Cancer Immunotherapy

Immune Surveillance, Cellular Senescence, and Age-Related Diseases: Mechanisms and Interventions

Cellular senescence is a stress-responsive state defined chiefly by durable proliferation arrest and frequently accompanied by a senescence-associated secretory phenotype (SASP).

Extracellular Vesicles: Pathogenesis and Therapy

Extracellular vesicles (EVs) are membrane-enclosed particles released by cells and include endosome-derived exosomes and plasma-membrane-derived microvesicles; they transport proteins, lipids, RNA, and other cellular constituents between cells.

Amino Acid Metabolism Reprogramming Mediates Aging and Tumorigenesis

Amino acid metabolism reprogramming describes coordinated changes in amino-acid uptake, synthesis, breakdown, transport, and nutrient sensing that alter cellular growth, stress responses, and metabolic homeostasis.

Nanomaterials Modulate Cellular Senescence to Enhance Tumor Therapy

Cellular senescence is a stable or terminal cell-cycle arrest triggered by stress and accompanied by extensive phenotypic changes, including a bioactive, frequently pro-inflammatory senescence-associated secretory phenotype (SASP).

Immune Surveillance Evasion by Senescent Cells and Intervention Strategies

Cellular senescence is a stable cell-cycle arrest coupled to a secretory program that remodels the tissue microenvironment.

Interplay Between Aging and Cancer

Aging is a progressive loss of physiological integrity that impairs function and increases vulnerability to major human diseases, including cancer.

Regulation of the cGAS-STING Pathway by Telomerase TERT

The cGAS-STING pathway is a central cytosolic DNA-sensing system in innate immunity: cGAS binds double-stranded DNA, generates the second messenger 2′3′-cGAMP, and activates STING to induce type I interferons and other immune-modulatory genes.

Anti-Tumor Effects of a Low-Temperature Metabolic Environment

A low-temperature metabolic environment can be operationally understood as an ambient-cold state that changes whole-body energy allocation, thermogenesis, glucose use, and immune metabolism in ways that alter tumor behavior.

The Nobel Prize in Physiology or Medicine: Molecular Mechanisms, Clinical Applications, and Future Therapeutic Frontiers

Recent Nobel Prizes in Physiology or Medicine illustrate how fundamental discoveries can develop into technologies that reshape biomedical research and clinical practice.

AACR: From RAS(ON) Inhibition to Molecular Glue Degradation

The AACR Annual Meeting 2026 was held in San Diego, USA, from April 17 to 22.

Circadian Rhythm Regulation of the Tumor Microenvironment and Immunotherapy

Circadian rhythm regulation of the tumor microenvironment describes the time-dependent control of tumor and immune biology by endogenous molecular clocks.

Chronotherapy: Impact on Efficacy and Pharmacokinetics in Cancer Treatment

Cancer chronotherapy aligns anticancer treatment delivery with endogenous circadian rhythms to improve therapeutic efficacy and tolerability, based on the observation that molecular clocks influence drug pharmacokinetics, toxicity, and pharmacodynamics across the 24-hour cycle.

Time-Based Nutrition Intervention for Obesity-Related Tumor Development

Time-based nutrition intervention for obesity-related tumor development refers to dietary strategies that control when food is consumed, including time-restricted eating or feeding and intermittent fasting, with the aim of modifying metabolic and circadian processes linked to obesity and cancer.

Clock Genes and Tumor Microenvironment Regulation

Circadian clock genes regulate approximately 24-hour biological timing through a transcriptional network centered on CLOCK and BMAL1, and cancer research has increasingly linked disruption of this machinery to tumor behavior and the tumor microenvironment (TME).

cGAS-STING Pathway: Biology, Activation, And Signaling

The cGAS-STING pathway detects double-stranded DNA in inappropriate cellular locations and converts it into innate immune signaling.

MAIT Cell Biology And Cross-Disease Regulation

Mucosal-associated invariant T cells are abundant innate-like T lymphocytes that link microbial metabolism to rapid tissue immunity.

Cell-Specific Inflammatory Signaling Regulation For Precision Therapy

Inflammatory disease is produced by signaling networks that differ across cell types even when patients share a clinical diagnosis.

Inhibitory Immune Receptors And Targeted Inflammation Therapy

Inhibitory immune receptors set activation thresholds and prevent protective inflammation from becoming destructive.

Applications And Challenges Of cfDNA Fragmentomics

Cell-free DNA fragmentomics extracts biological information from the physical patterns of circulating DNA rather than relying only on nucleotide variants.

Nervous System and Immune Regulation in TME

The nervous system is now recognized as an active component of the tumor microenvironment (TME), alongside malignant, immune, vascular, and stromal cells.

Nervous System Regulation in GI Cancer

Nervous-system regulation in gastrointestinal cancer refers to reciprocal signaling among autonomic, enteric, and sensory nerves; tumor cells; stromal cells; and immune populations.

PNS-Tumor-Immune Interplay in Cancer

The peripheral nervous system-tumor-immune axis is the reciprocal network linking autonomic and sensory fibers with malignant, stromal, vascular, and immune cells.

Neural Influence on NSCLC Immunotherapy Efficacy

Neural influence on non-small cell lung cancer immunotherapy refers to the capacity of autonomic and sensory signaling to alter the tumor, stromal, vascular, and immune conditions that determine response to immune checkpoint inhibition.

Tumor Innervation: Neural Regulation of Cancer Progression and Immunity

Tumor innervation describes the entry, expansion, and functional activity of autonomic or sensory nerve fibers within the tumor microenvironment.

