Microvascular invasion (MVI) is a major determinant of postoperative recurrence and poor prognosis in hepatocellular carcinoma (HCC), yet MVI cannot be reliably identified before surgery: pathologic evaluation is invasive, prone to sampling bias, and available only after resection. We aimed to develop and evaluate a preoperative radiomics biomarker for noninvasive MVI prediction and postoperative risk stratification of recurrence-free survival.

In this retrospective multicenter study, 567 patients with HCC from four centers were included. Based on pretreatment MRI and clinical variables available before surgery, radiomics models characterising the global tumour region (GTR) and intratumoral heterogeneity (ITH) were developed and integrated into a Fusion model for preoperative prediction of MVI. Discrimination, calibration, and clinical utility were assessed using AUC, calibration curves, and decision-curve analysis (DCA). Prognostic stratification was evaluated using C-index, time-dependent ROC analysis, and Kaplan-Meier analysis of recurrence-free survival, and benchmarked against the Barcelona Clinic Liver Cancer (BCLC), China Liver Cancer (CNLC), and American Joint Committee on Cancer (AJCC) staging systems.

The Fusion model showed higher discrimination than comparators in the validation and external test sets, achieving AUCs of 0.924 and 0.895, respectively. Ablation analyses showed incremental gains with the sequential addition of GTR features, ITH features, and clinical covariates. Fusion score-based stratification identified high- and low-risk groups with markedly divergent recurrence-free survival. In the external test set, the prognostic model achieved a C-index of 0.766 and time-dependent AUCs of 0.825 at 2 years and 0.878 at 5 years, showing higher discrimination than BCLC, CNLC, and AJCC staging (all p < 0.001). Performance remained robust across HBV status, histologic differentiation, and BCLC stage.

A radiomics biomarker integrating global tumour phenotype, intratumoral heterogeneity, and preoperative clinical variables enables noninvasive preoperative MVI assessment and may complement morphology-based staging for recurrence risk stratification in HCC.

Background Ovarian neoplasms represent a heterogeneous category of tumors with different histogenesis, clinical behavior, and prognosis, thus presenting a major challenge in gynecological oncology. The most popular biomarker in ovarian cancer is serum cancer antigen 125 (CA-125). Hence, the purpose of our study is to assess the diagnostic accuracy of serum CA-125 to differentiate between benign and malignant ovarian tumors using clinicopathological correlation in a tertiary care institution. Methods This is an observational study, retrospective in nature, carried out in the Department of Pathology at Rajendra Institute of Medical Sciences (RIMS), Ranchi, over 18 months. A total of 76 histopathologically confirmed ovarian tumor cases with available clinical, radiological, and serum CA-125 data were included. Preoperative serum CA-125 levels were measured using a cutoff value of 35 U/mL. Tumors were categorized as benign, borderline, or malignant based on histopathological criteria. Statistical analysis was performed using SPSS (IBM SPSS Statistics for Windows, IBM Corp., Version 27, Armonk, NY). Results Out of 76 ovarian tumors, 55 (72.4%) were benign, two (2.6%) were borderline, and 19 (25.0%) were malignant. Epithelial tumors (46, 60.5%) were the most common histological type. Serous cystadenoma (16, 21.1%) was the most frequent subtype. Elevated CA-125 levels were observed in all malignant tumors (19, 100%), while most benign tumors (49, 89.1%) showed normal levels. Serum CA-125 demonstrated sensitivity of 100%, specificity of 87.7%, positive predictive value of 73.1%, negative predictive value of 100%, and overall diagnostic accuracy of 90.7%. Conclusion The present study indicates that ovarian tumors are mainly benign, and most histological subtypes are epithelial tumors. Serum CA-125 demonstrated an excellent sensitivity in the detection of malignant tumors of the ovary, with all the malignant tumors portraying high levels of CA-125. These results show that CA-125 is a useful biomarker for identifying malignant ovarian tumors. However, its interpretation should be made in conjunction with clinical, radiological, and histopathological findings.

Thyroid nodules are one of the most frequently seen endocrine conditions in clinical practice and a major challenge in diagnosis, as only a small proportion of them are malignant. The current study aimed to compare the American College of Radiology Thyroid Imaging Reporting and Data System (ACR-TIRADS) ultrasonographic classification with the Bethesda cytological category in thyroid nodules with histopathological diagnosis.

