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Background: The clinical significance of protein tyrosine phosphatase nonreceptor type 11 mutation (PTPN11 mut ) in acute myeloid leukemia (AML) is underestimated., Methods: We collected the data of AML patients with mutated PTPN11 and wild-type PTPN11 (PTPN11 wt ) treated at our hospital and analyzed their clinical characteristics and prognosis., Results: Fifty-nine PTPN11 mut and 124 PTPN11 wt AML patients were included. PTPN11 mut was more common in myelomonocytic and monocytic leukemia, and was more likely to co-mutate with KRAS, KMT2C, NRAS, U2AF1, NOTCH1, IKZF1, and USH2A mutations than PTPN11 wt . The overall survival for AML patients with PTPN11 mut was significantly shorter than that for those with PTPN11 wt (p = 0.03). The negative impact of PTPN11 mut on overall survival was pronounced in the "favorable" and "intermediate" groups of ELN2017 risk stratification, as well as in the wild-type NPM1 group (p = 0.01, p = 0.01, and p = 0.04)., Conclusion: PTPN11 mut is associated with distinct clinical and molecular characteristics, and adverse prognosis in AML patients., (© 2023 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.)

CD7 has been found to be a promising chimeric antigen receptor (CAR) T cell target in several clinical trials. However, its expression on normal T cells poses additional challenges in CD7-directed CAR therapy, such as complete fratricide, contamination with malignant cells, and immune suppression due to T-cell aplasia. By taking advantage of evolved affinity between ligand and receptor, we constructed a CD7-directed CAR with the extracellular domain of SECTM1, a natural ligand of CD7, as the recognition domain. SECTM1 CAR T cells killed the majority of T cells with high CD7 expression in vitro. However, SECTM1 CAR T cells with low or negative CD7 expression survived, expanded, and showed strong cytotoxicity to CD7+ malignant cell lines and primary leukemic blasts from patients with T-cell acute lymphoblastic leukemia and acute myelogenous leukemia in vitro. It also exhibited efficacy in inhibiting xenograft tumor growth in vivo. More exploration is needed for clinical efficacy potential to patients with CD7+ malignancies., (© 2023 by The American Society of Hematology. Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0), permitting only noncommercial, nonderivative use with attribution. All other rights reserved.)

Acrolein is a highly toxic unsaturated aldehyde which is abundant in many circumstances. People exposed to acrolein may have significant clinical relevance in human cardiotoxicity situations. Paeoniflorin (PEF) is a bioactive glucoside isolated from the roots of Paeonia lactiflora Pall. It is reported that PEF performs a beneficial role in cardiovascular system. The aim of the current research was to evaluate the potential protective effect of PEF against acrolein-induced apoptotic damage in H9c2 cardiomyocytes. This study revealed that PEF exerted a protective effect on acrolein-induced cardiomyocyte apoptosis. Furthermore, treatment with acrolein could markedly increase the levels of reactive oxygen species (ROS) and expression of cleavage of caspase-9 and caspase-3 in H9c2 cardiomyocytes, which were significantly reversed by co-treatment with PEF (100uM). These results demonstrated that PEF protects H9c2 cardiomyocytes against acrolein-induced cardiomyocyte injury via decreasing ROS production and down regulating caspases cascade reaction, indicating that PEF is a potential therapeutic agent for cardiac toxic environmental pollutant injury.