We examined associations of county- and tract-level Social Vulnerability Index (SVI) with survival and treatment-related outcomes in adults with IDH-wildtype glioblastoma (GBM) or IDH-mutant grade 4 astrocytoma.

Adults treated at MD Anderson from 2020 to 2025 with PROACTIVE consent, survival follow-up, and Texas residential data were included. The 2022 CDC/ATSDR SVI was modeled per 0.1 increase (10 percentile points). Primary Cox models for GBM adjusted for age, sex, performance status, extent of resection, MGMT methylation, insurance, and distance. Proportional hazards were assessed using Grambsch-Therneau tests.

Cohorts included 398 patients with GBM and 62 with IDH-mutant grade 4 astrocytoma. In GBM, SVI was not associated with survival in county-level analyses (HR per 0.1 increase, 1.00; 95% CI, 0.96-1.05; P = 0.920) or Houston-area tract-level analyses (HR, 1.05; 95% CI, 0.98-1.13; P = 0.176). In exploratory time-varying analysis, the SVI-mortality association attenuated over follow-up (interaction P = 0.028). Higher tract-level SVI was associated with greater odds of not undergoing gross-total resection (OR, 1.19; 95% CI, 1.07-1.33; q = 0.010) and lower odds of clinical-trial treatment (OR, 0.81; 95% CI, 0.71-0.92; q = 0.008). No significant survival association was identified in exploratory astrocytoma analyses.

Among patients who reached tertiary neuro-oncology care, primary Cox models did not identify a statistically significant association between SVI and survival. Higher tract-level SVI was associated with less extensive resection and lower odds of clinical-trial treatment.

Postoperative hydrocephalus is a common complication following posterior fossa tumor resection, affecting 7-40% of patients. Although preoperative cerebrospinal fluid (CSF) diversion may be required in selected patients with hydrocephalus, decisions remain individualized in routine neurosurgical practice. We therefore developed and externally validated a model to provide supplementary preoperative risk stratification using routinely available variables. We retrospectively analyzed 1,073 patients following resection of posterior fossa tumors (PFTs) treated at five tertiary centers between 2013 and 2024, dividing them into a development cohort (n = 854) and an external validation cohort (n = 219). We initially screened 30 perioperative variables from the multicenter dataset and then selected a clinically implementable model restricted to variables available before tumor resection. Feature importance was ranked using Shapley additive explanations (SHAP), and seven distinct machine learning (ML) algorithms were evaluated. Model performance was comprehensively measured using the area under the receiver operating characteristic curve (AUC), sensitivity, specificity, precision-recall curves, and decision curve analysis. The final clinically implementable model included three preoperative variables: Evans index, tumor-fourth ventricle relationship, and preoperative cerebrospinal fluid diversion status. In the external validation cohort, the support vector machine model showed good external discrimination, with an area under the receiver operating characteristic curve of 0.877, accuracy of 81.3%, sensitivity of 80.8%, and specificity of 81.7%. Logistic regression achieved comparable discrimination. Calibration assessment suggested dataset shift between the development and external validation cohorts, indicating that absolute predicted probabilities should be interpreted cautiously in populations with different baseline risks. A concise three-variable preoperative model showed good external discrimination for clinically relevant postoperative hydrocephalus after posterior fossa tumor resection. The model may support preoperative risk communication and postoperative surveillance planning, but should not be used as a stand-alone indication for cerebrospinal fluid diversion. Prospective validation and local recalibration are warranted before routine clinical implementation.