Our study was conducted as a hospital-based cross-sectional observational analysis in the Departments of Pathology and Radiodiagnosis at Rajendra Institute of Medical Sciences (RIMS), Ranchi. A total of 50 consecutive patients fulfilling the eligibility criteria were included. Ultrasonographic examination was performed using ACR-TIRADS criteria, and fine needle aspiration cytology (FNAC) findings were interpreted according to The Bethesda System for Reporting Thyroid Cytopathology (TBSRTC). Histopathological examination served as the reference standard.

In our study, the mean age was 33.76 ± 12.85 years, and females constituted 34 (68.0%) cases. TIRADS 3 nodules constituted the largest subgroup with 16 (32.0%) cases. Histopathological examination identified 29 (58.0%) benign lesions and 21 (42.0%) malignant lesions. Bethesda cytology demonstrated superior concordance with histopathology, with a specificity of 100% and excellent diagnostic accuracy with an area under the curve (AUC) of 0.81. In contrast, ACR-TIRADS showed poor discriminatory ability with an AUC of 0.51.

Bethesda cytology showed superior concordance and diagnostic accuracy compared with ultrasonographic ACR-TIRADS classification in predicting malignant thyroid nodules. Combined radiological and cytological evaluation may improve diagnostic certainty and support appropriate surgical decision-making.

Despite the proven efficacy of KRAS G12C inhibitors (KRAS G12Ci) in solid tumors, evidence from direct comparisons with standard of care is scarce, and no analysis has investigated the potential immunological basis for differential responses.

PubMed, Embase, Cochrane Library, and ClinicalTrials.gov for randomized controlled trials (RCTs) involving solid tumors patients who had received KRAS G12Ci were retrieved from inception to March 28, 2026. Individual participant data on progression-free survival (PFS) and overall survival (OS) were extracted from the published Kaplan-Meier survival curves. When available, subgroup data by programmed death ligand 1 (PD-L1) expression were extracted to explore immune-related correlates of treatment response.

A total of 4 articles with 3 RCTs and 949 participants were selected. In 1-stage reconstructed individual patient data meta-analyses, PFS was better in the KRAS G12Ci group (HR, 0.62; 95% CI, 0.53-0.74; P < 0.001). However, no statistical difference in OS was observed (HR, 0.93; 95% CI, 0.74-1.16; P = 0.495). The results were confirmed by 2-stage meta-analyses which additionally exhibited an objective response rate (ORR) of 3.60 (95% CI; 2.01-6.46; P < 0.001; I² = 39.7%). Regarding PD-L1 expression, PFS benefits were observed in patients with expression levels <1% (HR, 0.56; 95% CI: 0.38-0.83; P = 0.004) and 1%-49% (HR, 0.58; 95% CI: 0.43-0.78; P < 0.001). KRAS G12Ci demonstrated a better safety profile, apart from diarrhea and rash.

A similar OS, but better PFS and ORR with a superior safety profile were observed in patients receiving KRAS G12Ci, suggesting that KRAS G12Ci may be more suitable for later-line therapy. Older patients, those without liver metastases, or those with PD-L1<50% may be the target population. These subgroup observations are hypothesis-generating and require prospective validation.

https://www.crd.york.ac.uk/PROSPERO/, identifier CRD420251146769.

Disease-related malnutrition can develop in colorectal cancer (CRC) patients, negatively affecting postoperative clinical outcomes. Nutritional status should be assessed using standardised tools and laboratory parameters to identify malnourished patients and introduce personalised, targeted dietary interventions based on epigenetics, immunologically-related aspects, and gut microbiome. The primary aim of this study is to analyse the immunonutritional status of CRC patients in the preoperative period. The secondary aim is to assess the link between albumin-to-globulin ratio (AGR), prognostic nutritional index (PNI), and TNM staging.

This study initially included 21 patients with histopathological confirmation of CRC qualified for surgical resection of the tumour. Immunologically-related nutritional status parameters, i.e., AGR and PNI, were calculated for selected 12 patients. The optimal cut-off value of PNI was determined, allowing patients to be divided into two independent groups: PNI-low and PNI-high. The link between AGR, PNI, and TNM was analysed.

