This study evaluates the effectiveness and safety of combining radiotherapy with first-line chemotherapy and immune checkpoint inhibitors in patients with locally advanced or metastatic urothelial carcinoma (la/mUC).

This retrospective study included patients with la/mUC who received first-line systemic treatment between January 2017 and December 2024. Two treatment strategies were compared: immunotherapy combined with chemotherapy followed by radiotherapy (ICRT group, n = 31) and immunotherapy combined with chemotherapy alone (ICT group, n = 73). Propensity score matching was used to reduce confounding and selection bias, yielding 30 matched patient pairs. Clinical endpoints included objective response rate (ORR), duration of response (DOR), progression-free survival (PFS), overall survival (OS), and treatment-related adverse events.

After propensity score matching, the ICRT group showed significantly prolonged PFS (18.70 vs. 7.93 months; P = 0.002) and OS (38.9 vs. 19.8 months; P = 0.031) compared with the ICT group. The ICRT cohort demonstrated higher PFS, OS, and ORR across all evaluated time points, with statistically significant differences at 6-month PFS, 12-month PFS, and 12-month OS (P < 0.05). Although the median DOR was numerically longer in the ICRT group (29.23 vs. 13.53 months), the difference did not reach statistical significance (P = 0.385). Radiation-related enteritis and cystitis were observed in the ICRT group, while no treatment-related deaths occurred. Multivariate Cox regression analysis identified lung metastases, elevated C-reactive protein levels, radiotherapy, and treatment response exceeding stable disease as independent predictors of PFS. Liver metastases, radiotherapy, and better treatment response were independently associated with OS.

The addition of radiotherapy to first-line immunotherapy and chemotherapy demonstrated favorable clinical activity and an acceptable safety profile in patients with la/mUC.

In patients with unresectable lung adenocarcinoma, whether cross-line immunotherapy (CIT) can improve clinical outcomes remains unclear.

This study enrolled patients with unresectable lung adenocarcinoma who received immune checkpoint inhibitors (ICIs)-based therapy and subsequently experienced disease progression. According to post-progression treatment strategies, patients were categorized into two groups: CIT group and Non-CIT group. The primary endpoints were second progression-free survival (PFS2), overall survival (OS), and post-progression survival (PPS), analyzed both using unadjusted and inverse probability for treatment weighting (IPTW) analyses. Survival outcomes were analyzed using the Kaplan-Meier method and compared with the log-rank test. Multivariate Cox regression was performed to identify independent prognostic factors. A nomogram for PPS prediction was built and internally validated with bootstrap resampling and receiver operating characteristic (ROC) curves.

A total of 185 patients met the inclusion criteria and were studied assessed, including 77 in the CIT group and 108 in the Non-CIT group. Baseline characteristics were generally balanced between two groups. After IPTW adjustment, median PFS2 was significantly longer in the CIT group compared with the Non-CIT group (6.3 vs. 2.8 months; hazard ratio (HR)=0.54, 95% confidence intervals (CI): 0.39-0.77, P<0.001). Similarly, the CIT group demonstrated improved median PPS and OS compared with Non-CIT group. Multivariate Cox analysis also identified CIT as independent predictors of PFS2, PPS and OS. The PPS nomogram showed good predictive performance.

In patients with unresectable lung adenocarcinoma who progressed after initial immunotherapy, continuation of immunotherapy beyond progression was associated with significantly improved survival. The PPS nomogram may facilitate risk stratification and personalized post-progression management.

Adding immune checkpoint inhibitors (ICIs) to neoadjuvant chemotherapy (NAC) enhances systemic efficacy in triple-negative breast cancer (TNBC). However, its impact on the survival outcomes of axillary surgical de-escalation remains undefined. This study evaluates whether chemo-immunotherapy mitigates survival risks historically associated with omitting axillary lymph node dissection (ALND) for sentinel lymph node biopsy (SLNB) in clinically node-positive (cN+) disease.

