International Journal of Clinical Oncology and Cancer Research
Volume 1, Issue 1, December 2016, Pages: 1-5
Received: Nov. 4, 2016;
Accepted: Dec. 3, 2016;
Published: Jan. 7, 2017
Views 2815 Downloads 100
Eman Abd Al-Halim, Department of Clinical Pathology, Faculty of Medicine, Al-Azher University, Cairo, Egypt; Department of Basic Medical Sciences, Al Farabi College of Medicine, Riyadh, KSA
M. Raouf Emam, Department of Clinical Pathology, Faculty of Medicine, Al-Azher University, Cairo, Egypt; Department of Basic Medical Sciences, Al Farabi College of Medicine, Riyadh, KSA
Abdulwahab Ali Abuderman, Department of Basic Medical Sciences, College of Medicine, Salman Bin Abdulaziz University, Riyadh, KSA
Fas-mediated cell death is involved in drug-induced apoptosis in various cell types. Hence, failure of apoptosis could lead to chemoresistance in acute leukemia. The participants of this study were 80 adult acute leukemia patients classified as follows: 40 acute myeloid leukemia (AML) patients, 40 acute lymphoblastic leukemia (ALL) patients. In addition, 10 healthy controls were also included in the study. Fas expression was measured using flow cytometry. The mean value of Fas expression by blast cells from AML patients at diagnosis was 41.72 ± 10.3%. AML patients were divided into the Fas-positive group [30 patients (72.5%)] and the Fas-negative group [10 patients (27.5%)]. The mean value of expression increased significantly in M5 (52.91 ± 11.3%) with highly significant differences (P < 0.001) between Fas expression levels in different FAB subtypes of AML. The mean value of Fas expression in ALL patients was 43.87± 11.5%. 23 (57.5%) patients were positive for Fas expression, whereas 17 (42.5%) were negative. Fas expression was positive in 14/24 (63.2%) precursor B-ALL patients and in 12/16 (84.6%) T-ALL patients. The mean value of Fas expression was significantly higher (P = 0.039) in T-ALL (55.15 ± 7.8%) in comparison with precursor B-ALL (34.47 ± 5.76%). The mean value of Fas expression by blast cells from AML and ALL, patients at diagnosis was 41.72± 10.3 and 43.87 ± 11.5. We can conclude that Fas receptor expression on blast cells from ALL and AML patients could serve as an independent prognostic factor.
Eman Abd Al-Halim,
M. Raouf Emam,
Abdulwahab Ali Abuderman,
The Prognostic Value of Apoptotic Marker (CD95) in Adult Acute Leukemias, International Journal of Clinical Oncology and Cancer Research.
Vol. 1, No. 1,
2016, pp. 1-5.
Steller H. Mechanisms and genes of cellular suicide Science; (1995) 267: 1445–1448.
Evan G, Wyllie A, Gilbert C. Induction of apoptosis in fibroblasts by C-myc protein. Cell; (1992) 69: 119–128.
Sessler T, Healy S, Samali A, Szegezdi E. (2013) Structural determinants of DISC function: New insights into death receptor-mediated apoptosis signaling. Pharmacol Ther; (2013) 140: 186–199.
Knipping E, Debatin K, Stricker K, Heilig B, Eder A, Krammer P. Identification of soluble Apo-1 in supernatants of human B- and T-cell lines and increased serum levels in B- and T-cell leukemias. Blood;. (1995) 85: 1562–1569.
Yonehara S, Ishii A, Yonehara M. A cell-killing monoclonal antibody (anti-Fas) to a cell surface antigen co-downregulated with the receptor of tumor necrosis factor. J Exp Med; (1989) 169: 1747–1756.
Fischer U, Schulze-Osthoff K. New approaches and therapeutics targeting apoptosis in disease. Pharmacol Rev; (2005) 57: 187–215.
Takahashi T, Tanaka M, Inazawa J, Abe T, Suda T, Nagata S. Human Fas ligand: Gene structure, chromosomal location and species specificity. Int Immunol; (1994) 6: 1567–1574.
Laurent G, Jaffrezou J. Signaling pathways activated by daunorubicin. Blood; (2001) 98: 913–924.
Fulda S, Los M, Friesen C, Debatin K. Chemosensitivity of solid tumor cells is associated with activation of the CD95 system. Int J Cancer; (1998) 76: 105–114.
Schimmer A, Hedley D, Penn L, Minden M. Receptor and mitochondrialmediated apoptosis in acute leukemia: A transitional view. Blood; (2001) 98: 3541–3553.
Bennet J, Catovasky D, Danial M. Proposed revised criteria for classification of acute leukemia: A report of the French-American-British Cooperation group. Ann Intern Med; (1985) 103: 620–625.
