Anti-tumor Therapeutics often cause anemia in advanced gastric cancer (AGC) patients. Currently, anemia is often diagnosed based on hemoglobin levels, but these tests are reactive rather than predictive. Erythrocyte lifespan (ELS) a crucial physiological parameter, yet its relationship with anemia after anti-tumor treatment in AGC patients remains unclear. We aimed to investigate the potential of ELS in predicting the development of moderate and severe anemia in patients with AGC following anti-tumor therapeutics.

Colorectal cancer (CRC) is a prevalent malignancy with the efficacy of current treatments limited. Nitidine chloride (NC), a natural alkaloid, exhibits antitumor potential, but its mechanism in CRC remains unclear.

To develop a CT-based decision tree model integrating clinical and imaging features for the preoperative differentiation of gastric ectopic pancreas (GEPs) and gastrointestinal stromal tumors (GISTs) with a maximum diameter of less than 3 cm.

Dysbiosis of the oral microbiota has been shown to be associated with the development of esophageal and gastric cancer. Nevertheless, little research explores how oral microbiota might contribute to the occurrence and progression of adenocarcinoma of the esophagogastric junction (AEG).

Ferroptosis, an iron-dependent form of programmed cell death, has garnered significant attention in tumor research in recent years. Its core characteristics include aberrant accumulation of lipid peroxides and impairment of antioxidant defense mechanisms, such as dysfunction of glutathione peroxidase 4. These features are closely intertwined with the initiation, progression, and therapeutic resistance of hepatocellular carcinoma (HCC). This review presents a systematic overview of the fundamental molecular mechanisms underlying ferroptosis, encompassing iron metabolism, lipid metabolism, and the antioxidant system. Furthermore, it summarizes the potential applications of targeting ferroptosis in liver cancer treatment, including the mechanisms of action of anticancer agents (e.g., sorafenib) and relevant ferroptosis-related enzymes. Against the backdrop of the growing potential of artificial intelligence (AI) in liver cancer research, various AI-based predictive models for liver cancer are being increasingly developed. On the one hand, this review examines the mechanisms of ferroptosis in HCC to explore novel early detection markers for liver cancer, to provide new insights for the development of AI-based early diagnostic models. On the other hand, it synthesizes the current research progress of existing liver cancer predictive models while summarizing key challenges that AI predictive models may encounter in the diagnosis and treatment of HCC.

Chen et al demonstrated that regulator of G protein signaling (RGS) 4 promotes gastric cancer (GC) progression by activating the focal adhesion kinase/phosphatidyl-inositol-3-kinase/protein kinase B pathway and inducing epithelial-mesenchymal transition. Although their multilevel approach integrating clinical data, functional assays, and xenograft models demonstrated a key role for RGS4 in GC pathogenesis, several limitations should be considered. The mechanism of the RGS4-focal adhesion kinase interaction remains unclear, specifically whether it involves direct binding or intermediaries. The clinical analysis of 90 patients lacks stratification by GC subtypes or immune features, potentially limiting generalizability. Furthermore, fully validating RGS4's oncogenic role requires additional studies, including functional assays in chemotherapy-resistant and metastatic cell lines, metastasis models including orthotopic implantation and tail vein injection, and comparison with other RGS family members. Addressing these via targeted mechanistic studies and expanded clinical validation could strengthen RGS4's potential as a therapeutic target in GC.

Gastrointestinal bleeding due to metastasis of an invasive mole to the small intestine is very rare. Most reported cases of metastatic invasive mole are diagnosed after surgery, and lack rich illustrations, which leads to insufficient understanding by clinicians, misdiagnosis, and unnecessary surgeries.

High expression of pescadillo ribosomal biogenesis factor 1 (PES1) has been reported across multiple cancer types and is significantly associated with poor prognosis. Hu et al in their recent paper described their investigation of PES1 in gastric cancer and head and neck squamous cell carcinoma, demonstrating positive correlations between PES1 and programmed death-ligand 1 (PD-L1) expression (51.72% for PES1 and 58.62% for PD-L1), as well as associations with lymph node metastasis and tumor invasion depth. However, the relationship between PES1 and PD-L1 remains incompletely defined. To further address this gap, we analyzed The Cancer Genome Atlas gastric adenocarcinoma dataset and found a negative correlation between PES1 expression and CD8+ T cell infiltration, alongside a positive correlation with PD-L1 expression. Based on prior findings, we hypothesize that PES1 may regulate PD-L1 through the phosphatidylinositol 3-kinase/protein kinase B pathway or cellular Myc-mediated mechanisms. While these pathways require experimental validation, our observations highlight PES1 as a potential regulator of immune evasion and a promising target for cancer immunotherapy.

