Colorectal cancer (CRC) remains a major contributor to global cancer mortality, ranking second worldwide for cancer-related deaths in 2022, and is characterized by marked heterogeneity in prognosis and therapeutic response. We sought to construct a machine-learning prognostic model based on a complement-related risk signature (CRRS) and to situate this signature within the CRC immune microenvironment.

Gastric Cancer (GC) is a highly prevalent and poorly prognostic gastrointestinal malignancy with low overall treatment efficacy worldwide. Early diagnostic markers and potential therapeutic targets for GC treatment are urgently needed. UFMylation, a novel ubiquitin-like modification is indispensable for numerous fundamental cellular processes. Deficiency in this modification is reported to be associated with several human diseases including cancer. Accumulating evidence suggests that the expression of the key UFMylation components is closely associated with GC cell proliferation, invasion, metastasis, and chemotherapy resistance. Recent clinical studies have further highlighted the prognostic value and therapeutic potential of UFMylation in the clinical management of GC. However, the precise molecular mechanisms through which UFMylation contributes to GC remain largely unclear. This review aims to summarize recent findings on the functional roles of UFMylation in diverse cellular processes, such as endoplasmic reticulum (ER) homeostasis, DNA damage response (DDR), protein translation, and quality control pathways, discuss potential underlying mechanisms in GC development and progression, and to explore potential therapeutic implications targeting the UFMylation pathway in GC.

Breast cancer is characterized by significant metabolic dysregulation, in which altered enzyme activity plays a central role. Malate dehydrogenase 2 (MDH2), a key enzyme in the tricarboxylic acid cycle, has been implicated in several malignancies, but its role in breast cancer tumorigenesis and progression remains unclear. We aimed to elucidate the oncogenic role of MDH2 in breast cancer and to evaluate its potential as a diagnostic, therapeutic, and prognostic biomarker.

Alisol A is a natural compound isolated from , known for its diverse pharmacological activities, including anticancer and neuroprotective effects. This study aimed to explore the anticancer effects of Alisol A on oral cancer cells and elucidate its underlying mechanisms.

Despite the fact that prostate cancer is one of the most common tumors in men, this study intends to evaluate the predictive significance of immune and metabolic genes in prostate cancer using multi-omics data and experimental validation.

Glioblastoma (GBM) remains the most aggressive primary brain tumour in adults, marked by pronounced cellular heterogeneity, diffuse infiltration, and resistance to conventional treatment. In recent years, transcriptomic profiling has provided valuable insights into the molecular mechanisms that govern the progression of glioblastoma. This aims to synthesise the current literature on dysregulated gene expression in GBM, focusing on gene signatures associated with stemness, immune modulation, extracellular matrix remodelling, metabolic adaptation, and therapeutic resistance.

The tumor microenvironment plays a pivotal role in prostate cancer progression and may differ across metastatic sites. This study aimed to evaluate and compare the primary and metastatic prostate adenocarcinoma tumor microenvironment.

Monitoring of Cancer Antigen 125 (CA125) during ovarian cancer (OC) maintenance treatment with poly(ADP-ribose) polymerase inhibitors (PARPis) may be insufficient when using Gynecologic Cancer Intergroup (GCIG) biochemical progression criteria. This study aimed to evaluate the usefulness of CA125 monitoring in detecting OC recurrence during PARPis maintenance treatment.

[This retracts the article DOI: 10.3727/096504016X14685034103752.].