TNM classification of the 12 selected participants revealed that most participants classified as T3 (67%), lymph node metastasis was identified in 50% of patients, and there were no distant metastases. Among selected patients, the analysis of mean values of immunological laboratory tests showed that they were within the normal range, except for lymphocyte levels, which were reduced (22.03 ± 7.31%). The optimal cut-off value was set at 51.74 for PNI; thus, patients were accordingly divided into PNI-low and PNI-high groups (<51.74, 34% of cases; ≥51.74, 66%, respectively). PNI-low was initially associated with more advanced cases (based on T assessment) compared to PNI-high (100% versus 75%; respectively); however, it failed to reach statistical significance (p = 0.515; effect size 0.2889; CI 95%, CI = 0.0110-7.5681). Therefore, this finding should be interpreted with caution. Lymph node metastasis was found more often in the PNI-high group than in the PNI-low group.

Overall concentrations of albumin and total protein were not decreased in CRC patients; however, these parameters allow calculation of AGR and PNI. The link between PNI-low and locally advanced cases of CRC based on T assessment can potentially exist; nevertheless, it should be confirmed with more clinical data. Lymph node metastasis was more often observed in the PNI-high group. This status is also related to higher levels of AGR. A PNI-low value is more related to local than distant pathological processes associated with CRC.

Radiotherapy (RT) has evolved from a purely cytotoxic treatment into a potent immune modulator capable of inducing systemic anti-tumor responses. High-dose precision approaches such as stereotactic body radiotherapy or stereotactic radiosurgery can trigger immunogenic cell death, enhance antigen presentation, and promote tumor-specific T-cell priming. However, the magnitude and quality of these radiation-induced immune effects depend critically on the biological age of the host immune system. Immunosenescence-defined by the gradual decline and remodeling of immune competence with age-profoundly alters both innate and adaptive immunity. The aged immune landscape is characterized by reduced responsiveness, chronic low-grade inflammation, and impaired coordination between immune effector cells. In this context, RT may not elicit the same immunogenic signals observed in younger patients. Instead, aging-associated immune alterations can dampen the anti-tumor potential of radiation or shift the balance toward prolonged inflammation and immune dysregulation. These effects highlight the need to consider immune aging as a key determinant of therapeutic response. Understanding how immunosenescence modulates radiation-induced immunity is essential for developing age-informed and immune-adaptive RT strategies. Integrating biomarkers of immune aging into treatment planning could enable truly personalized immuno-oncology approaches-optimizing efficacy, minimizing toxicity, and improving outcomes in older patients with cancer.

Pancreatic ductal adenocarcinoma (PDAC) has an extremely poor prognosis. Immune checkpoint inhibitor (ICI) monotherapy has shown limited efficacy in PDAC, whereas the potential clinical value of first-line ICI-based combination regimens remains unclear. Through a systematic review and meta-analysis, this study aimed to evaluate the efficacy and safety of first-line ICI-based combination regimens in advanced PDAC.

PubMed, Embase, The Cochrane Library, Scopus, Web of Science, CNKI, Wanfang Data, VIP, and CBM were searched up to April 4, 2026, to identify clinical studies evaluating first-line ICI-based combination therapy for advanced PDAC. Study screening and data extraction were performed in accordance with PRISMA guidelines.

Eight clinical trials involving 379 patients were included. In RCT-only analyses, ICI-based combination regimens showed favorable but statistically non-definitive trends for OS (HR = 0.83, 95% CI: 0.65-1.06) and PFS (HR = 0.75, 95% CI: 0.53-1.05), while ORR was improved (OR = 2.19, 95% CI: 1.32-3.64). Single-arm pooled analysis showed a median PFS of 6.2 months and an ORR of 38.0%. In terms of safety, combination therapy increased the risk of specific Grade 3 or higher adverse events, but the overall incidence was clinically manageable.

