Browse Articles

Oral Magnetoelectric Neuroimmunomodulation via the Gut–Brain–Spleen–Heart Axis for Noninvasive Atrial Fibrillation Therapy

ABSTRACT Atrial fibrillation (AF), the most common cardiac arrhythmia, is closely associated with autonomic imbalance and inflammation. While low‐level vagus nerve stimulation (LL‐VNS) offers therapeutic benefits, its clinical application is limited by the need for surgical implants. Here, we present a noninvasive, orally delivered magnetoelectric neuroimmunomodulation platform that targets the gut–brain–spleen–heart axis to deliver LL‐VNS for AF therapy. The platform comprises ingestible microparticles (MPs) embedding magnetostrictive Fe 3 O 4 @BaTiO 3 nanogenerators (FO@BTO NGs) within a conductive matrix of poly(3,4‐ethylenedioxythiophene):poly(styrenesulfonate) (PEDOT:PSS), which facilitates electrical signal transmission, and dopamine–alginate, which promotes gastric adhesion via catechol‐mediated interactions. After oral gavage in a rat AF model, MPs adhere to the stomach lining and, upon alternating magnetic activation, FO@BTO NGs generate pulsed electrical currents that stimulate vagal afferent fibers. This activates brainstem autonomic circuits, enhancing parasympathetic tone and suppressing sympathetic activity. Concurrently, it engages the splenic neuroimmune circuit via the cholinergic anti‐inflammatory pathway, thereby reducing systemic inflammation. This dual neuroimmune modulation significantly shortens AF duration and mitigates cardiac inflammation and electrical remodeling. These findings establish a clinically translatable, implant‐free strategy for delivering LL‐VNS through coordinated neural and immune pathways, offering a safe and accessible alternative to implantable systems for AF management.

ASPIRE: A randomized phase III trial of androgen deprivation therapy (ADT) plus apalutamide (A) with or without docetaxel (D) in metastatic castration-sensitive prostate cancer (mCSPC) stratified by tumor suppressor gene alterations (Alliance A032302).

TPS290 Background: Landmark randomized trials established the survival benefit of adding D to ADT in mCSPC. Building on this foundation, subsequent trials (PEACE-1 and ARASENS) demonstrated further survival improvements when androgen receptor pathway inhibitors (ARPI) were added to the ADT + D backbone. However, the independent contribution of D within the triplet regimen remains unclear given lack of prospective evaluation. Additionally, tumor suppressor gene (TSG) alterations involving TP53, PTEN, and RB1 are frequently observed in PC and are associated with aggressive biology and poor outcomes, providing an opportunity to enhance prognostic accuracy and optimize selection of candidates for treatment intensification. We hypothesize that adding D to ADT plus A will improve survival compared to ADT + A in mCSPC and stratification by TSG status may identify different treatment effects across molecular subgroups. Methods: ASPIRE is an open-label, two-arm, randomized phase 3 study to assess the benefit of D added to ADT plus A for patients with mCSPC. Eligible patients include those with confirmed adenocarcinoma of the prostate with evidence of distant metastatic disease on conventional imaging and are appropriate to receive D. Patients with metachronous low-volume disease or PSMA-PET only disease are excluded. Candidates must have next-generation sequencing (NGS) results from a CLIA-certified tissue test available for TSG status stratification at registration. Eligible patients will receive ADT plus A (240 mg PO daily) +/- D for up to 6 cycles until progression of disease by PCWG3/RECIST version 1.1 criteria. Prior therapy with ADT (with or without ARPI) initiated within 120 days before registration is permitted. The primary endpoint is overall survival (OS). Secondary endpoints include OS by TSG status; radiographic progression-free survival (rPFS); time to castration resistance; symptomatic skeletal event–free survival; time to worsening of disease-related symptoms (NCCN-FACT FPSI-17); safety and tolerability (CTCAE v5.0); PSA90 response at 6 weeks and 6 months; time to PSA progression; and objective response rate in patients with measurable disease. The study will enroll 1200 patients and is currently actively accruing patients. Clinical trial information: NCT06931340 .

Educational representation of genitourinary malignancies in medical student curricula: A cross-sectional review of oncologic education in Caribbean and South American schools.

4 Background: Genitourinary (GU) malignancies, including prostate, bladder, renal, and testicular cancers, comprise a major proportion of global oncologic morbidity and mortality. Despite their significance, GU oncology receives limited attention in medical student curricula. Insufficient exposure may impair clinical competency, delay diagnosis, and reduce interest in urologic subspecialties. Methods: A cross-sectional content analysis was performed on publicly available curricula from 12 accredited medical schools (8 Caribbean, 4 South American) between May and August 2025. Each school’s preclinical and clinical syllabi, curriculum maps, and lecture schedules were extracted and standardized. Oncology-related content was identified using keyword-based text mining (“cancer,” “carcinoma,” “neoplasm,” “tumor,” “oncology,” “genitourinary,” “prostate,” “bladder,” “renal,” “testicular”). Content was categorized by organ system (genitourinary, gastrointestinal, hematologic, breast, pulmonary, endocrine, neurologic, dermatologic) and stratified by level (preclinical, clerkship, elective). Quantitative variables included total lecture hours, dedicated GU sessions, and number of assessment items. Data were independently verified by two reviewers. Comparative analyses assessed GU oncology representation relative to other malignancy categories. Continuous variables were summarized as means ± SD, and group comparisons used paired t-tests and ANOVA with p < 0.05. Results: Across the 12 programs, 486 oncology-related instructional hours were identified. GU malignancies accounted for 8.4% (40.8 ± 9.6 hours) of total oncology instruction, significantly lower than gastrointestinal (23.5%) and breast (17.9%) content (p < 0.01). Only 3 programs included a dedicated prostate cancer lecture, and none covered bladder cancer screening or testicular cancer survivorship. GU oncology appeared mainly within general pathology modules without clinical integration in 10 schools. Conclusions: GU malignancies are markedly underrepresented in medical student education across Caribbean and South American schools. This gap may hinder early detection competency and reduce interest in urologic oncology. Incorporating structured GU modules and clinical exposure could align curricula with cancer epidemiology and strengthen future physician readiness.

