This review synthesizes current evidence on the global epidemiology and prevention of lung cancer, with a focused analysis of the Southeastern Europe region. Lung cancer remains the leading cause of cancer-related mortality worldwide, reflecting persistent exposure to modifiable risk factors and substantial inequities in early detection and treatment access. Data from GLOBOCAN, the Global Burden of Disease study, randomized controlled trials, and population-based registries were used to assess trends in incidence, mortality, and survival, and to examine the evolving distribution of histological subtypes and molecular profiles. While tobacco smoking remains the leading risk factor, a growing proportion of lung cancer, especially among never-smokers, is attributable to non-tobacco exposures, including ambient and household air pollution, occupational carcinogens, and residential radon. Despite advances in targeted therapies and immunotherapy, overall survival remains poor, largely due to late-stage diagnosis. Evidence from landmark trials demonstrates that low-dose computed tomography (LDCT) screening reduces lung cancer mortality primarily through stage migration, enabling detection at earlier, more treatable stages. Southeastern Europe continues to experience a high burden driven by tobacco exposure, limited screening implementation, and restricted access to molecular diagnostics. Inequities in screening eligibility, uptake, and access to advanced therapies worsen survival outcomes across socioeconomic and demographic groups. CONCLUSIONS: Effective lung cancer control requires a multilevel prevention strategy integrating strengthened tobacco control policies, risk-stratified LDCT screening, and equitable access to molecular testing and treatment. Future research priorities include understanding lung cancer in never-smokers, evaluating long-term risks of emerging exposures such as e-cigarettes, and utilizing multi-omics approaches to refine risk stratification and guide targeted therapy.

e15181 Background: Androgen receptor splice variant 7 ( AR-V7 ) is a constitutively active androgen receptor isoform lacking the ligand-binding domain. AR-V7 is a well-established mediator of resistance to androgen receptor (AR) targeting therapies in prostate cancer (PCa). Although AR-V7 has been increasingly reported in non-prostatic malignancies, its prevalence, biological significance, and clinical relevance outside the prostate remain poorly defined. Methods: A systematic review was conducted in accordance with PRISMA guidelines. Major databases and oncology/pathology conference proceedings were searched until October 2025. Studies reporting AR-V7 expression in non-prostatic malignancies were included. Data on cancer type, AR-V7 detection methods, prevalence, treatment context, and clinical outcomes were extracted and synthesized narratively due to methodological heterogeneity. Results: Thirty-four studies encompassing 4855 clinical cases and 60 cancer cell lines were included. Overall, AR-V7 was detected in 948 cases (19.5%). Breast cancer accounted for the largest absolute number of AR-V7 –positive cases (815/948; 86.0%), although its within-cancer prevalence was modest (815/4,057; 20.1%) and highly sensitive to detection methodology. Higher proportional prevalence was observed in salivary duct carcinoma (55.2%), hepatocellular carcinoma (57.1%), and non–muscle-invasive bladder carcinoma (82.6%). AR-V7 was mostly detected in treatment-naïve cancers across several malignancies. Across breast cancer cell lines, AR-V7 expression was exclusive to AR-positive contexts and commonly co-existed with additional splice variants. Conclusions: AR-V7 is detectable across multiple non-prostatic malignancies, with marked heterogeneity by cancer type and detection method. Unlike prostate cancer, where AR-V7 typically emerges as a mechanism of acquired resistance after androgen-directed therapy, AR-V7 is present in a substantial subset of treatment-naïve extra-prostatic cancers, supporting its role as an intrinsic, tumor-specific molecular feature. Larger, prospective studies are warranted to define its prognostic and predictive utility to refine future AR-targeted strategies in precision oncology. Protocol registration: https://www.crd.york.ac.uk/PROSPERO/view/CRD420251083307.