Treatment choices for metastatic non-small-cell lung cancer (NSCLC) after first-line targeted therapy progression are heterogeneous. This study aimed to characterize real-world treatment patterns and outcomes of advanced NSCLC harboring actionable genomic alterations (AGAs) in second- (2 L) or third-line (3 L) settings. This retrospective cohort study across six Chinese centers included stage IV NSCLC patients with confirmed AGAs. Therapies were divided into six categories: targeted monotherapy (T), targeted combinations (T+), chemotherapy monotherapy (C), chemotherapy combinations (C+), anti-angiogenic monotherapy (A), and other regimens (O). The primary outcome was the treatment pattern. Secondary outcomes included biomarker testing and effectiveness. A total of 658 patients were enrolled, with the majority harboring EGFR mutations (n = 590, 89.7%). In the 2 L-enrolled group (n = 602), T use declined from 75.3% in the 1 L setting to 49.3% in 2 L, while utilization of A + C increased to 16.5%. Within the EGFR-mutant subgroup, therapeutic sequences were highly dependent on 1 L TKI generation and T790M resistance status. Over half (51.1%) of T790M-negative patients continued T in 2 L following progression on 1 L first- or second-generation TKIs. Among the 3 L-enrolled patients (n = 56), A + C (35.7%) and C (14.3%) were predominant. The overall median real-world progression-free survival for the 2 L-enrolled group was 7.4 months in the 2 L setting (7.5 months for the EGFR-mutant subgroup) and 5.4 months in 3 L. This multicenter real‑world cohort predominantly comprised patients with EGFR‑mutant NSCLC, with smaller numbers of other AGA subtypes. Targeted therapies remain the cornerstone of later-line advanced NSCLC management. The prevalent real-world reliance on continued TKI therapy, even in T790M-negative patients, highlights the clinical dilemma of limited post-resistance options and the need to integrate emerging novel therapeutics.

Breast cancer (BC) is the most commonly diagnosed malignant disease in women worldwide. Resistance to neoadjuvant chemotherapy (NAC) still limits treatment efficacy despite the enormous progress in systemic therapy. Because pathological complete response (pCR) is strongly associated with favorable clinical outcomes, especially in triple-negative and HER2-positive breast cancer, the discovery of reliable predictive biomarkers before treatment has become a key clinical goal. This narrative review summarizes the available evidence of genetic and transcriptomic biomarkers associated to responses to conventional anthracycline, taxane and platinum-based NAC. Current evidence suggests biomarkers can be broken down into three interconnected biological pathways. Dysregulation of immune and interferon signaling, including interferon-stimulated genes (ISG15, IFIH1, MX1, OAS family, IFI27, and IFITM1), affects chemotherapy response by modulating immune activation, apoptosis, and DNA damage tolerance. Second, alterations in DNA damage response (DDR) pathways for BRCA1, TP53, PARP1, ATM, and CHK1 affect the cells' vulnerability to genotoxic stress and contribute to the subtype-specific differences in treatment efficacies. Third, dysregulated cell cycle components (CCND1, CDK4/6, RB1, and E2F1) affect proliferation, checkpoint control, and susceptibility to chemotherapy-induced apoptosis. These pathways act in concert, rather than as independent mechanisms, to influence NAC sensitivity. Available data suggest that no single biomarker has sufficient predictive accuracy for all breast cancer subtypes. Subtype-specific multi-gene models integrating immune, DDR and cell-cycle biomarkers represent a more powerful tool to predict pCR and improve patient stratification before NAC. Further prospective clinical validation is needed before these biomarkers can be implemented in routine clinical practice.

This study aimed to evaluate the role and optimal timing of radiotherapy following intensive chemotherapy in infants with medulloblastoma (MB), and to explore whether molecular subtyping may inform radiotherapy timing strategies.

We conducted a retrospective cohort study including 105 children aged < 3 years with MB treated at Beijing Shijitan Hospital, Capital Medical University, between 2013 and 2023. Clinical data were collected to compare clinical characteristics and survival outcomes across different radiotherapy strategies.

Among 105 infants with MB, 67 (63.8%) were classified as SHH, 18 (17.1%) as Group 3, and 20 (19.0%) as Group 4, with no WNT cases identified. The SHH subgroup demonstrated significantly better survival than the Non-SHH subgroup (comprising Group 3 and Group 4), with 3-year overall survival (OS) of 80.2% versus 46.0% and progression-free survival (PFS) of 62.6% versus 30.4% (both P < 0.001). Patients were stratified into chemotherapy-only, upfront radiotherapy, and salvage radiotherapy groups based on treatment timing. In SHH patients, upfront radiotherapy did not confer additional survival benefit over chemotherapy alone (P = 0.658), whereas salvage radiotherapy was associated with longer observed OS (P = 0.005). In contrast, in the Non-SHH subgroup, chemotherapy alone was associated with a high progression rate (85.7%), and radiotherapy was associated with improved survival outcomes.

