Prognostic significance of β‐catenin and topoisomerase IIα in de novo acute myeloid leukemia |
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| Authors: | Chih‐Cheng Chen Jyh‐Pyng Gau Jie‐Yu You Kuan‐Der Lee Yuan‐Bin Yu Chang‐Hsien Lu Jen‐Tsun Lin Chieh Lan Wan‐Hsia Lo Jacqueline Ming Liu Ching‐Fen Yang |
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| Institution: | 1. Division of Hematology Oncology, Department of Medicine, Chang Gung Memorial Hospital‐Chiayi, Chiayi, Taiwan;2. Graduate Institute of Clinical Medical Sciences, Chang Gung University, Tao‐Yuan, Taiwan;3. Division of Hematology Oncology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan;4. School of Medicine, National Yang‐Ming University, Taipei, Taipei, Taiwan;5. Institute of Cancer Research, National Health Research Institutes, Taipei, Taiwan;6. Department of Pathology, Taipei Veterans General Hospital, Taipei, Taiwan |
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| Abstract: | The Wnt/β‐catenin signaling is important for controlling self‐renewal of hematopoietic stem cells and its constitutive activation has recently been documented in a significant proportion of acute myeloid leukemia (AML) cases. Topoisomerase IIα (Topo IIα) is a marker of cell proliferation and a crucial target for anthracycline cytotoxicity, the mainstay of management employed in AML. We retrospectively investigated the prognostic roles of β‐catenin and topo IIα in a cohort of 59 patients with newly diagnosed AML by immunohistochemistry. Aberrant β‐catenin expression was demonstrated in 13 patients (22%), and it was more likely to occur in those with unfavorable karyotypes. Advanced age and poor performance status adversely influenced the achievement of complete remission, while neither aberrant β‐catenin expression nor enhanced topo IIα activity did. On multivariate survival analysis, four factors independently predicted a shortened overall survival: aberrant β‐catenin expression, high topo IIα activity, poor‐risk cytogenetics, and presence of at least one comorbidity factor. Our results suggest that both β‐catenin and topo IIα independently predicted an adverse prognosis and might serve as new markers for risk stratification in AML patients. Am. J. Hematol., 2009. © 2008 Wiley‐Liss, Inc. |
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