Summary Introduction:  CIP2A is a newly identified inhibitor of PP2A. It can stabilize c‐Myc and promote anchorage‐independent cell growth and tumour formation. CIP2A is over‐expressed in some solid tumours although its expression in acute myeloid leukaemia (AML) is still unknown. Methods:  CIP2A mRNA and protein expressions were determined in bone marrow mononuclear cells of both patients with AML and healthy controls using reverse transcription polymerase chain reaction and Western blot, respectively. We used siRNA to knock‐down CIP2A expression in HL60 cells and then examined its potential roles during the pathological progression of AML. Results:  CIP2A mRNA was present in 54 of 70 (77.14%) patients with newly diagnosed AML and in 11 of 14 (70.86%) patients with relapsed AML, which was significantly higher than complete remission specimens and healthy controls (P < 0.001). Knock‐down of CIP2A in HL60 cells slowed down cell proliferation, decreased clonogenic activity and promoted cell differentiation. Conclusion:  These results suggest that CIP2A is over‐expressed in patients with newly diagnosed/relapsed AML and the expression of CIP2A could have potential use as a clinical marker for AML relapse after treatment. The high expression of CIP2A in HL60 cells may be related to active cell proliferation and arrest of cell differentiation. This study may shed light on the molecular function of CIP2A in myeloid leukemogenesis.

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The results indicate that exercise training can prevent the attenuation of anesthetic cardioprotection in obesity. Preventing the attenuation of this strategy may be associated with reduced basal oxidative stress and normalized ROS-mediated AMPK pathway, but the causal relationship remains to be determined.

Background: The aim of this study was to investigate the effect of pyrotinib, an irreversible pan-ErbB inhibitor, and capecitabine in the treatment of human epidermal growth factor receptor 2 (HER2)-positive breast cancer (BC) patients with untreated brain metastases.

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