Mitelman F. ISCN: An International System for Human Cytogenetic Nomenclature. Basel, Switzerland: S. Karger;. (1995)
Mrozek K, Carroll A, Maharry K Central review of cytogenetics is necessary for cooperative group correlative and clinical studies of adult acute leukemia: The Cancer and Leukemia Group B experience. Int J Oncol; (2008) 33: 239–244.
Grimwade D, Walker H, Oliver F, Wheatley K, Harrison C, Harrison G. The importance of diagnostic cytogenetics on outcome in AML: Analysis of 1612 patients entered into the MRC AML 10 Trial. Blood; (1998) 92: 2322–2333.
Büchner T, Hiddemann W, Wörmann B, Löffler H, Ludwig Wd, Schoch C, et al. Acute myeloid leukemia in adults: Is postconsolidation maintenance therapy necessary? Int J Hematol; (2000) 72: 285–289.
Lengfelder E, Reichert A, Schoch C, Haase D, Haferlach T, Löffler H, et al. Double induction strategy including high dose cytarabine in combination with all-trans retinoic acid: Effects in patients with newly diagnosed acute promyelocytic leukemia. Leukemia; (2000) 14: 1362–1370.
De Greef GE, van Putten WL, Boogaerts M, Huijgens PC, Verdonck LF, Vellenga E, et al Dutch-Belgian Hemato-Oncology Co-operative Group HOVON, Swiss Group for Clinical Cancer Research SAKK. Criteria for defining a complete remission in acute myeloid leukaemia revisited. An analysis of patients treated in HOVON-SAKK co-operative group studies. Br J Haematol;.( 2005) 128: 184–191.
Gökbuget N, Hoelzer D, Arnold R, Bohme A, Bartram CR, Freund M, et al. Treatment of adult ALL according to the protocols of the German Multicenter Study Group for Adult ALL (GMALL). Hematol Oncol Clin North Am; (2000) 14: 1307–1325.
Debatin K, Krammer P. Death receptors in chemotherapy and cancer. Oncogene; (2004) 23: 2950–2966.
Zapata J, Pawlowski K, Haas EA diverse family of proteins containing tumor necrosis factor receptor-associated factor domains. J Biol Chem;.(2001) 276: 24242–24252.
Krammer P. CD95’s deadly mission in the immune system. Nature; (2000) 407: 789–795.
Miyawaki T, Uehara T, Nibu R, Tsuji T, Yachie A, Yonehara S, Taniguchi N. Differential expression of apoptosis-related Fas antigen on lymphocyte subpopulations in human peripheral blood. J Immunol; (1992) 149: 3753–3758.
Druilhe A, Cai Z, Haile S, Chouaib S, Pretolani M Fas-mediated apoptosis in cultured human eosinophils. Blood; (1996) 87: 2822–2830.
Min Y, Lee S, Lee J, Chong S, Hahn J, Ko Y. Expression of Fas antigen in acute myeloid leukemia is associated with therapeutic response to chemotherapy. Br J Hematol; (1996) 93: 928.
Iijima N, Miyamura K, Itou T, Tanimoto M, Sobue R, Saito H. Functional expression of Fas (CD95) in acute myeloid leukemia cells in the context of CD34 and CD38 expression: Possible correlation with sensitivity of chemotherapy. Blood;. (1997) 90: 4901–4909.
Min Y, Lee H, Choi S, Chi H, Lee J, Kim W, Lee K. Prognostic significance of Fas (CD95) and TRAIL receptors (DR4/DR5) expression in acute myelogenous leukemia. Leuk Res 2004; 28: 359–365.
Maciejewski J, Selleri C, Anderson S, Young N. Fas antigen expression on CD34+ human marrow cells is induced by interferon γ and tumour necrosisfactor α potentiates cytokine-mediated hematopoietic suppression in vitro. Blood; (1995) 85: 3183–3190.
Iwai K, Miyawaki T, Takizawa T, Konno A, Ohta K, Yachie A, et al. Differential expression of bcl-2 and susceptibility to anti-Fas-mediated cell death in peripheral blood lymphocytes, monocytes and neutrophils. Blood; (1994) 84: 1201–1208.
Beltinger C, Kurz E, Bohler T, Schrappe M, Ludwing W, Debatin K. CD95(Apo-1/Fas) mutation in childhood T-lineage acute lymphoblastic leukemia. Blood; (1998) 91: 3943–3951.
Karawajew L, Wuoter C, Ruppert V, Drexler H, Gruss H, Ludwig W. Differential CD95 expression and function in T and B lineage acute lymphoblastic leukemia cell. Leukemia; (1997) 11: 1245–1252.