Hepatocellular carcinoma (HCC) is characterized by its highly invasive and metastatic potential, as well as a propensity for recurrence, contributing to treatment failure and increased mortality. Under physiological conditions, the liver maintains a balance in lipid biosynthesis, degradation, storage, and transport. HCC exhibits dysregulated lipid metabolism, driving tumor progression and therapeutic resistance. This review aims to elucidate the roles of fatty acid, sphingolipid, and cholesterol metabolism in HCC pathogenesis and explore emerging therapeutic strategies targeting these pathways. Key findings demonstrate that upregulated enzymes like fatty acid synthase (FASN), acetyl-CoA carboxylase (ACC), enhance lipogenesis and β-oxidation, and promote HCC proliferation, invasion, and apoptosis evasion. Sphingolipids exert dual functions: ceramides suppress tumors, while sphingosine-1-phosphate (S1P) drives oncogenic signaling. Aberrant cholesterol metabolism, mediated by HMG-CoA reductase (HMGCR), liver X receptor α (LXRα), and sterol regulatory element-binding protein 1 (SREBP1), contributes to immunosuppression and drug resistance. Notably, inducing ferroptosis by disrupting lipid homeostasis represents a promising approach. Pharmacological inhibition of key nodes-such as FASN (Orlistat, TVB-3664), sphingomyelin synthase (D609), or cholesterol synthesis (statins, Genkwadaphnin)-synergizes with sorafenib/lenvatinib and overcomes resistance. We conclude that targeting lipid metabolic reprogramming, alone or combined with conventional therapies, offers significant potential for novel HCC treatment strategies. Future efforts should focus on overcoming metabolic plasticity and optimizing combinatorial regimens.

KIT proto-oncogene, receptor tyrosine kinase (KIT, CD117) and platelet-derived growth factor-alpha (PDGFRA) are key drivers of gastrointestinal stromal tumors (GIST), but resistance to targeted therapy often arises from tumor protein p53 (p53) alterations and loss of cell cycle control. However, the role of p53 status in GIST therapeutic potential has rarely been studied, so this study aimed to employ both wild-type and mutant p53 GIST models to investigate how p53 dysfunction influences the efficacy of p53 pathway-targeted therapies.

[This retracts the article DOI: 10.3727/096504018X15251282086836.].

This review aims to explore the development, challenges, and future directions of UCAR cell therapy as a scalable alternative to autologous CAR-T for cancer treatment. Consequently, limitations of autologous CAR-T, including long production, variable quality, and cost, drive off-the-shelf UCAR development to standardize manufacturing and improve access. Current UCAR-T cell strategies focus on mitigating the risks of graft-vs.-host disease and host-vs.-graft rejection through advanced gene editing technologies, including clustered regularly interspaced short palindromic repeat-associated system Cas9-mediated knockout of the T cell receptor, human leukocyte antigen, and cluster of differentiation 52 (CD52. Beyond conventional T cells, cell types such as double-negative T cells, γδT cells, and virus-specific T cells are being engineered with CARs to improve tumor targeting and minimize off-tumor toxicity. UCAR-T therapy is frequently used for hematologic malignancies, including acute lymphoblastic leukemia, non-Hodgkin lymphoma, and multiple myeloma, with efficacy and safety supported by numerous clinical studies. Although trials for solid tumors (e.g., CYAD-101, CTX130) show modest responses, challenges such as tumor heterogeneity and T cell exhaustion remain. Future research should focus on optimizing gene editing precision, integrating combination therapies, and advancing scalable manufacturing platforms. With expanded targets and cell types, UCAR therapies show promise for both hematologic and solid tumors, reshaping cancer treatment and patient outcomes.

Chimeric antigen receptor T (CAR-T) cell therapies have demonstrated significant clinical efficacy in hematological malignancies. However, their application to solid tumors remains substantially limited by multiple challenges, including the risk of off-target effects. Hence, optimizing CAR-T cells for stronger antigen binding is essential.

[This retracts the article DOI: 10.3727/096504016X14826089198805.].

Pancreatic cancer (PC) is an extremely aggressive cancer of the digestive system with insidious onset and the lack of effective biomarkers, resulting in late-stage diagnosis and poor prognosis. Exosomal non-coding RNAs (ncRNAs) are key mediators of intercellular communication that drive PC initiation and advancement. By modulating gene expression, they impact tumor microenvironment (TME) remodeling, proliferation, migration, apoptosis, and immune evasion. Critically, exosomal ncRNAs serve as promising biomarkers for early diagnosis and prognostic assessment. This review summarizes the current research achievements regarding exosomal ncRNAs in PC, systematically elaborating on their roles in tumor occurrence, metastasis, chemoresistance and the TME. Furthermore, by integrating the potential of exosomal ncRNAs in the diagnosis, treatment and prognosis of PC and by highlighting the challenges and future directions, this review aims to offer novel insights for future research and clinical translation of exosomal ncRNAs in PC.

