35.
Li H, Li J, Cheng J, Chen X, Zhou L, Li Z. AML‑derived mesenchymal stem cells upregulate CTGF expression through the BMP pathway and induce K562‑ADM fusiform transformation and chemoresistance. Oncology reports. 2019;42(3):1035-46.
Devemy E, Li B, Tao M, Horvath E, Chopra H, Fisher L et al. Poor prognosis acute myelogenous leukemia: 3-biological and molecular biological changes during remission induction therapy. Leukemia research. 2001;25(9):783-91.
Erreni M, Solinas G, Brescia P, Osti D, Zunino F, Colombo P et al. Human glioblastoma tumours and neural cancer stem cells express the chemokine CX3CL1 and its receptor CX3CR1. European Journal of Cancer. 2010;46(18):3383-92.
Zeng Y, Jiang J, Huebener N, Wenkel J, Gaedicke G, Xiang R et al. Fractalkine gene therapy for neuroblastoma is more effective in combination with targeted IL-2. Cancer letters. 2005;228(1-2):187-93.
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