Real-world data demonstrate distinct differences between SHH and Non-SHH infant MBs in survival outcomes and radiotherapy strategies. The SHH subtype showed favorable survival with systemic chemotherapy, whereas the Non-SHH subtype exhibited limited disease control with chemotherapy alone, suggesting a more critical role for radiotherapy in this population.

Dasatinib absorption is pH-dependent, and concomitant use of Proton Pump Inhibitors (PPIs) can substantially reduce dasatinib exposure. Whether this interaction has clinical relevance and affects treatment outcomes in patients with chronic myeloid leukemia (CML) remains unclear. This retrospective cohort study used German statutory health insurance claims data (2010 - 2024). Adults with CML who initiated dasatinib treatment were selected. Patients were classified according to concomitant PPI use around dasatinib initiation. The primary endpoint was time to switch to another systemic CML therapy. Two analytical cohorts were evaluated (incident and prevalent cohorts). Propensity score matching and Cox proportional hazards models were used to compare patients with and without PPI co-medication. Sensitivity analyses censored follow-up at severe adverse events and restricted the population to users of the originator dasatinib formulation. Among 297 dasatinib patients in the incident and 372 in the prevalent cohort, PPI co-medication was observed in approximately 19-21% of patients. After matching, concomitant PPI use was consistently associated with earlier treatment switching. This association reached statistical significance in the prevalent cohort (hazard ratio: 1.87, 95% CI 1.18-2.95; p = .008) and was directionally consistent in the incident cohort. Sensitivity analyses yielded directionally consistent findings. In this large real-world analysis, concomitant PPI use was associated with earlier treatment switching in dasatinib-treated patients with CML. While causality cannot be established, these findings are consistent with the known pH-dependent interaction and reinforce existing recommendations to avoid PPI co-medication during dasatinib therapy whenever feasible.

Children with solid tumors are highly vulnerable to treatment-related nutritional compromise. However, longitudinal data describing how dietary intake and nutritional risk evolve during therapy remain limited. This study aimed to examine longitudinal changes in dietary intake adequacy and nutritional risk across different phases of oncological treatment and to identify clinically vulnerable periods requiring intensified supportive care.

In this prospective longitudinal study, children aged 8-18 years with newly diagnosed solid tumors were assessed at three predefined treatment phases (early-, mid-, and late-treatment). Dietary intake was evaluated using interviewer-verified 3-day food records at each time point. Energy and nutrient intakes were expressed as percentages of age- and sex-specific estimated requirements. Nutritional risk was assessed using the Screening Tool for Childhood Cancer Nutrition Risk (SCAN). Longitudinal changes were analyzed using non-parametric repeated-measures methods, and associations with gastrointestinal symptoms and taste alterations were explored.

Sixty children completed all assessments. Energy adequacy was below recommended levels at all assessment points and declined significantly over time (p = 0.001), with most patients failing to meet recommended energy requirements throughout treatment. Significant reductions were observed in carbohydrate, fat, dietary fiber, and selected micronutrients, particularly iron and magnesium. Absolute protein intake remained statistically unchanged over time, whereas the relative contribution of protein to total energy intake increased significantly. More than 80% of patients were classified as being at nutritional risk at all time points. Higher nutritional risk scores were significantly associated with greater gastrointestinal symptom burden and taste alterations (all p < 0.05). Nutritional vulnerability was present across all assessment points. The mid-treatment phase was characterized by relatively greater deterioration in dietary adequacy and nutritional risk indicators; however, inadequate intake and elevated nutritional risk persisted throughout treatment.

Children with solid tumors experience progressive deterioration in dietary intake adequacy during oncological treatment, with nutritional vulnerability evident across the treatment trajectory and relatively greater deterioration observed during mid-treatment. Future supportive care strategies should move beyond monitoring intake alone and focus on identifying modifiable factors driving dietary decline, including gastrointestinal symptoms and taste alterations, to determine the extent to which this deterioration can be prevented or reversed and when nutritional interventions may be most effective.

