Chronic stress, gut microbiota, and immunity: interconnections and implications for health.

Psychological stress influences the hypothalamic-pituitary-adrenal (HPA) and the sympathetic-adrenal -medullary (SAM) axes which directly impact the immune system. Stress not only affects hematopoietic stem cell activity but also increases the circulating levels of inflammatory cells, thereby potentially exacerbating pathogenic conditions. Moreover, stress affects hormone release, inflammation, and autonomic changes, which can modify the composition of the gut microbiota and indirectly alter the immune system.

Genomic profile helps to predict the clonal evolution and outcome of BCR-ABL-negative myeloproliferative neoplasms.

Classical BCR-ABL-negative myeloproliferative neoplasms (MPNs) are a clonal expansion of myeloid precursors caused by somatic stem cells. Although driver mutations were observed in most MPN patients, the potential clonal disorder remains unclear. We analyzed a total of 1004 newly diagnosed MPN patients and next-generation sequencing was performed on the genomic DNA.

Inhibition of tumor-intrinsic NAT10 enhances antitumor immunity by triggering type I interferon response via MYC/CDK2/DNMT1 pathway.

Posttranscriptional modifications are involved in cancer progression. However, the function and regulatory mechanism of mRNA acetylation modification remains largely unknown. Here, we discover an unexpected role of N4-acetylcytidine (ac4C) RNA acetyltransferase NAT10 in reshaping the tumor immune microenvironment.

A novel LncRNA risk model for disulfidptosis-related prognosis prediction and response to chemotherapy in acute myeloid leukemia.

Acute myeloid leukemia (AML), the most prevalent acute leukemia in adults, is characterized by its heterogeneity, which contributes to a poor prognosis and high recurrence rate. Recently, a unique form of cell death, called disulfidptosis, has been identified, which could transforming our understanding of and strategy for cancer treatment. Consequently, further inquiry is necessary to explore the possible link between disulfidptosis and AML.

Immune-related genetic single-nucleotide polymorphisms contribute to prognosis and response to chemotherapy in patients with acute lymphoblastic leukemia.

The immune system is essential for immuno-surveillance and the generation of anti-tumor immunity. However, the role of immune-related single-nucleotide polymorphisms (SNPs) in the susceptibility and progression of acute lymphoblastic leukemia (ALL) is currently unknown. Here, we selected and analyzed 28 immune-related SNPs in 201 ALL patients and 228 healthy controls.

FpCDP1 From Fusarium pseudograminearum Is Recognized as a Novel Pathogen-Associated Molecular Pattern That Induces Plant Immunity.

Fusarium crown rot, caused by Fusarium pseudograminearum (F. pseudograminearum), poses a significant threat to wheat production in China. Growing evidence suggests that Fusarium secretes a large number of effectors into host, but the biological function of these effectors remains poorly understood.

Exosomal circ_0006896 promotes AML progression via interaction with HDAC1 and restriction of antitumor immunity.

Background: Drug resistance and immune escape continue to contribute to poor prognosis in AML. Increasing evidence suggests that exosomes play a crucial role in AML immune microenvironment.

Methods: Sanger sequencing, RNase R and fluorescence in situ hybridization were performed to confirm the existence of circ_0006896.

Genetic variations in DNA excision repair pathway contribute to the chemosensitivity and prognosis of acute myeloid leukemia.

Acute myeloid leukemia (AML) is a hematologic malignancy with a high recurrence rate and poor long-term prognosis. DNA excision repair systems, such as base excision repair (BER) and nucleotide excision repair (NER), play a major role in maintaining genomic stability and integrity. Further intensive investigations are necessary to uncover additional AML prognosis loci.

circFAM193B interaction with PRMT6 regulates AML leukemia stem cells chemoresistance through altering the oxidative metabolism and lipid peroxidation.

Most forms of chemotherapy for acute myeloid leukemia (AML) are often ineffective in eliminating leukemic stem cells (LSCs), as their underlying mechanisms remain unclear. Here, we have identified circFAM193B, which regulates the redox biology of LSCs and is associated with unfavorable outcomes in AML patients. In vitro and in vivo assays suggested that circFAM193B significantly inhibits LSCs chemotherapy resistance and AML progression.

Analysis of gene mutation characteristics and its correlation with prognosis in patients with myelodysplastic syndromes.

Gene mutations are a pivotal component of the pathogenesis of MDS, and they hold profound prognostic significance for predicting treatment responses and survival outcomes. However, reports about mutation patterns in Chinese MDS patients are limited. In this study, we analyzed the genetic mutation of 23 genes in 231 patients with MDS using next-generation sequencing (NGS) technology, and explored the characteristics of gene mutations in MDS patients and their associations with clinical outcomes, survival, and transformation outcomes.