Androgen receptor splice variant 7 (AR-V7) is associated with resistance to androgen receptor-targeting therapies in prostate cancer, but its prevalence and clinical relevance in non-prostatic cancers remain incompletely characterized. A systematic review was conducted in accordance with PRISMA guidelines. Thirty-four studies, including 4855 clinical cases and 60 cell lines, were included. Overall, AR-V7 positivity was reported in 948/4855 clinical cases (19.5%); however, this represents a descriptive estimate across heterogeneous tumor types, study designs, and detection methods. Breast cancer accounted for 4057 of 4855 clinical cases (83.6%) and 815 of 948 AR-V7-positive cases (86.0%), with a within-cancer prevalence of 20.1%. However, after excluding the TCGA cohort in which AR-V7 was inferred through splice-junction analysis, the prevalence of AR-V7-positive breast cancer decreased to 9%. Higher tumor-specific proportions were observed in salivary duct carcinoma (55.2%), hepatocellular carcinoma (57.1%), and non-muscle-invasive bladder cancer (82.6%), but these estimates were based on smaller cohorts and should be interpreted cautiously. AR-V7 was present in several treatment-naive non-prostatic cancers, suggesting that it may represent a preexisting molecular feature in selected contexts. Current evidence suggests that AR-V7 warrants further investigation as a candidate biomarker. Standardized detection methods and prospective studies are needed before its clinical utility can be established.

Non-small cell lung cancer (NSCLC) remains the leading cause of cancer mortality worldwide; however, precision oncology has fundamentally transformed its treatment landscape. In 2025, seven approvals by the U.S. Food and Drug Administration (FDA) further accelerated biomarker-driven care across critical molecular subsets. These include MET-directed and trophoblast cell-surface antigen-2 (TROP-2) antibody-drug conjugates (ADCs), expanded strategies targeting epidermal growth factor receptor (EGFR), notably those addressing exon 20 insertion mutations, a ROS proto-oncogene 1 (ROS1) inhibitor, and various human epidermal growth factor receptor 2 (HER2) options that encompass both tumor-agnostic and mutation-selected approaches. These advancements underscore the necessity for integrated diagnostics—such as next-generation sequencing (NGS), fluorescence in situ hybridization (FISH), and immunohistochemistry (IHC)—while also emphasizing ongoing challenges in biomarker selection, therapeutic sequencing, and equitable global implementation.

BACKGROUND:Developing countries face limited access to targeted treatments for patients with advanced epithelial ovarian cancer (EOC). The CA-125 ELIMination rate constant K (KELIM), calculated from longitudinal CA-125 measurements during the first 100 days of treatment, serves as an early indicator of tumour chemosensitivity. The primary objective of this study was to evaluate the value of the KELIM score in predicting progression-free survival (PFS) and overall survival (OS) in patients with EOC treated with adjuvant or neoadjuvant chemotherapy. METHODS:The records of patients with EOC (International Federation of Gynecology and Obstetrics stage II-IV) treated at the University Clinical Hospital Mostar (Bosnia and Herzegovina) between 2013 and 2023 were analysed retrospectively. Patient characteristics, outcomes and KELIM score were assessed during the first 100 days of treatment. KELIM scores were categorized as favourable (≥1.0) or unfavourable (<1.0). RESULTS:KELIM scores were assessed in 92 patients: 36 (39 %) were classified in the favourable group and 56 (61 %) in the unfavourable group. Patients in the favourable KELIM group achieved complete cytoreduction significantly more often (p < 0.001) and demonstrated longer platinum-free intervals (PFI), with most having PFI > 12 months (p = 0.005). In contrast to OS (p = 0.442), PFS was significantly longer in the favourable KELIM group [29.0 months, 95 % confidence interval (CI) 8.45-49.55] compared with the unfavourable KELIM group (13.0 months, 95 % CI 10.56-15.44; p < 0.001). CONCLUSION:In this real-world cohort from a resource-limited setting, a favourable KELIM score was associated with greater early chemosensitivity, longer PFI, improved PFS, and a higher rate of complete cytoreduction in patients with EOC. The KELIM score has been validated in real-world settings and post-hoc analyses of prospective studies, and can be applied easily in routine clinical practice for patients with EOC treated with adjuvant or neoadjuvant chemotherapy, providing a useful prognostic, predictive, pragmatic and cost-effective tool to support risk stratification and inform therapeutic decision-making. Further prospective validation is still required for biomarker-guided treatment selection.

