DNA damage-inducing endogenous and exogenous factors and research progress.

The substances that cause abnormal DNA structures are known as DNA damage-inducing factors, and their resulting DNA damage has been extensively studied and proven to be closely related to cancer, neurodegenerative diseases, and aging. Prolonged exposure to DNA damage-inducing factors can lead to a variety of difficult-to-treat diseases, yet these factors have not been well summarized. It is crucial to use a combination of environmental science and life science to gain a deep understanding of the environmental sources and biological consequences of DNA damage-inducing factors for mechanistic research and prevention of diseases such as cancer.

Quantifying the Level of 8-oxo-dG Using ELISA Assay to Evaluate Oxidative DNA Damage in MCF-7 Cells.

8-Oxo-7,8-dihydro-2'-deoxyguanosine (8-oxo-dG) base is the predominant form of commonly observed DNA oxidative damage. DNA impairment profoundly impacts gene expression and serves as a pivotal factor in stimulating neurodegenerative disorders, cancer, and aging. Therefore, precise quantification of 8-oxoG has clinical significance in the investigation of DNA damage detection methodologies.

Deletion of TECRL promotes skeletal muscle repair by up-regulating EGR2.

Myogenic regeneration relies on the proliferation and differentiation of satellite cells. TECRL (trans-2,3-enoyl-CoA reductase like) is an endoplasmic reticulum protein only expressed in cardiac and skeletal muscle. However, its role in myogenesis remains unknown.

Investigations of the prognostic value of RUNX1 mutation in acute myeloid leukemia patients: Data from a real-world study.

RUNX1 is one of the recurrent mutated genes in newly diagnosed acute myeloid leukemia (AML). Although historically recognized as a provisional distinct entity, the AML subtype with RUNX1 mutations (AML-RUNX1) was eliminated from the 2022 WHO classification system. To gain more insight into the characteristics of AML-RUNX1, we retrospectively analyzed 1065 newly diagnosed adult AML patients from the First Affiliated Hospital of Soochow University between January 2017 and December 2021.

Targeting PRMT9-mediated arginine methylation suppresses cancer stem cell maintenance and elicits cGAS-mediated anticancer immunity.

Current anticancer therapies cannot eliminate all cancer cells, which hijack normal arginine methylation as a means to promote their maintenance via unknown mechanisms. Here we show that targeting protein arginine N-methyltransferase 9 (PRMT9), whose activities are elevated in blasts and leukemia stem cells (LSCs) from patients with acute myeloid leukemia (AML), eliminates disease via cancer-intrinsic mechanisms and cancer-extrinsic type I interferon (IFN)-associated immunity. PRMT9 ablation in AML cells decreased the arginine methylation of regulators of RNA translation and the DNA damage response, suppressing cell survival.

Types of DNA damage and research progress.

DNA damage is a modification in the structure of DNA under the influence of endogenous or exogenous factors. DNA damage can cause different types of diseases and is closely related to genetic mutations, cancer, and aging. The cause of the corresponding reaction process is essential for the study of related cancers and other genetically related diseases.

Zyxin inhibits the epithelial-mesenchymal transition process in gastric cancer by upregulating SIRT1.

Tumor development relies on the stemness of cancer stem cells, which is regulated by environmental cues. Previous studies have shown that zyxin can inhibit the expression of genes for embryonic stem cell status. In the present study, the expression levels of zyxin protein in cancer tissues and adjacent noncancerous tissues from 73 gastric cancer patients with different clinical stages were analyzed by Western blot.

Effects of Aflatoxin B on growth performance, carcass traits, organ index, blood biochemistry and oxidative status in Chinese yellow chickens.

In this study, the effects of different levels of aflatoxin B (AFB) on the growth performance, carcass traits, organ index, blood biochemistry, and antioxidant capacity of yellow-feathered broilers were investigated to provide a reference for the application of AFB-containing feed ingredients. In this test, yellow-feathered broilers were chosen as the research objects and divided into five treatment groups, with seven replicates in each group and 75 broilers in each replicate. The AFB concentration in the diets of groups 1 to 5 were 1.

Inhibition of FEN1 promotes DNA damage and enhances chemotherapeutic response in prostate cancer cells.

Prostate cancer (PCa) refers to epithelial malignancies occurring in prostate and is the most commonly diagnosed cancer among men. Flap structure-specific endonuclease 1 (FEN1) is one of the major base excise repair enzymes and is abnormally expressed in a variety of cancers, which contributes to cancer progression. Targeting FEN1 serves as a potent strategy for cancer therapy.

The roles of TPL in hematological malignancies.

Triptolide (TPL) is a diterpenoid isolated from the traditional Chinese medicine Tripterygium wilfordii. It has powerful antitumor, immunosuppressive and anti-inflammatory properties. Recent studies have shown that TPL can induce apoptosis of hematological tumor cells, inhibit their proliferation and survival, promote autophagy and ferroptosis, and enhance the efficacy of traditional chemotherapy and targeted therapies.

High FAAP24 expression reveals poor prognosis and an immunosuppressive microenvironment shaping in AML.

Background: As a core member of the FA complex, in the Fanconi anemia pathway, FAAP24 plays an important role in DNA damage repair. However, the association between FAAP24 and patient prognosis in AML and immune infiltration remains unclear. The purpose of this study was to explore its expression characteristics, immune infiltration pattern, prognostic value and biological function using TCGA-AML and to verify it in the Beat AML cohort.