Cluster of differentiation 47 (CD47), an immune checkpoint commonly referred to as the "don't eat me" signal, plays a pivotal role in tumor immune evasion by inhibiting phagocytosis through interaction with signal regulatory protein alpha (SIRPα) on macrophages and dendritic cells (DCs). Although early enthusiasm drove broad clinical development, recent discontinuations of major CD47-targeted programs have prompted re-evaluation of its therapeutic potential. The purpose of this commentary is to contextualize the setbacks observed with first-generation CD47 inhibitors and to highlight strategies aimed at overcoming their limitations. Clinical challenges, including anemia, thrombocytopenia, suboptimal pharmacokinetics, and limited single-agent efficacy, underscore the need to develop safer, more selective approaches. Emerging next-generation strategies, such as SIRPα-directed agents, bispecific antibodies, and conditionally active therapeutics, are designed to enhance safety and tumor selectivity and reduce systemic toxicity. In addition, spatial profiling and biomarker-driven patient selection are advancing toward guiding rational therapeutic combinations, including with "eat-me" signals (e.g., calreticulin [CALR]) or DNA damage response therapies (e.g., poly(ADP-ribose) polymerase [PARP] inhibitors). Rather than signaling failure, these developments underscore the need for precision, context-specific applications, and adaptive trial designs to realize the durable therapeutic promise of CD47 blockade in cancer immunotherapy.

Head and neck squamous cell carcinoma (HNSCC) is an aggressive cancer with high recurrence rates and prevalent resistance to therapeutic interventions. Tumor behavior is largely dependent on the tumor microenvironment (TME) that includes immune cells, stromal components, cancer-associated fibroblasts (CAFs), the extracellular matrix (ECM), and an associated cytokine network. In this review, we examine principal mechanisms of the tumorigenic transformation, encompassing immune checkpoint disruption, therapy resistance mediated through CAFs, the contribution of hypoxic niches, and several metabolic dependencies that hold potential as future targets. Novel therapeutics developed and/or repurposed, such as immune checkpoint inhibitors (ICIs), TME modulation therapeutics, CAF reprogramming, hypoxia targeting agents, and ECM remodeling, aim to overcome TME-mediated resistance. We also examine the rationale and progress of integrating TME-targeted therapies with other treatment modalities. By identifying actionable, molecular targets within the HNSCC TME, this review presents a translational perspective for implementing TME modulation in personalized treatment. The challenges comprise TME heterogeneity, a paucity of predictive biomarkers, and a translational gap between pre-clinical and clinical practice. Future studies must be aimed at proper stratification of patients, optimization of combination treatment, and cost-effectiveness analysis of TME-modifying therapies to enable personalized medicine in HNSCC treatment.

Radiation sensitive 23 homolog B (RAD23B), a DNA repair-related protein, plays a contributory role in the development of multiple malignancies. This study aimed to explore the role of RAD23B in promoting colorectal cancer (CRC) metastasis and to elucidate the underlying molecular mechanisms.

Cancer immunotherapy has long been established as an important treatment option for cancers. In particular, Immune Checkpoint Inhibitor (ICI) has been reported to be effective against various gastrointestinal cancers (esophageal cancer, gastric cancer, colorectal cancer); however, the treatment phase in which ICI should be used and how it should be incorporated into the treatment strategy vary depending on the cancer type being treated. Multiple clinical trials and basic research on ICIs are currently underway, and new insights from these results will continue to change the clinical treatment strategy of gastrointestinal cancers. While it is desirable to have an increasing number of treatment strategy options for gastrointestinal cancers, it is necessary to organize increasingly complex treatments and select more appropriate ICI-based treatments. In addition, as gastrointestinal cancers are being controlled through multidisciplinary treatment using ICI-based treatment, local control by conversion surgery is becoming an important treatment option. We may soon see an era in which gastrointestinal cancers can be systematically controlled with ICI-based treatment, while difficult-to-control lesions can be removed by conversion surgery. In this review, we summarize the evidence of ICI-based treatment for gastrointestinal cancers and provide an overview of the treatment strategies currently underway.

Motif interacting with ubiquitin-containing novel DUB family-1 (MINDY1) could enhance the stability of programmed death-ligand 1 (PD-L1). The study aimed to investigate whether MINDY1 regulates the immune escape of hepatocellular carcinoma (HCC) mediated by PD-L1.