In this retrospective cohort study using the National Cancer Database (2018-2022), we identified women with cN1-3, cM0 TNBC who received NAC ± ICIs and achieved ypN0 (axillary pathological complete response), followed by axillary surgery (SLNB or ALND). Overall survival (OS) was evaluated using restricted mean survival time (RMST) and propensity score matching. Multivariable Cox models assessed the independent effect of surgical extent (SLNB vs. ALND) on OS.

Out of 1,315,170 breast cancer cases, 4,336 eligible patients were included. The therapeutic regimen significantly interacted with the survival impact of axillary de-escalation. With NAC alone, SLNB was independently associated with inferior OS compared to ALND [5-year OS: 83.0% vs. 87.8%, P = .027; adjusted hazard ratio (aHR)=1.63, 95% CI = 1.12-2.38, P = .01]. Strikingly, adding ICIs neutralized this disparity: in the NAC+ICI cohort, SLNB yielded OS comparable to ALND (5-year OS: 90.1% vs. 93.6%, P = .99; identical 48-month RMST), with no significant survival detriment in multivariable analysis (aHR=1.19, 95% CI = 0.54-2.61, P = .67).

The enhanced systemic control conferred by ICIs appears to compensate for the reduced surgical clearance of the axilla when ALND is omitted, effectively mitigating the survival risks associated with omitting ALND in cN+ TNBC. These real-world findings suggest modern chemo-immunotherapy facilitates axillary de-escalation without compromising overall survival, establishing a compelling rationale for prospective clinical trials.

Tumor immune evasion is a fundamental hallmark of cancer progression and a major barrier to effective immunotherapy. RNA epitranscriptomic modifications have emerged as a critical layer of post-transcriptional regulation that links RNA fate control with tumor immune remodeling. These reversible modifications, including m⁶A, m⁵C, ac⁴C, m¹A, m⁷G, pseudouridine, m⁶Am, Nm, and A-to-I RNA editing, are dynamically regulated by writers, erasers, and readers. By modulating RNA stability, splicing, nuclear export, translation efficiency, degradation, and innate immune recognition, RNA modifications reshape multiple immune-related processes in cancer. Mechanistically, they regulate tumor immune visibility by influencing antigen processing, MHC-I expression, interferon signaling, and dendritic cell-mediated cross-presentation. They also control immune checkpoint expression, particularly the PD-1/PD-L1 axis, inflammatory signaling pathways, immune-cell recruitment and exhaustion, and metabolic immunosuppression within the tumor immune microenvironment. Importantly, the functions of RNA modification regulators are highly context dependent. The same regulator may either promote immune escape or enhance antitumor immunity depending on cancer type, cellular source, target transcript, reader protein, and microenvironmental state. From a clinical perspective, RNA modification-based molecular subtypes, prognostic signatures, and risk-score models show potential for predicting patient prognosis, immune infiltration, and response to immune checkpoint blockade. In parallel, targeting RNA modification regulators, alone or in combination with immunotherapy, radiotherapy, chemotherapy, or targeted therapy, represents an emerging therapeutic strategy. However, clinical translation remains limited by insufficient specificity, tumor heterogeneity, complex crosstalk among RNA modifications, potential toxicity, and delivery barriers. Future studies integrating RNA modification mapping with single-cell, spatial, and multi-omics technologies will be essential to define cell-type-specific regulatory networks and develop precise RNA epitranscriptomic biomarkers and therapies for cancer immunotherapy.

Helicobacter pylori (H. pylori) is a primary etiological agent for various gastric pathologies. Although numerous studies have described the association between H. pylori and individual stages of the Correa cascade, data comprehensively evaluating its prevalence across the full histopathological spectrum-from non-atrophic gastritis (NAG) to gastric cancer (GC)-within a single Chinese cohort remain limited. This study aimed to investigate the association between H. pylori infection and specific endoscopic stages, and further analyzed its influence on histopathological progression in a longitudinal sub-cohort.