Background: Breast cancer (BC) is one of the most common cancers worldwide, and metastasis is its worst aspect and the first cause of death. Metastasis is a multistep process, where invasion is a recurring event. The process of BC cell invasion involves, in general, three major factors including, cell adhesion molecules (CAM), proteinases, and growth factors. CD44, a family of CAM proteins and the hyaluronic acid (HA) cell surface receptor, acts as cell differentiation, cell migration/invasion, and apoptosis regulator. To better understand the molecular mechanisms that underpin CD44-promoted BC cell invasion, our previous microarray gene expression profiling, using “TET-OFF” BC CD44-inducible cell experimental model, identified ITGB1BP1 as a novel potential transcriptional target of CD44. Methods: to test this hypothesis, both in vitro BC cell model, as well as ex-vivo tissue microarray (TMA) slides, containing adjacent sections from breast tumors of 113 BC patients were examined for the expression of both CD44 and its potential target gene expression, ITGB1BP1, by immunohistochemistry (IHC). Results: in vitro results revealed that HA-activation and induction of CD44 increased significantly the expression of its target gene, ITGB1BP1. Furthermore, IHC analysis of TMAs showed that overall 90% of the samples exhibited high CD44-immunostaining in the membrane while its target ITGB1BP1 was mainly observed in the cytoplasm and occasionally in the membrane. More interestingly, the patterns of expression of CD44 and its target ITGB1BP1 showed a parallel increase in the majority of highly invasive/metastatic tumor tissues when compared to less invasive breast tumor tissues. Consclusion: the present study provides for the first time substantial evidence supporting our hypothesis that ITGB1BP1is a potential novel transcriptional target that underpin CD44-promoted BC tumor cell progression.

Objective: To investigate paper mill involvement and fake peer review among retracted systematic reviews and meta-analyses (SR/MAs), and to compare paper mill–associated and non–paper mill retracted SR/MAs with respect to temporal patterns, disciplinary profile, country of origin, and retraction characteristics. Study Design and Setting: Cross-sectional study based on the Retraction Watch database. Records were screened to identify retracted SR/MAs. Paper mill status was assigned only when paper mill involvement was explicitly stated in the retraction information. Fake peer review was coded separately. Group comparisons used Pearson χ² and Mann–Whitney U tests. Associations with paper mill status were estimated using univariable Poisson regression with robust variance and reported as prevalence ratios (PRs) with 95% confidence intervals (CIs). Results: Among 69,163 retracted publications in the Retraction Watch dataset, 1,071 (1.5%) were identified as retracted SR/MAs. Of those, 191 (17.8%) were paper mill–associated and 880 (82.2%) were not. China accounted for 732/1,071 (68.3%) of all retracted SR/MAs and 177/191 (92.7%) of paper mill–associated SR/MAs. The annual number of paper mill–associated SR/MAs peaked in 2023 (n=152). Compared with non–paper mill SR/MAs, paper mill–associated SR/MAs had a longer median time to retraction (511 vs 459 days; p=0.024), more frequent results-related concerns (89.0% vs 30.0%), data issues (53.4% vs 17.5%), referencing concerns (53.9% vs 13.6%), and ethical concerns (8.9% vs 2.6%) (all p<0.001), and less frequent multi-country authorship (8.9% vs 17.6%; p=0.004). In univariable Poisson regression analyses, paper mill status was associated with Chinese origin (PR 5.86, 95% CI 3.45–9.93), more recent publication year (PR 1.20 per 1-year increase, 95% CI 1.16–1.23), medical broad domain (PR 3.66, 95% CI 1.66–8.08), and results-related concerns (PR 11.88, 95% CI 7.68–18.39). Conclusion: Paper mill activity has affected the evidence-synthesis literature and accounted for a substantial proportion of retracted SR/MAs in this Retraction Watch–based analysis. Paper mill–associated SR/MAs showed a distinct profile characterized by strong concentration in China, clustering in recent years, and higher prevalence of major publication-related concerns, supporting the view that paper mill contamination poses a direct threat to the credibility of SR/MAs.