To evaluate the proportion of expressed programmed cell death ligands-1 (PD-L1) in epithelial ovarian carcinoma patients, and the association with the clinicopathological, surgical outcomes, and oncologic outcomes. To compare PD-L1 protein expression with messenger ribonucleic acid (mRNA) expression.

The patients who had pathology of epithelial ovarian/tubal/peritoneal carcinoma were enrolled. The demographic data, tumor characteristics, surgical outcomes, treatment details, and treatment response were analyzed by descriptive statistics. Spearman's rank correlation coefficient test was used to determine the correlation between protein expression and mRNA expression. The survival curve was developed utilizing the Kaplan-Meier method, the log-rank test was used to compare survival distributions of patients according to the PD-L1 protein expression.

A total of 100 patients, with high-grade serous carcinoma being the most common subtype (42%). Advanced-stage disease was present in 49% of patients, and 65% achieved optimal cytoreduction. PD-L1 protein expression was detected in 23% of tumors, while the median normalized mRNA expression was 0.015 (IQR 0.004-0.037). A moderate positive correlation was observed between PD-L1 protein and mRNA expression (Spearman's rho = 0.407, p < 0.001). The mean progression-free survival (PFS) and overall survival (OS) were 44.32 ± 4.04 months and 74.19 ± 3.33 months, respectively.

PD-L1 protein expression was observed in a minority of patients and was not significantly associated with survival outcomes. There was a moderate correlation between PD-L1 protein and mRNA expressions.

Persistent oncogenic HPV infection can cause cervical epithelial changes leading to premalignant lesions such as CIN2. Active surveillance, a conservative option, reduces exposure to excisional risks while allowing timely treatment when needed. However, little is known about clinicians' perspectives, acceptability, and experience of offering active surveillance in the Australian healthcare context.

To explore gynaecologists' perspectives, acceptability, and experiences in providing active surveillance to women diagnosed with CIN2.

Individual semi-structured interviews were conducted with obstetrics and gynaecology specialists and trainees in secondary and tertiary healthcare settings across Australia. Data were analysed using inductive thematic analysis.

Twenty-five in-depth interviews were conducted. Participants expressed positive views about active surveillance, regarding it as a safe option that does not increase long-term cancer risk. When formulating management recommendations for CIN2, participants considered various interrelated diagnostic, patient, clinician, and policy-level factors. To support shared decision-making, participants used several communication strategies such as anatomical models and visual images to help address patient knowledge gaps and they provided patients with time and space to reflect on their preferred management plan. Participants identified strategies that could support offering active surveillance and patients' adherence to this, including enhanced clinician education and training, increased resourcing, and improved use of information technology to support follow-up tests for active surveillance.

A deeper understanding of multi-level factors influencing clinicians' recommendations and implementation of active surveillance for CIN2 may inform the development of targeted interventions to address barriers and strengthen enablers, ultimately supporting wider offering of active surveillance.

Parental cancer effects millions of children worldwide. We estimated the number of children influenced by paternal cancer and paternal orphans, and examined changes in their numbers and annual rates over time, with a focus on time trends and the influence of cancer type.

Male cancer patients aged ≥15 years, diagnosed since 1953, were identified from the Finnish Cancer Registry. Cancer deaths and information on live births were obtained from Statistics Finland. Annual number of new children and prevalent children whose father was diagnosed with cancer and the annual number of new orphans and prevalent orphans due to paternal cancer death for 1970-2022 were estimated indirectly by combining cancer incidence and mortality data with population-level fertility rates.

The estimated age-standardized rate of new children with paternal cancer increased from 96/100,000 children in 1970-1974 to 163/100,000 in 2017-2021. The annual rate of new paternal orphans decreased from 56/100,000 in 1970-1974 to 35/100,000 in 2017-2021. The rate of new children increased 1.1% per year while the rate of new orphans decreased 1.1% in 1970-2021.

Although the number of paternal orphans is decreasing due to improved cancer survival, the number of children influenced by paternal cancer is rising reflecting the increasing cancer incidence and resulting in more children vulnerable to the harmful effects of paternal cancer.