A retrospective study was conducted using data from participants who underwent concurrent gastroscopy and a ¹⁴C-Urea breath test (UBT) at the endoscopy center at Fengqing people's Hospital between January 2019 and December 2024. Gastric mucosa status was assessed based on endoscopic and histopathological biopsy findings. Statistical associations were evaluated using the chi-square test. Correlations were analyzed using Spearman coefficients. A longitudinal sub-cohort was analyzed to compare disease progression between baseline H. pylori-positive and -negative groups. The hazard ratio (HR) and 95% confidence interval (CI) for incident disease progression were calculated by Cox proportional hazards regression.

A total of 13,579 participants were included, and the overall prevalence of H. pylori infection was 62.54%. A statistically significant association was found between H. pylori infection and gastric sequential stages of Correa's cascade. The infection rate varied across pathological groups, being highest in participants with low-grade intraepithelial neoplasia (LGIN) (77.46%), and lowest in those with non-atrophic gastritis (NAG) (61.05%). In the longitudinal sub-cohort, the disease progression rate was higher among participants who were H. pylori-positive at baseline compared to their negative counterparts (9.67% vs. 5.60%, p = 0.0043). The HR for disease progression was significantly increased among H. pylori-positive participants compared with H. pylori-negative participants after sex- and age-adjustment [adjusted HR = 1.60 (1.07-2.39), p=0.021].

Our study reveals a significant association between H. pylori infection and advanced gastric lesions, and confirms its significant impact on disease progression. This evidence solidifies the importance of eradication in clinical management to halt disease advancement.

Chemotherapy-induced oral mucositis (CIOM) is a prevalent toxic side effect of cancer treatment, severely compromising patients' quality of life, nutritional intake, and treatment adherence. Its pathogenesis has evolved from the traditional model of simple epithelial damage to a complex pathological process involving the interplay of chemotherapy toxicity, host immunity, and oral microbiota. Research indicates that chemotherapy can disrupt the oral microbiota, promoting the proliferation of pathogenic bacteria and exacerbating damage to the mucosal barrier and local inflammatory responses. Current clinical interventions, such as mouth rinses and cryotherapy, have limited efficacy and lack standardized protocols. In recent years, modulating the oral microbiota has emerged as a promising therapeutic strategy. Probiotic preparations have demonstrated potential in clinical studies to alleviate CIOM severity through mechanisms including competitive colonization, metabolic regulation, and immunomodulation. This review systematically summarizes the clinical manifestations, epidemiological characteristics, pathogenesis, and existing treatment strategies of CIOM. It highlights the critical role of the oral microbiota in CIOM pathogenesis and further outlines the promising application prospects of microbiome-targeted interventions, particularly probiotic preparations, aiming to provide novel insights for CIOM prevention and treatment.

Solid pseudopapillary neoplasms (SPNs) are rare, low-grade malignant tumors of the pancreas comprising 1%-2% of pancreatic neoplasms. Predominantly affecting young women, these tumors are typically slow-growing and often discovered incidentally during imaging for non-specific symptoms. This case describes a young female patient who presented with acute-onset back pain without prior significant medical history or trauma. Initial evaluation suggested a musculoskeletal etiology; however, persistent symptoms prompted further imaging, which revealed a pancreatic mass. Subsequent diagnostic workup, including cross-sectional imaging and histopathological analysis, confirmed the diagnosis of an SPN of the pancreas. The patient underwent surgical resection with a favorable postoperative recovery. This case highlights the atypical presentation of SPN as isolated back pain and underscores the importance of maintaining a broad differential diagnosis when evaluating persistent, unexplained pain in young patients.

Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine disorder associated with both reproductive and metabolic dysregulation. While anti-Müllerian hormone (AMH) and the triglyceride-glucose (TyG) index have been independently linked to PCOS, their combined and interactive effects remain unclear. This study aimed primarily to investigate the independent and synergistic associations of AMH and the TyG index with PCOS, and secondarily to evaluate their predictive performance for PCOS risk.