A commercial biorepository of tumor samples with associated clinical data is crucial for discovering and validating biomarkers and advancing all stages of cancer research. Although oncogenic fusions are highly specific and attractive drug targets, the progress is limited by their diversity and low (1-4%) prevalence in solid tumors, outside prostate adenocarcinoma (>30% with a characteristic TMPRSS2::ERG fusion). Systematic, cost effective evaluation of banked tumor samples for the oncogenic fusions could accelerate such research efforts. We examined formalin-fixed paraffin-embedded tumor samples from a commercial biorepository (Reference Medicine, Phoenix, AZ) using a workflow which included expert pathology review, whole slide scanning, construction of multi-tumor tissue microarrays (TMA) immunohistochemistry (IHC) and genomic profiling with commercially available next generation sequencing (NGS) panels. More than 500 tumors were reviewed by board-certified pathologists; selected cases were then cored for TMAs. Immunohistochemistry for ALK and ROS1 proteins' expression were performed on TMAs. IHC for ALK and ROS1 identified two positive cases, one for ROS1 and one for ALK. Thirty eight tumors underwent NGS and both IHC-positive cases were confirmed to harbor gene fusions (EML4::ALK and EZR::ROS1, respectively). All other cases were fusion-negative, concordant with the IHC result. Properly characterized tissue samples are essential for image analysis, biomarker detection and genomic profiling. Rigorous pathologic review helps avoid archiving of poorly preserved samples. IHC screening of TMAs provides a cost-effective approach for identification of fusion events, particularly in non-small cell lung carcinomas, while preserving material for multiple downstream applications. Zoran Gatalica, Inga Rose, Semir Vranic. Detection of fusion oncogenes in routinely collected biorepository samples [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Fusion-Positive Cancer: From Discovery to Therapy; 2026 Jan 13-15; Philadelphia PA. Philadelphia (PA): AACR; Cancer Res 2026;86(1_Suppl):Abstract nr A005.

Immunohistochemistry (IHC) is central to precision oncology in advanced non-small cell lung cancer (NSCLC), although its predictive value and the need for molecular confirmation differ across biomarkers. This narrative review aimed to summarize the clinical utility, validated assays, scoring systems, diagnostic performance, and testing algorithms for predictive IHC biomarkers in NSCLC. Recent guidelines, regulatory documents, and selected analytical and clinical studies were reviewed for programmed death-ligand 1 (PD-L1), anaplastic lymphoma kinase (ALK), ROS proto-oncogene 1 receptor tyrosine kinase (ROS1), mesenchymal–epithelial transition factor receptor (c-Met), B-Raf proto-oncogene serine/threonine kinase V600E (BRAF V600E), pan-tropomyosin receptor kinase (pan-TRK), human epidermal growth factor receptor 2 (HER2), and epidermal growth factor receptor (EGFR). PD-L1 and ALK are established IHC-based predictive assays, although PD-L1 interpretation remains assay-, platform-, and cutoff-specific. VENTANA ALK D5F3 and VENTANA MET SP44 RxDx are clinically validated companion diagnostics, whereas HER2 IHC score 3+ may support eligibility for trastuzumab deruxtecan in the tumor-agnostic setting. ROS1, BRAF V600E, pan-TRK, and non-companion-diagnostic c-Met or HER2 assays are best used for screening or triage and generally require molecular confirmation. EGFR mutation-specific IHC is not recommended because of insufficient diagnostic performance. Overall, IHC enables rapid, tissue-sparing biomarker assessment but should be integrated with broad genomic and transcriptomic next-generation sequencing (NGS), particularly when alteration-specific findings are negative, equivocal, or discordant.