First-line ICI-based combination regimens showed encouraging antitumor activity in advanced PDAC, particularly for radiological response. However, definitive survival benefits were not established in RCT-only analyses, and further large-scale randomized trials are needed.

https://www.crd.york.ac.uk/PROSPERO/view/CRD420261440306, identifier CRD420261440306.

Population aging is a major global health challenge and a principal risk factor for cancer. Aging does not simply increase mutational burden; it reshapes tissue homeostasis across genetic, epigenetic, metabolic, immune, and systemic dimensions. Genomic instability, epigenetic drift, mitochondrial dysfunction, and metabolic rewiring collectively establish a tumor-permissive landscape that enhances clonal diversification and lowers the threshold for malignant transformation. Concurrently, accumulation of senescent cells and the senescence-associated secretory phenotype (SASP) remodel the microenvironment, promote immune suppression, and weaken tumor surveillance, further exacerbated by immunosenescence and gut microbiota dysbiosis. Importantly, cancer progression feeds back to accelerate organismal aging. Tumor burden and therapy-induced stress destabilize hematopoietic and non-hematopoietic stem cell niches, disrupt systemic metabolic homeostasis, and induce neuroendocrine reprogramming, thereby amplifying multi-organ functional decline. Aging and cancer therefore constitute a bidirectional and self-reinforcing network rather than a linear cause-effect relationship. In this review, we synthesize mechanistic, clinical, and translational evidence defining the tumor-aging axis and discuss emerging strategies aimed at interrupting this pathogenic cycle.

This study aims to summarize and appraise the credibility of existing epidemiological evidence on the association between periodontal diseases (PDs) and the risk of site-specific cancers.

PubMed, Embase, and Cochrane Library were searched from inception to June 2026. Meta-analyses of observational studies investigating PDs and cancer risk were included. Each association was classified into five levels according to a predefined criterion, which included statistical significance, heterogeneity, sample size, and bias assessment. AMSTAR 2 was used to evaluate the quality of studies. Corrected covered area and the author's own meta-analysis were performed to ensure a rigorous methodology.

In total, 66 associations from 38 meta-analyses investigating 14 cancer types were appraised, including head and neck cancer (HNC), oral, lung, breast, esophageal, gastric, pancreatic, liver, colorectal, bladder, kidney, prostate, melanoma, and hematopoietic and lymphatic cancers. Among 23 main associations, highly suggestive evidence was identified in associations between PDs (odds ratio [OR], 2.42; 95% confidence interval [CI], 1.85-3.17) in HNC, and PDs in oral cancer (OR, 2.94; 95% CI, 2.13-4.07). Another seven associations were recommended as suggestive evidence (class III). Fourteen associations were classified as weak (class IV) or showing no significant evidence (class V).

Associations between PDs and site-specific cancers demonstrated varying levels of evidence. This analysis highlighted strong correlations in HNC and oral cancer, while failing to show credible evidence for the remaining 12 cancers. Overall, our study yielded novel insights into oral health interventions, calling for the incorporation of periodontal health into public health policy.

https://www.crd.york.ac.uk/PROSPERO/view/CRD42024585375, identifier CRD42024585375.

Immune checkpoint inhibitors (ICIs) have revolutionized cancer treatment; however, durable clinical benefit is limited to a subset of patients. Long non-coding RNAs (lncRNAs) have emerged as important regulators of tumor biology and immune responses and may serve as novel biomarkers to predict prognosis and response to ICIs.

The systematic review was conducted according to PRISMA guidelines and registered in PROSPERO (CRD420251030158). Databases were searched from January 2010 to July 2025 for studies evaluating lncRNA expression in adult cancer patients treated with ICIs. Eligible studies assessed associations between lncRNAs expression and survival outcomes after ICI treatment.

After selection, 31 studies across multiple cancer types, were included. Most studies were retrospective bioinformatic analyses of public datasets and focused on ICI therapies. lncRNA-based signatures consistently demonstrated prognostic value by stratifying patients into groups with significantly different survival outcomes and were associated with variations in ICI response across multiple cancer types.

LncRNAs represent promising prognostic and predictive biomarkers for ICI. Prospective validation and standardized analytical approaches are needed to support their clinical translation in precision immuno-oncology.

https://www.crd.york.ac.uk/PROSPERO/, identifier CRD420251030158.