Autoimmune gastritis (AIG) is frequently associated with one or more comorbid conditions, among which type I gastric neuroendocrine tumors (gNETs) warrant significant clinical concern. However, risk factors for the development of gNETs in AIG populations remain poorly defined.

Hodgkin lymphoma (HL) is characterized by rare Hodgkin/Reed-Sternberg (H/RS) cells surrounded by a predominant immune infiltrate that shapes tumor biology and influences prognosis. FKBP51, an immunophilin and NF-κB/Akt modulator, is implicated in cancer progression, but its role within the HL tumor microenvironment (TME) remains unclear.

Understanding the impacts of low-dose ionizing radiation exposure has significant public health implications. However, the effects of low-dose ionizing radiation on immune modulation and cancer progression remain contentious. This study aimed to investigate the impact of chronic low-dose gamma radiation on mammary tumorigenesis and immune homeostasis using a transgenic mouse model. Female MMTV-neu transgenic mice were exposed to continuous whole-body 60Co gamma radiation over a period of 56 days, thereby receiving cumulative absorbed doses of 10, 100 and 2,000 mGy. Mice were analyzed at 3.5, 6 and 8 months of age for changes in immune cell composition and function, as well as tumor development. We found that mice exposed to LDR exhibited transient increases in NK cell frequency, along with improved IFN-γ production following ex vivo stimulation. Notably, the expression of NKG2D on NK cells was upregulated following LDR exposure. Low-dose radiation also modulated inflammatory cytokine profiles and immune cell populations, such as macrophages and myeloid-derived suppressor cells. Despite these immune changes, the overall impact on tumorigenesis was minimal. Although our data indicated that the LDR treatment did not impact survival and cancer progression, the observed results of NK cell proportion, activation and function provide evidence of the stimulatory effects of LDR on NK cells. These findings aim to contribute to health risk assessments and advise radiation protection regulations.

RNA epigenetic modifications critically regulate gene expression, with 5-methylcytosine (m5C) emerging as an important mark in cancer biology. NSUN2, a key m5C methyltransferase, modifies diverse RNA species, thereby influencing RNA stability, processing, export, and translation. Accumulating evidence indicates that NSUN2 promotes tumorigenesis by enhancing cell proliferation, supporting drug resistance, driving epithelial-mesenchymal transition, and reprogramming metabolic pathways. Clinically, its dysregulated expression is associated with poor prognosis and potential as a biomarker or therapeutic target. Beyond intrinsic tumor functions, NSUN2 also shapes the tumor immune microenvironment by regulating immune checkpoint molecules, cytokine networks, and immune cell activities, ultimately contributing to immune evasion and influencing immunotherapy efficacy. This review summarizes current insights into the roles and mechanisms of NSUN2 in cancer progression and immune modulation, and discusses challenges and future opportunities for therapeutic exploration.

The inflammatory microenvironment formed by chronic inflammation is not only a major risk factor for cancer but also a well-recognized precursor to bladder cancer. However, the immunological transitions that occur along the inflammation-to-cancer continuum remain incompletely understood. This mini-review synthesizes recent advances in understanding how the immune microenvironment evolves from an inflamed yet non-malignant urothelium to invasive carcinoma. First, we discuss how persistent stimuli-such as chronic infection or exposure to carcinogens-disrupt immune homeostasis, leading to sustained interferon signaling, cytokine secretion, and immune cell infiltration. Second, during preneoplastic and dysplastic stages, the immune landscape gradually shifts toward an environment enriched in regulatory T cells and characterized by dysfunctional cytotoxic T cells. Furthermore, in established tumors, immune evasion is primarily driven by T cell exhaustion, myeloid cell-mediated immunosuppression, and fibroblast-associated immune exclusion. Finally, advances in spatial transcriptomics, single-cell technologies, and urinary exosomal profiling have enabled precise "immune snapshots" of these transitions, providing new avenues for biomarker development and therapeutic strategy selection. Mapping these dynamic immune states holds great promise for improving risk stratification, facilitating early detection, and enabling personalized immunotherapy, ultimately translating immune snapshots into actionable strategies for bladder cancer prevention and treatment.

Gastric cancer (GC) is a highly heterogeneous malignancy with poor prognosis, underscoring the urgent need for reliable biomarkers to guide precise stratification and therapy. Transfer RNA-derived small RNAs (tsRNAs) have emerged as potential key regulators in cancer, yet their systematic role in defining GC subtypes remains unexplored.