Introduction:Mucoepidermoid carcinoma (MEC) of the breast is an exceptionally rare salivary gland-type malignancy with uncertain prognostic behaviour. This study compared the clinicopathologic characteristics, treatment patterns, and survival outcomes of MEC and invasive ductal carcinoma not otherwise specified (IDC-NOS) using Surveillance, Epidemiology, and End Results (SEER) data. Material and methods:A retrospective cohort analysis of SEER data (1975-2022) identified cases with MEC (n = 42) and IDC-NOS (n = 50,881). Demographic, clinicopathologic, and treatment variables were compared using χ2 and one-way analysis of variance tests. Overall survival (OS) and disease-specific survival (DSS) were analysed with Kaplan-Meier and Cox proportional hazards models. Results:Mucoepidermoid carcinoma cases were older (≥ 70 years: 91.0% vs. 31.1%; p < 0.001) and predominantly White. Compared with IDC-NOS, MEC exhibited lower HER2 positivity (0.0% vs. 31.4%), oestrogen receptor/progesterone receptor expression (31.0% and 0.0% vs. 60.1% and 52.3%), and distant metastasis (0.0% vs. 20.1%) (all p < 0.001). Mucoepidermoid carcinoma cases were less likely to undergo surgery (85.7%) or receive systemic therapy (40.5%, p < 0.05). Only five deaths (OS) and three (DSS) occurred among MEC cases. Kaplan-Meier curves showed similar early survival, but MEC survival plateaued after 120 months, whereas IDC-NOS declined steadily. Multivariable Cox analysis revealed higher all-cause mortality for IDC-NOS (adjusted hazard ratios [HR] = 3.80, 95% CI: 1.18-12.22), with no significant difference in cancer-specific mortality (HR = 2.32, 95% CI: 0.71-7.58). Conclusions:Mucoepidermoid carcinoma exhibits distinct clinicopathologic features, limited metastatic potential, and favourable long-term survival despite frequent triple negativity. Its indolent course supports conservative management for low-grade cases, warranting further molecular and prognostic studies.

This response to the letter expands the discussion on the evolving demands of peer review for systematic reviews and meta-analyses. We emphasize that the main concern surrounding artificial intelligence is not its limited and disclosed use for language support, but undisclosed application and insufficient human verification, which may compromise citation accuracy, interpretation, and overall trustworthiness. We also argue that similarity reports should be interpreted contextually, particularly in evidence syntheses where standardized methodological language is unavoidable, and that low similarity does not necessarily exclude manuscript manipulation. Finally, we highlight reference verification as a central research-integrity challenge that should not rest on peer reviewers alone. Preserving the credibility of evidence synthesis requires shared responsibility across authors, reviewers, editors, and publishers.

Colorectal cancer (CRC) is the second leading cause of cancer-related death. The tumor immune microenvironment plays a critical role in tumor progression and immune evasion. B7-H3 (CD276), a member of the B7 family of immune checkpoint molecules, is frequently overexpressed in a variety of malignancies, including CRC. A systematic search of the literature was performed to identify studies evaluating B7-H3 in CRC. Data were extracted on study characteristics, B7-H3 expression and detection methods, molecular and signaling pathways, and clinical outcomes. Study quality and risk of bias were assessed using the MASTER scale, and findings were synthesized using a structured narrative approach. Sixty-three studies were included. B7-H3 expression was commonly reported but demonstrated substantial variability, largely driven by differences in detection and scoring methodologies. Preclinical evidence suggests that B7-H3 may contribute to tumor growth, invasion, immune evasion, and resistance to radio- and chemotherapy, potentially through pathways such as PI3K–AKT–mTOR, JAK–STAT, MAPK/ERK, NF-κB, VEGF/hypoxia, and Wnt/β-catenin. Preclinical studies have demonstrated that targeting B7-H3 may improve radiotherapy response and reduce metastatic burden in murine CRC models. However, these findings should be considered preliminary and are not yet supported by clinical evidence in humans. B7-H3 targeting remains an emerging therapeutic approach that requires further clinical validation. However, significant methodological heterogeneity in detection and scoring limits comparability across studies and precludes definitive conclusions regarding its clinical utility. B7-H3 should therefore be considered a candidate biomarker and further standardized. Prospective studies are needed to clarify its diagnostic, prognostic, and therapeutic relevance in CRC.