Nanomaterial-Based Tumor Therapy Targeting Mitochondrial Metabolism

Nanomaterial-based therapy targeting mitochondrial metabolism uses engineered carriers or reactive platforms to concentrate drugs, metals, photosensitizers, or metabolic inhibitors in tumors and then direct their action toward mitochondrial functions.

Pattern Recognition Receptors for Pathogen Detection

Pattern recognition receptors (PRRs) are germline-encoded sensors that detect conserved microbial structures and signals of cellular damage, converting recognition into innate defense and instruction of adaptive immunity.

Therapeutic Targeting of Non-Apoptotic Cell Death

Non-apoptotic regulated cell death comprises mechanistically defined programs that kill cells without relying primarily on canonical apoptotic execution.

Apoptosis Resistance in Metastatic Cancer

Apoptosis resistance is the capacity of malignant cells to avoid caspase-dependent death despite oncogenic stress, therapy, immune attack, or loss of tissue attachment.

Ammonia-Induced Death and Immunotherapy

Ammonia-induced cell death describes a recently reported metabolic vulnerability of activated effector CD8-positive T cells.

Pyroptosis, PANoptosis, and Immunity

Pyroptosis is a lytic inflammatory death program executed by gasdermin pores, whereas PANoptosis describes coordinated inflammatory death with pyroptotic, apoptotic, and necroptotic components that cannot be explained by any one pathway alone.

Epigenetics and Cell Death in Cancer Therapy

Epigenetics regulates gene activity without changing DNA sequence through DNA methylation, histone modification, chromatin remodeling, non-coding RNAs, and RNA modifications.

RCDs in Tumor Metabolism and Tumor Immunity

Metabolic context determines death susceptibility.

The Dual Role of NAD+ in Cancer Immunity

Nicotinamide adenine dinucleotide (NAD+) connects redox metabolism, energy production, DNA repair, epigenetic regulation, and immune-cell function.

Drug-Tolerant Persister Cells: Barriers to Cancer Therapy and Strategies for Elimination

Persistence is inherently treatment-dependent.

Remodeling the Tumor Dormancy Ecosystem and Targeting Tumor Recurrence

Latency can persist after treatment.

Degradation of the Glycocalyx Barrier: A Key Strategy in Tumor Immunity

This barrier is biologically dynamic.

Epigenetic Metabolic Interactions Regulate T Cell Exhaustion

T cell exhaustion is a differentiated state that develops during persistent antigen exposure in chronic infection and cancer and is characterized by diminished effector function, sustained inhibitory-receptor expression, altered metabolism, and a distinct chromatin landscape.

Chemical-assisted techniques and applications for appearance modification

'Epigenetic modification' refers to the use of chemical methods to assist in modifying observable cellular states or phenotypes by targeting epigenetic regulatory mechanisms.

Epigenetic Regulatory Targets Overcome Tumor Treatment Resistance

Tumor treatment resistance is not exclusively a genetic endpoint; it can also arise from reversible chromatin states that let a small fraction of cancer cells survive otherwise lethal therapy.

Epigenetic Mechanisms of Metalloproteinases and Interventions for Metastasis

Metalloproteinases are zinc-dependent proteases that remodel extracellular matrix and process cell-surface receptors, growth factors, cytokines, and adhesion molecules.

Epigenome Editing: Mechanistic Exploration and Disease Applications

Epigenome editing uses programmable DNA-binding systems to deposit, remove, or recruit regulatory marks at selected genomic loci without changing the underlying nucleotide sequence.

Multimodal Notch Signaling Mediates Development And Disease

Notch is an evolutionarily conserved, contact-dependent signaling system that controls cell-fate decisions, tissue patterning, stem-cell maintenance, and adult homeostasis.

Research on Circular RNA Characteristics and Diseases

Circular RNAs are covalently closed RNA molecules produced mainly by back-splicing, in which a downstream splice donor joins an upstream acceptor.

Transcriptional condensates mediate the integration of temporal signals.

Transcriptional condensates are dynamic, high-concentration assemblies of transcription factors, coactivators, RNA polymerase II, chromatin, and RNA at active regulatory loci.

Epigenetic Regulation and the Tumor Immune Microenvironment

The tumor immune microenvironment is a spatial ecosystem of malignant, immune, stromal, endothelial, and extracellular-matrix components.

Epigenetics of Neuroendocrine Neoplasms (NENs)

Neuroendocrine neoplasms comprise well-differentiated neuroendocrine tumors and poorly differentiated neuroendocrine carcinomas arising in several organs.

Epigenetics of Esophageal Cancer

Esophageal cancer includes squamous-cell carcinoma and adenocarcinoma, diseases with distinct epidemiology, precursor lesions, and molecular landscapes.

Cancer Epigenetic Plasticity and CRISPR/dCas9 Editing

Cancer epigenetic plasticity is the capacity of malignant cells to adopt reversible transcriptional states that alter differentiation, invasion, immune recognition, and drug response.

Cancer Epigenetics: From Pathophysiology to Therapeutic Strategies

Cancer epigenetics studies heritable or persistent changes in gene regulation that do not require alteration of the underlying DNA sequence.

Frontiers in Cancer Suppression: Targeting Super-Enhancer-Driven Oncogenic Transcription

Super-enhancers are extended clusters of enhancers with unusually dense occupancy by lineage-defining transcription factors, Mediator, BRD4, and active histone marks.