miRNAs play multiple roles in the tumour microenvironment of pancreatic cancer, including angiogenesis, interactions with cancer-associated fibroblasts, the immune microenvironment, exosome communication, the neural microenvironment and metabolic reprogramming.

• Malignant T cells in T-cell lymphoblastic lymphoma (T-LBL) are predominantly blocked in double negative (DN) and double positive (DP) stages.
• Block bias induces an immunosuppressive tumour microenvironment (TME) and mediastinal preference.
• Block bias upregulates UHRF1 leading to hypermethylation of tumour suppressor genes.
• Demethylation therapy exhibits potential in the treatment of T-LBL.

1. FTO regulates the translation of IGFBP3 by demethylating m6A sites in the 3′-untranslated region of IGFBP3 mRNA.
2. Binding of the m6A reader protein IMP3 to 3′UTR m6A sites in IGFBP3 mRNA promoted its localisation and sequestration in cellular organelles known as to P-bodies, thereby suppressing IGFBP3 mRNA translation.
3. IGFBP3 regulates activation of the AKT signalling pathway, and that FTO-mediated regulation of IGFBP3 influences LUAD malignant behaviours.

1. Combination of Kras activation and Arid1a loss induces pancreatic cancer in mice.

2. ARID1A deficiency enhances immune cell infiltration and lipid metabolism in pancreatic cancer.

3. Fatty acid synthase (FASN) is a druggable target in ARID1A-deficient pancreatic cancer.

1. The interaction between m6A and APA is mediated by the m6A regulator IGF2BP2 and the APA factor CPSF6

2. The transcripts harbouring m6A modification tend to use the proximal polyadenylation signal (PAS) in ovarian cancer (OC)

3. PUM2 promotes the malignant progression of OC through its m6A methylation and APA processing

1. MiR-501-3p and miR-502-3p expression is elevated in AD CSF exosomes, AD serum exosomes, AD B-lymphocytes and Aβ- and Tau-treated cells.

2. MiR-501-3p and miR-502-3p are correlated with amyloid plaque and NFT tangle density in specific brain regions.

3. MiR-501-3p and miR-502-3p are highly expressed in neurons and astrocytes, suggesting that these cells are the source of miRNA secretion.

4. MiR-501-3p and miR-502-3p could be a promising biomarker panel for AD.

CD70 is aberrantly overexpressed in diverse tumours with limited normal tissue expression, making it a compelling diagnostic and therapeutic target. Immuno-PET/CT facilitates tumour detection, staging, and treatment monitoring. Multiple CD70-targeted therapies are under early evaluation. Rational combination strategies are emerging to enhance antitumor efficacy.

Spatial omics technologies reveal unprecedented insights into cancer therapy resistance (CTR) by resolving spatial heterogeneity of tumour and microenvironment. This review highlights cutting-edge spatial omics and computational technologies, showcasing their transformative potential in deciphering CTR mechanisms and uncovering novel diagnostic and therapeutic opportunities.

Cancer stem cells (CSCs) drive tumor progression through their dynamic self-renewal capacity, epigenetic plasticity, and drug resistance. These cells interact bi-directionally with the tumor ecosystem to promote immunosuppressive reprogramming and metastatic spread. We systematically evaluated current targeting of CSC-specific markers, signaling pathways and tumor microenvironment interactions, and clinical therapeutic strategies.

Osteoblast senescence, a key driver of age-related osteoporosis, disrupts bone formation and homeostasis through multiple pathways. Addressing this senescence to combat osteoporosis is challenging but holds promise.

IL-11 drives tumour progression and is linked to poor survival in lung adenocarcinoma patients, as well as an immunosuppressive tumour microenvironment. Antibody targeting of the IL-11 receptor (IL-11RA) shows significant anti-tumour effects in a patient-derived xenograft model highlighting IL-11 as a compelling therapeutic target.

1. Tumour cells evade immune surveillance by downregulating MHC expression through transcriptional repression, lysosomal degradation and post-translational modifications.

2. Pharmacological agents interventing epigenetic and metabolic can upregulate MHC expression and improve T cell activation.

3. Combination strategies potentiate immunotherapy efficacy by reinvigorating tumour immunogenicity.

• Itaconate alleviates NEC by reprogramming M1 macrophage metabolism.
• ACOD1 deficiency exacerbates NEC severity.
• 4OI maintains intestinal barrier integrity.
• 4OI rescues NEC by regulating macrophage mitochondrial activity.

Mitochondrial disease triggers opposite responses in different muscles. Mitochondrial integrated stress response (ISRmt) and aerobic glycolysis characterize large muscles. Eye muscles show no ISRmt but activate PDK4—inhibitor of glucose oxidation—thereby upregulating beta-oxidation, which is non-optimal in mitochondrial disease and can explain eye muscle atrophy in mitochondrial disease.

YOD1 binds to PKM2 and reduces its ubiquitination level by removing the K63 ubiquitin chain of PKM2, thereby increasing the tetramer level and reducing the dimer level of PKM2. It then inhibited dimerized PKM2 entry into the nucleus and activated the Nrf2 signaling pathway, thus promoting oxidative stress.

1. HGSC intra-tumour heterogeneity is predominantly driven by stroma, as revealed by spatial proteomic compartmentalization (tumour/stroma).

2. Spatial proteomics expands the therapeutic target database, enabling prediction of platinum-based chemotherapy response.

3. Chemo-resistant patients exhibit pre-treatment metabolic activation rather than proliferative signatures.

4. TFRC (iron transport) and PDLIM3 (cytoskeletal remodelling) are spatially validated as chemo-response biomarkers.