Mutation spectrum of FLT3 and significance of non-canonical FLT3 mutations in haematological malignancy.

Fms-like tyrosine kinase 3 (FLT3) is frequently mutated in haematological malignancies. Although canonical FLT3 mutations including internal tandem duplications (ITDs) and tyrosine kinase domains (TKDs) have been extensively studied, little is known about the clinical significance of non-canonical FLT3 mutations. Here, we first profiled the spectrum of FLT3 mutations in 869 consecutively newly diagnosed acute myeloid leukaemia (AML), myelodysplastic syndrome and acute lymphoblastic leukaemia patients.

Case Report: Blinatumomab therapy for the treatment of B-cell acute lymphoblastic leukemia patients with central nervous system infiltration.

The treatment of B-cell acute lymphoblastic leukemia (B-ALL) with central nervous system (CNS) involvement poses a significant clinical challenge because most chemotherapeutic agents exhibit weak permeability to the blood-brain barrier (BBB). In addition, current anti-CNS leukemia treatments often bring short or long-term complications. Immunotherapy including chimeric antigen T-cell therapy and bispecific antibody have shown profound treatment responses in relapsed/refractory B-ALL.

Loss of CRY2 promotes regenerative myogenesis by enhancing PAX7 expression and satellite cell proliferation.

The regenerative capacity of skeletal muscle is dependent on satellite cells. The circadian clock regulates the maintenance and function of satellite cells. Cryptochrome 2 (CRY2) is a critical component of the circadian clock, and its role in skeletal muscle regeneration remains controversial.

Comprehensive analysis of ERCC3 prognosis value and ceRNA network in AML.

Background: Acute myeloid leukemia (AML) is a hematological malignancy with high molecular and clinical heterogeneity, and is the most common type of acute leukemia in adults. Due to limited treatment options, AML is prone to relapse and has a poor prognosis. Excision repair cross-complementing 3 (ERCC3) is an important member of nucleotide excision repair (NER) that is overexpressed in types of solid cancers and potentially regarded as a prognostic factor.

Developments and challenges of FLT3 inhibitors in acute myeloid leukemia.

FLT3 mutations are one of the most common genetic alterations in acute myeloid leukemia (AML) and are identified in approximately one-third of newly diagnosed patients. Aberrant FLT3 receptor signaling has important implications for the biology and clinical management of AML. In recent years, targeting FLT3 has been a part of every course of treatment in FLT3-ITD/TKD-mutated AML and contributes to substantially prolonged survival.

Development and Validation of Prognostic Model for Lung Adenocarcinoma Patients Based on m6A Methylation Related Transcriptomics.

Existing studies suggest that mA methylation is closely related to the prognosis of cancer. We developed three prognostic models based on mA-related transcriptomics in lung adenocarcinoma patients and performed external validations. The TCGA-LUAD cohort served as the derivation cohort and six GEO data sets as external validation cohorts.

Integration of immune and hypoxia gene signatures improves the prediction of radiosensitivity in breast cancer.

Immunity and hypoxia are two important factors that affect the response of cancer patients to radiotherapy. At the same time, considering the limited predictive value of a single predictive model and the uncertainty of grouping patients near the cutoff value, we developed and validated a combined model based on immune- and hypoxia-related gene expression profiles to predict the radiosensitivity of breast cancer patients. This study was based on breast cancer data from The Cancer Genome Atlas (TCGA).

A Radiosensitivity Prediction Model Developed Based on Weighted Correlation Network Analysis of Hypoxia Genes for Lower-Grade Glioma.

Background And Purpose: Hypoxia is one of the basic characteristics of the physical microenvironment of solid tumors. The relationship between radiotherapy and hypoxia is complex. However, there is no radiosensitivity prediction model based on hypoxia genes.

Rapid and Efficient Response to Gilteritinib and Venetoclax-Based Therapy in Two AML Patients with FLT3-ITD Mutation Unresponsive to Venetoclax Plus Azacitidine.

The presence of FLT3-ITD mutation is associated with relapse and poor survival in AML patients. Venetoclax combined with hypomethylating agents (VEN+HMA) was approved for the frontline treatment of elderly or unfit AML patients, which leads to noteworthy impacts on AML management. The combination therapy is associated with encouraging efficacy in FLT3-mutated AML among both newly diagnosed unfit and relapsed/refractory patients.

An 11-Gene Signature Based on Treatment Responsiveness Predicts Radiation Therapy Survival Benefit Among Breast Cancer Patients.

Purpose: We developed a strategy of building prognosis gene signature based on clinical treatment responsiveness to predict radiotherapy survival benefit in breast cancer patients.

Methods And Materials: Analyzed data came from the public database. PFS was used as an indicator of clinical treatment responsiveness.

A Combined Histone Deacetylases Targeting Strategy to Overcome Venetoclax Plus Azacitidine Regimen Resistance in Acute Myeloid Leukaemia: Three Case Reports.

The management of patients with relapsed or refractory (R/R) acute myeloid leukaemia (AML) remains a challenge with few reliably effective treatments. Chidamide, a new selective HDAC inhibitor, has demonstrated some effectiveness in AML patients. Herein, we reported three patients with R/R AML who were unresponsive to venetoclax plus azacitidine (VA) but were successfully treated with VA when chidamide was added to the regimen.