OBJECTIVES:To investigate reported paper mill involvement among retracted systematic reviews and meta-analyses (SR/MAs), and to compare retracted SR/MAs with and without reported paper mill involvement with respect to temporal patterns, disciplinary profile, country recorded in the database, and retraction characteristics. STUDY DESIGN AND SETTING:Cross-sectional study based on the Retraction Watch Database. Records were screened to identify retracted SR/MAs. Reported paper mill involvement was assigned only when explicitly stated in the Retraction Watch record or associated retraction information; fake peer review was coded separately. Group comparisons used the Pearson chi-square and Mann-Whitney U tests. Associations with reported paper mill involvement were estimated using univariable Poisson regression with robust variance and reported as prevalence ratios (PRs) with 95% confidence intervals (CIs). These analyses were treated as exploratory, noninferential internal contrasts within the dataset of already retracted SR/MAs. RESULTS:Among 69,163 retracted publications in the Retraction Watch dataset, 1071 (1.5%) were identified as retracted SR/MAs. Of those, 191 (17.8%) were paper mill-associated and 880 (82.2%) were not. In the database country field, China was recorded for 732/1071 retracted SR/MAs (68.3%) and 177/191 SR/MAs with reported paper mill involvement (92.7%). The annual number of paper mill-associated SR/MAs peaked in 2023 (n = 152). Within this restricted dataset, paper mill-associated SR/MAs had a longer median time to retraction (511 vs 459 days; P = .024), more frequent results-related concerns (89.0% vs 30.0%), data issues (53.4% vs 17.5%), referencing concerns (53.9% vs 13.6%), and ethical concerns (8.9% vs 2.6%) (all P < .001), and less frequent multicountry authorship (8.9% vs 17.6%; P = .004). In univariable Poisson regression analyses restricted to retracted SR/MAs, larger observed proportions of reported paper mill involvement were seen among records linked to China in the database country field (PR: 5.86, 95% CI: 3.45-9.93), more recent publication years (PR 1.20 per 1-year increase, 95% CI 1.16-1.23), the medical broad domain (PR 3.66, 95% CI 1.66-8.08), and records with results-related concerns (PR 11.88, 95% CI 7.68-18.39). These PRs should not be interpreted as likelihoods, risks, or rates beyond the analyzed Retraction Watch subset. CONCLUSION:In this Retraction Watch-based analysis, reported paper mill involvement was identified in 191/1071 retracted SR/MAs (17.8%). These records were most often linked to China in the database country field (177/191; 92.7%) and clustered in recent years, particularly 2023. These findings should be interpreted as descriptive patterns within detected and retracted records, not as country-level rates, comparative performance indicators, or estimates of the true prevalence of paper mill activity. PLAIN LANGUAGE SUMMARY:Paper mills are organizations that produce fraudulent scientific papers for payment. Most research on paper mills has focused on primary studies, but less is known about their role in systematic reviews and meta-analyses (SR/MAs), which represent high-level evidence and can directly influence clinical decisions, guidelines, and future research. This study examined retracted SR/MAs in the Retraction Watch Database to describe how often paper mill involvement was reported and how these records differed from other retracted SR/MAs. Among 1071 retracted SR/MAs, 191 were explicitly identified as paper mill-associated. These records were most often linked to China in the database country field, were more common in recent retraction years, and more often involved concerns related to results, data, references, and ethics. These findings describe detected and retracted records indexed in Retraction Watch and should not be interpreted as country-level rates or as the true prevalence of paper mill activity in all SR/MAs. The study highlights the need for clearer retraction notices and better safeguards for identifying unreliable evidence syntheses.

Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with a high risk of early central nervous system dissemination and poor outcomes after brain metastasis (BM). This systematic review summarizes current evidence on incidence, treatment strategies, outcomes, guidelines, and ongoing trials in TNBC-associated BM. The review followed PRISMA guidance and was registered in the Open Science Framework (OSF.IO/6TDRF). MEDLINE, Scopus, Web of Science, DOAJ, and ClinicalTrials.gov were searched through January 17, 2026. Eligible records comprised randomized trials, prospective, retrospective, and ambispective cohorts, registry analyses, case series, guideline or consensus documents, and registered clinical trials reporting TNBC-specific CNS data. Data were extracted independently and synthesized descriptively because clinical and methodological heterogeneity precluded quantitative meta-analysis. Forty-three records met the inclusion criteria: 27 clinical studies (25 addressing parenchymal brain metastases and two addressing leptomeningeal metastases), seven guideline or consensus documents, and nine ongoing clinical trials. Across clinical studies, 67,290 patients were included; 2,555 patients had TNBC and developed CNS involvement. SRS achieved 1-year local control rates of 90–99

