Ethyl acetate as an acetyl source and solvent for acetylation of alcohols by KOH.

A KOH mediated mild, efficient, convenient and gram-scalable protocol for the acetylation of alcohols with EtOAc as acetyl source and solvent. Various types of alcohols were successfully transformed into according acetylated products. Good to excellent yields were offered by primary alcohols and low to moderate yields were offered by secondary alcohols.

The role of pyroptosis and gasdermin family in tumor progression and immune microenvironment.

Pyroptosis, an inflammatory programmed cell death, distinguishes itself from apoptosis and necroptosis and has drawn increasing attention. Recent studies have revealed a correlation between the expression levels of many pyroptosis-related genes and both tumorigenesis and progression. Despite advancements in cancer treatments such as surgery, radiotherapy, chemotherapy, and immunotherapy, the persistent hallmark of cancer enables malignant cells to elude cell death and develop resistance to therapy. Recent findings indicate that pyroptosis can overcome apoptosis resistance amplify treatment-induced tumor cell death. Moreover, pyroptosis triggers antitumor immunity by releasing pro-inflammatory cytokines, augmenting macrophage phagocytosis, and activating cytotoxic T cells and natural killer cells. Additionally, it transforms "cold" tumors into "hot" tumors, thereby enhancing the antitumor effects of various treatments. Consequently, pyroptosis is intricately linked to tumor development and holds promise as an effective strategy for boosting therapeutic efficacy. As the principal executive protein of pyroptosis, the gasdermin family plays a pivotal role in influencing pyroptosis-associated outcomes in tumors and can serve as a regulatory target. This review provides a comprehensive summary of the relationship between pyroptosis and gasdermin family members, discusses their roles in tumor progression and the tumor immune microenvironment, and analyses the underlying therapeutic strategies for tumor treatment based on pyroptotic cell death.

Advances in radiotherapy and immunity in hepatocellular carcinoma.

Primary liver cancer is one of the most common malignant tumours worldwide; it caused approximately 830,000 deaths in 2020. Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer, accounting for over 80% of all cases. Various methods, including surgery, chemotherapy, radiotherapy, and radiofrequency ablation, have been widely used in the treatment of HCC. With the advancement of technology, radiotherapy has become increasingly important in the comprehensive treatment of HCC. However, due to the insufficient sensitivity of tumour cells to radiation, there are still multiple limitation in clinical application of radiotherapy. In recent years, the role of immunotherapy in cancer has been increasingly revealed, and more researchers have turned their attention to the combined application of immunotherapy and radiotherapy in the hope of achieving better treatment outcomes. This article reviews the progress on radiation therapy in HCC and the current status of its combined application with immunotherapy, and discusses the prospects and value of radioimmunotherapy in HCC.

Metabolism, metabolites, and macrophages in cancer.

Tumour-associated macrophages (TAMs) are crucial components of the tumour microenvironment and play a significant role in tumour development and drug resistance by creating an immunosuppressive microenvironment. Macrophages are essential components of both the innate and adaptive immune systems and contribute to pathogen resistance and the regulation of organism homeostasis. Macrophage function and polarization are closely linked to altered metabolism. Generally, M1 macrophages rely primarily on aerobic glycolysis, whereas M2 macrophages depend on oxidative metabolism. Metabolic studies have revealed that the metabolic signature of TAMs and metabolites in the tumour microenvironment regulate the function and polarization of TAMs. However, the precise effects of metabolic reprogramming on tumours and TAMs remain incompletely understood. In this review, we discuss the impact of metabolic pathways on macrophage function and polarization as well as potential strategies for reprogramming macrophage metabolism in cancer treatment.

Gasdermin D Plays an Oncogenic Role in Glioma and Correlates to an Immunosuppressive Microenvironment.

BACKGROUND: Understanding the molecular mechanisms driving oncogenic processes in glioma is important in order to develop efficient treatments. Recent studies have proposed gasdermin D (GSDMD) as a newly discovered pyroptosis executive protein associated with tumorigenesis. However, the precise effect of GSDMD on glioma progression remains unknown. METHODS: The expression levels of GSDMD in 931 glioma and 1157 normal control tissues were collected. A series of bioinformatic approaches and in vivo and in vitro experiments were used to investigate the roles and mechanisms of GDSMD in glioma. RESULTS: Significant upregulation of GSDMD was detected in glioma tissues compared to normal brain tissues. Patients with glioma and higher GSDMD levels had shorter overall survival, and the Cox regression analysis revealed that GSDMD was an independent risk factor. In addition, upregulation of GSDMD was associated with higher tumor mutation burden and PD-1/PD-L1 expression. Immune infiltration and single-cell analyses indicated that GSDMD was positively associated with an immunosuppressive microenvironment with more infiltrated macrophages and cancer-associated fibroblasts. Furthermore, the in vitro and in vivo experiments revealed that GSDMD knockdown inhibited glioma proliferation, migration, and growth in vivo. CONCLUSION: Our analyses revealed a relatively comprehensive understanding of the oncogenic role of GSDMD in glioma. GSDMD is a promising prognostic biomarker and a potential target for glioma treatment.

Harnessing NK cell-based immunotherapy to prevent the high-dose radiotherapy-inducing tumor survival recurrence.

Natural killer cells play crucial roles in tumor immunosurveillance and serve as first responders to recognize abnormal cells. Radiotherapy is the mainstay of cancer treatment. However, the effect of high-dose radiotherapy on NK cells remains elusive. Here, we used tumor-bearing mice in the murine colorectal cancer cell line, MC38. The function of NK cells in tumor-draining lymph nodes and tumors was explored after the mice were treated using radiotherapy with 20 Gy and/or blocking antibody αTIGIT at the indicated time. High-dose radiotherapy shaped an immunosuppressive tumor microenvironment to support tumor growth, showing a decreased anti-tumor immunity phenotype in which effector T cells were reduced significantly. Furthermore, the production of functional cytokines and markers in NK cells, including CD107a, granzyme B, and IFN-γ, also remarkably decreased after radiotherapy, while the inhibitory receptor TIGIT was significantly upregulated by FACS analysis. The effect of radiotherapy was significantly elevated after treatment with the combination of radiotherapy and TIGIT inhibition. Moreover, this combination significantly decreased tumor recurrence. Our findings reported that local single high-dose radiotherapy shaped the immunosuppressive microenvironment and inhibited the function of NK cells. Our study revealed compelling evidence suggesting that the enhancement of NK cell function through TIGIT targeting is an effective strategy to mitigate immune suppression caused by high-dose radiotherapy, thereby promoting the inhibition of tumor recurrence.