Small cell lung cancer (SCLC) presents challenges due to its high invasiveness and rapid progression, resulting in an inferior prognosis. Approximately 70% of patients have developed an extensive stage at the time of diagnosis. While most patients with extensive-stage SCLC (ES-SCLC) are sensitive to chemotherapy, they remain at high risk of local recurrence and distant metastasis in the short term. In the era of chemotherapy, studies have indicated the potential survival benefits of consolidative thoracic radiotherapy (cTRT) for patients responding to systemic treatment. The introduction of immunotherapy has significantly transformed the treatment landscape for SCLC. The combination of immune checkpoint inhibitors (ICIs) with chemotherapy has emerged as the new standard for first-line treatment of ES-SCLC. Nevertheless, controversy surrounds the role of cTRT after the first-line treatment of ES-SCLC in the context of immunotherapy, especially considering advancements in imaging staging methods and precise radiotherapy technology. This review focuses on the application value and latest research advancements in cTRT following first-line immunotherapy combined with chemotherapy in ES-SCLC, providing valuable insights for clinical practice.

Pheochromocytomatosis, defined as the implantation of pheochromocytoma cells to the intraoperatively opened surfaces during surgical manipulation, is an infrequent complication of surgical intervention of pheochromocytomas. Only a handful of pheochromocytomatosis cases have been reported since the first case was described in 2001.

Pancreatic cancer (PC) is one of the deadliest malignancies due to early metastasis, therapy resistance, and a highly immunosuppressive microenvironment. Although oncogenic mutations such as KRAS and TP53 are well characterized, the role of protein tyrosine phosphatase non-receptor type 14 (PTPN14)-a Hippo-pathway regulator implicated in other cancers-remains unclear in PC. PTPN14 expression was analyzed in PC tissues and cell lines using immunohistochemistry and western blotting. Functional effects of PTPN14 knockdown or overexpression on proliferation, apoptosis, migration, and invasion were evaluated in vitro using CCK-8, flow cytometry, wound healing, and Transwell assays. Molecular mechanisms were explored via western blotting, immunofluorescence, and rescue experiments focusing on β-catenin and NF-κB signaling. In vivo, a xenograft mouse model assessed tumor growth, histopathology, apoptosis (TUNEL), Ki67 expression, and serum cytokine levels (ELISA). PTPN14 was markedly upregulated in PC tissues and cell lines. Silencing PTPN14 significantly inhibited cell proliferation, migration, and invasion, while enhancing apoptosis in vitro. Mechanistically, PTPN14 activated β-catenin and NF-κB signaling, promoting β-catenin nuclear translocation and p65 phosphorylation, with increased IL-6, TNF-α, and IL-1β secretion. In vivo, PTPN14 knockdown suppressed xenograft tumor growth, reduced Ki67 expression, enhanced apoptosis, and lowered serum pro-inflammatory cytokines. PTPN14 drives PC progression by co-activating β-catenin and NF-κB pathways and promoting a pro-tumor inflammatory milieu. These findings highlight PTPN14 as a promising therapeutic target to inhibit PC aggressiveness and inflammation-driven tumor progression.

The promising therapeutic outcomes of neoadjuvant chemoimmunotherapy (NCIT) in locally advanced esophageal squamous cell carcinoma (ESCC) have been confirmed by multiple phase II clinical trials and are widely used in clinical practice. However, there are some cases, such as clinical T3N+ stage, that achieve poor tumor regression after receiving NCIT, reflecting the insufficient efficacy of NCIT for advanced T-type tumors. It may be necessary to add concurrent radiotherapy to further improve the local control effect of tumor, but it also means higher adverse events and immune suppression when irradiating tumor-draining lymph nodes. Nevertheless, node-sparing radiotherapy can enhance the effect of NCIT with fewer adverse effects, which has been applied to other solid tumors. The aim of this study was to evaluate the safety and efficacy of NCIT combined with node-sparing radiotherapy for clinical T3N+ locally advanced ESCC (CINSREC trial).

Approximately 15%-25% paragangliomas and pheochromocytomas (PPGL) can metastasize. Untreated metastatic PPGL (MPP) patients have a 5-year survival rate below 50%, while standardized diagnosis and treatment can significantly improve prognosis. Currently, there has been no established national guidelines for MPP management in China. To address this gap, the Adrenal Group of Chinese Society of Endocrinology convened a multidisciplinary panel of experts from endocrinology, oncology, surgery, nuclear medicine, radiation oncology, pathology, laboratory medicine, and interventional therapy. Based on evidence-based medicine, the latest global research, and clinical data from China, the panel has developed a consensus statement. This consensus encompasses various aspects of MPP, including its epidemiology, pathogenesis, risk factors and prediction for dissemination, clinical manifestations, diagnosis, treatment, and prognosis. A total of 16 recommendation statements have been formulated, with the aim of assisting clinicians in developing standardized strategies for the diagnosis and treatment of MPP.

The purpose of this study was to evaluate the safety of omitting radioiodine (RAI) ablation in low-risk papillary thyroid cancer.