A single-center retrospective cross-sectional study included 628 participants (2020-2024). Clinical, hormonal, and metabolic parameters were assessed. Associations and predictive ability were examined using logistic regression restricted cubic splines (RCS), subgroup analysis, and receiver operating characteristic (ROC) curves.

Adjusted analyses confirmed AMH and the TyG index as independent risk factors for PCOS (ORs = 1.252, 1.981; both P < 0.05). A significant interaction was identified (OR = 1.029, P < 0.001). In subgroup analyses, a significant positive association was observed between the TyG index and PCOS risk in the low AMH subgroup (OR = 4.561, P = 0.002). Compared with the double-low group (low AMH and low TyG), the risk for PCOS showed a sequential increase in the low AMH/high TyG, high AMH/low TyG, and double-high groups (ORs = 3.582, 5.894, and 12.082; all P < 0.05), demonstrating a clear dose-response relationship. The predictive model combining AMH and the TyG index demonstrated the highest accuracy (AUC = 0.693), which was slightly higher than that of either indicator alone.

Beyond their independent roles, AMH and the TyG index interact synergistically in the pathogenesis of PCOS.

CD19- and B-cell maturation antigen (BCMA)-directed chimeric antigen receptor T-cell (CAR T-cell) therapies have improved outcomes in relapsed or refractory B-cell lymphoid malignancies and multiple myeloma, but late hematologic complications are increasingly relevant as survivorship expands. This narrative review examines how pre-infusion clonal hematopoiesis (CH), clonal hematopoiesis of indeterminate potential (CHIP), clonal cytopenia of undetermined significance (CCUS), marrow reserve, prior genotoxic exposure, inflammatory stress, and disease-platform context shape the risks of prolonged cytopenia and therapy-related myeloid neoplasms (t-MN) after CAR T-cell therapy. Available evidence suggests that high-risk clonal architecture, particularly TP53-mutated or DNA damage response-associated clones, clonal cytopenia, larger or multiple clones, and heavy prior cytotoxic exposure, is more clinically informative than CHIP positivity alone. By contrast, associations between unstratified CH and prolonged cytopenia remain heterogeneous. CD19 lymphoma and BCMA myeloma settings share clonal-selection biology but differ in marrow ecology, treatment history, baseline cytopenia, inflammatory burden, and surveillance windows. For clinical translation, risk assessment should not rely on universal CHIP screening or binary genomic classification. Instead, clonal-risk models, hematotoxicity-risk models, baseline blood counts, inflammatory markers, prior therapy exposure, and disease-platform context should be integrated to identify patients who may benefit from intensified myeloid surveillance, supportive-care planning, and earlier marrow reassessment while preserving access to CAR T-cell therapy.

The impact of protein quality on lung cancer risk in the U.S. population remains unclear. We conducted a large-scale prospective cohort study with 101,755 American adults enrolled in the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial (1993-2001).

The Healthy Plate Protein Quality Index (HPPQI) was used to assess dietary protein quality. Cox proportional hazards regression was applied to analyze the relationships between HPPQI and lung cancer incidence and mortality. Subgroup and sensitivity analyses were conducted.

Over a mean follow-up of 8.82 ± 1.95 years (897,809 person-years; median 9.40 years), 1,706 lung cancer cases (1,464 NSCLC and 242 SCLC) and 1,217 related deaths (1,005 NSCLC and 212 SCLC) were recorded. Higher HPPQI was significantly linked to lower lung cancer incidence (HR Q4 vs. Q1: 0.63; 95% CI: 0.55-0.73; P < 0.001 for trend) and mortality (HR Q4 vs. Q1: 0.62; 95% CI: 0.52-0.74; P < 0.001 for trend), consistent in both NSCLC and SCLC. Sensitivity analysis confirmed the study's robustness across various participant characteristics.

Adherence to a dietary pattern characterized by a higher HPPQI is associated with reduced lung cancer risk.