Aim: To determine whether immunohistochemical B7-H3 expression is associated with magnetic resonance imaging (MRI)-derived tumour volume, peritumoral brain oedema volume, and oedema index in adult gliomas. Methods: This retrospective radiopathological correlation study included 99 consecutive patients with histopathologically confirmed intracranial gliomas surgically treated between 2013 and 2021. B7-H3 expression (clone RBT-B7H3, Bio SB, USA) was evaluated using staining intensity, percentage of positive tumour cells, and a composite immunoreactive score (IRS). Tumour volume (TV), peritumoral brain oedema volume (PTBE), and oedema index (EI) were calculated from orthogonal MRI measurements. Spearman correlation and crude and adjusted linear regression were used. Adjusted models included age, sex, tumour grade, and Ki-67. Results: Median TV was 29.31 cm3 (IQR 12.17-49.12), median PTBE was 84.51 cm3 (IQR 47.59-178.18), and median EI was 4.56 (IQR 3.83-5.00). B7-H3 IRS correlated strongly with TV (r=0.921, p<0.001) and PTBE (r = 0.920, p < 0.001), but not with EI (r = -0.105, p = 0.299). After adjustment, B7-H3 IRS remained associated with ln(TV) (beta = 0.228, 95% CI 0.190-0.265, p < 0.001) and ln(PTBE) (beta = 0.178, 95% CI 0.152-0.204, p < 0.001), but not with EI (beta = 0.001, 95% CI -0.083 to 0.084, p = 0.990). Conclusion: B7-H3 expression is independently associated with MRI-derived tumour volume and peritumoral brain oedema volume in adult gliomas, but not with oedema index, supporting its relationship with absolute MRI-visible lesion burden.

Immunotherapy with immune checkpoint inhibitors (ICI) has become a transformative pillar in cancer treatment, offering significant improvements in survival and reducing treatment-related side effects compared to traditional therapies. In gynecologic cancers, ICIs have transformed the treatment of endometrial (EC) and cervical cancers, whereas they have not demonstrated clinical benefit in ovarian cancer. This review examines the current state of ICI advancements in EC. Given the unique immunological characteristics of EC, a comprehensive understanding of advancements is crucial for optimizing decision-making and patient outcomes. While ICIs have demonstrated robust and durable efficacy in dMMR/MSI-H EC, the magnitude of benefit in pMMR disease remains modest. Additionally, we examine promising future directions, including personalized immunotherapy approaches and novel combination therapies (e.g. antibody-drug conjugates, PARP inhibitors, antiangiogenic drugs).

PURPOSE:Acinic cell carcinoma (ACC) of the breast is a very rare, primary salivary gland-type breast malignancy, with ~100 reported cases in the literature. Limited information about the clinical features and outcomes of patients with ACC is available. METHODS:We utilized the Surveillance, Epidemiology, and End Results (SEER) database to identify ACC patients. For comparison, we also examined a cohort of invasive breast carcinomas of no special type (NST). RESULTS:Thirty ACC patients were identified among the more than 248 000 invasive breast carcinoma NST patients. ACCs were predominantly grade 3 carcinomas (44%) and were diagnosed at an earlier stage (67%). Hormone receptor (HR) and HER2 status data were available for only 13 patients, revealing molecular heterogeneity: HR-/HER2- (four patients), HR-/HER2+ (two patients), HR+/HER2- (four patients), and HR+/HER2+ (three patients). The median survival time for ACC patients was 19 months vs. 48 months for NST patients (p < 0.001). A complete-case approach was utilized for the adjusted analyses, restricting the sample to 46 257 patients without missing data on all relevant covariates. The adjusted Kaplan-Meier analysis indicated a more pronounced decline in survival probabilities among patients with ACC compared to those with NST, with the number at risk in the ACC group diminishing to four patients by the 30-month mark. In contrast, NST patients exhibited a more gradual decrease. In the multivariable Cox regression, which adjusted for age, TNM stage, HR/HER2, and chemotherapy, ACC histology was correlated with a 1.69-fold increase in the hazard of death (HR: 1.69; 95% CI: 0.63-4.56), although this result was not statistically significant. Age and advanced stage continued to be strong predictors of poor survival, and the inclusion of an age-time interaction enhanced the model fit. CONCLUSION:Acinic cell carcinoma of the breast is a very rare primary breast malignancy. Our study indicates potentially aggressive clinical behavior in mammary ACC; however, findings must be interpreted cautiously given inherent SEER limitations, especially regarding histologic and molecular subtyping accuracy. Further centralized studies are urgently needed for the accurate characterization of this rare entity.