Propionate promotes ferroptosis and apoptosis through mitophagy and ACSL4-mediated ferroptosis elicits anti-leukemia immunity.

Short-chain fatty acids (SCFAs), particularly propionate and butyrate, have been reported in many cancers. However, the relationship between propionate and acute myeloid leukemia (AML) remains unclear. Additionally, Acyl-CoA synthetase long chain family member 4 (ACSL4) has been reported to regulate immunity in solid tumors, but there are still many gaps to be filled in AML.

Hematopoietic stem cells suppress proliferation and enhance differentiation of leukemia cells through regulating apoptotic and inflammatory genes.

Purpose: Stem cells are known to play an important role in tumor treatment and many of them have shown tumor-suppressing ability in different cancers; however, whether hematopoietic stem cells (HSCs) have growth-inhibiting effects on leukemia cells has not been fully evaluated. Herein, we aimed to demonstrate the growth-restraining function of HSCs in acute leukemia treatment.

Methods: Cell fusion experiment was conducted by PEG-1500.

Mitochondrial transfer in hematological malignancies.

Mitochondria are energy-generated organelles and take an important part in biological metabolism. Mitochondria could be transferred between cells, which serves as a new intercellular communication. Mitochondrial transfer improves mitochondrial defects, restores the biological functions of recipient cells, and maintains the high metabolic requirements of tumor cells as well as drug resistance.

Clinical and prognostic profile of SRSF2 and related spliceosome mutations in patients with acute myeloid leukemia.

Background: Mutations in splicing factor (SF) genes are frequently detected in myelodysplastic syndrome, but their clinical and prognostic relevance in acute myeloid leukemia (AML) have rarely been reported.

Methods: A total of 368 newly diagnosed non-M3 AML patients were included in this study. Next generation sequencing including four SF genes was performed on the genomicDNA.

The genetic polymorphisms of immune-related genes contribute to the susceptibility and survival of lymphoma.

Background: Though immunological abnormalities have been proven involved in the pathogenesis of lymphoma, the underlying mechanism remains unclear.

Methods: We investigated 25 single nucleotide polymorphisms (SNPs) of 21 immune-related genes and explored their roles in lymphoma. The genotyping assay of the selected SNPs was used by the Massarray platform.

EIF4A3-induced Circ_0001187 facilitates AML suppression through promoting ubiquitin-proteasomal degradation of METTL3 and decreasing m6A modification level mediated by miR-499a-5p/RNF113A pathway.

Aberrant expression of circRNAs has been proven to play a crucial role in the progression of acute myeloid leukemia (AML); however, its regulatory mechanism remains unclear. Herein, we identified a novel circRNA, Circ_0001187, which is downregulated in AML patients, and its low level contributes to a poor prognosis. We further validated their expression in large-scale samples and found that only the expression of Circ_0001187 was significantly decreased in newly diagnosed (ND) AML patients and increased in patients with hematological complete remission (HCR) compared with controls.

Chenodeoxycholic acid suppresses AML progression through promoting lipid peroxidation via ROS/p38 MAPK/DGAT1 pathway and inhibiting M2 macrophage polarization.

Purpose: Bile acids are steroid synthesized in liver, which are essential for fat emulsification, cholesterol excretion and gut microbial homeostasis. However, the role of bile acids in leukemia progression remains unclear. We aim at exploring the effects and mechanisms of chenodeoxycholic acid (CDCA), a type of bile acids, on acute myeloid leukemia (AML) progression.

[Molecular regulatory mechanisms of hypoxia-inducible factor and interventional effect of Chinese herbal medicine].

Hypoxia-inducible factors(HIFs)are the key transcription factors that sense and regulate cellular oxygen concentration in vivo. HIF-1 is composed of 2 subunits,α and β,in which,the molecular regulatory mechanism of HIF-1α involves the main processes of its degradation and activation. The degradation of HIF-1α is regulated by oxygen-dependent pathways,including "von hippel-lindau protein(pVHL)-dependent pathway" and "pVHL-independent pathway".

Antiproliferative and Immunoregulatory Effects of Azelaic Acid Against Acute Myeloid Leukemia the Activation of Notch Signaling Pathway.

Acute myeloid leukemia (AML) is a common type of hematological malignancy that can progress rapidly. AML has a poor prognosis and a high incidence of relapse due to therapeutic resistance. Azelaic acid (AZA), a small molecular compound is known to exhibit antitumor effect on various tumor cells.