Explainable machine learning prediction of tracheostomy after craniotomy for supratentorial intracerebral hemorrhage

CCL21 as a treatment-linked prognostic biomarker in metastatic castration-resistant prostate cancer.

257 Background: Metastatic castration-resistant prostate cancer (mCRPC) is an immunologically “cold” tumor with a low-inflamed microenvironment and limited sensitivity to immune checkpoint inhibitors. Treatment selection still lacks validated blood biomarkers. C-C motif chemokine ligand 21 (CCL21) orchestrates lymphocyte trafficking and lymphoid niche formation; thus, circulating levels may mirror the patient’s systemic immune state. Yet, the serum dynamics of CCL21 in mCRPC before and after treatment and their clinical relevance remain poorly defined. Methods: Observational translational cohort in mCRPC. Patients received systemic treatment according to clinical guidelines: androgen receptor pathway inhibitors (ARPIs) or chemotherapy (CT). Serum was collected at baseline (≤14 days pre-start) and week 12 (pre–cycle 3). CCL21 was quantified by enzyme-linked immunosorbent assay (ELISA) in batched runs under standard operating procedures, blinded to clinical outcomes. Primary outcome was whether on-treatment CCL21 dynamics associate with overall survival (OS); secondary outcome assessed whether these dynamics differ by treatment class (ARPIs vs CT). CCL21 value was dichotomized into HIGH/LOW using the median as the threshold. OS was estimated by Kaplan–Meier and compared using log-rank. Statistical significance was set at p<0.05. Results: 98 patients with mCRPC were included: 47 received ARPI (48%), of which 35 abiraterone and 12 enzalutamide, and 51 CT (52%). Most patients had bone disease (94.9%); 54.1% had nodal involvement and 15.3% had visceral disease. 59 patients had Gleason ≥ 8. Classical prognostic factors in prostate cancer were comparable across treatment groups. Median CCL21 value was 423.61 at baseline and 465.33 at week 12. Survival analysis showed differences when CCL21 value at 12 weeks was used as classifier. Those patients with HIGH values had a worse prognosis. No significant differences were observed at baseline by treatment class. But at week 12, CCL21 levels showed differences regarding to prognosis by treatment class. Among patients receiving ARPI therapy, HIGH week-12 CCL21 value was associated with shorter OS (p=0.03); while no association was observed with CT. Conclusions: In mCRPC, serum CCL21 measured at week 12 showed treatment-related differences and association with OS. In patients receiving ARPI therapy, CCL21 emerges as a candidate biomarker to monitor treatment and inform therapeutic selection. External validation and definition of clinically actionable thresholds will be required for clinical implementation.

A guide to cancer screening

Energetic Disorder in A‐D‐A Type Acceptors for Organic Photovoltaics: Fused‐Ring vs. Nonfused‐Ring Systems

ABSTRACT Reducing the energetic disorder is crucial to improve the efficiencies of organic photovoltaics. Given the high performance of both fused‐ring and nonfused‐ring A‐D‐A type acceptors, a fundamental question arises: is a fused‐ring D‐unit necessary to obtain low energetic disorder? Here, we have systematically investigated the energetic disorder for electrons (described by the standard deviation of the lowest unoccupied molecular orbital (LUMO) energy, σ LUMO ) in representative fused‐ring and nonfused‐ring A‐D‐A type acceptors by combining molecular dynamics simulations with density functional theory calculations. The results point out that the σ LUMO is dominated by the dynamic disorder for both fused‐ring and nonfused‐ring systems. Moreover, for all these acceptors, the LUMO is delocalized over the entire molecular backbone, which benefits to reduce the electron‐vibration coupling. Consequently, both fused‐ring and nonfused‐ring systems exhibit low σ LUMO values of 48–56 and 50–71 meV, respectively. Compared to the fused‐ring systems with similar conjugation lengths, the σ LUMO is slightly increased for the nonfused‐ring systems due to the extra rotation‐induced static disorder. Notably, the σ LUMO of the nonfused‐ring systems can be effectively reduced by extending the D‐units and restricting the conformational rotation. This work provides helpful insights for developing cost‐effective nonfused‐ring acceptors with low energetic disorder.

First-in-human assessment of actinium-225-prostate-specific membrane antigen ( ²²⁵ Ac-PSMA)-Trillium (BAY 3563254) in mCRPC: Dose-escalation results of the phase 1 PAnTHa study.

19 Background: PSMA is a validated target in the treatment of mCRPC. We investigated 225 Ac-PSMA-Trillium, a novel PSMA-targeting molecule which comprises a highly specific PSMA-binding motif, an albumin-binding domain to optimize the agent’s pharmacokinetic profile, and a Macropa chelator complexed with the alpha-emitter 225 Ac. We present results of the global, Phase 1 PAnTHa (NCT06217822) study, assessing safety and efficacy of 225 Ac-PSMA-Trillium in patients (pts) with mCRPC. Methods: PAnTHa consists of dose-escalation and dose-expansion parts; the former is reported here. Pts had mCRPC with metastases overexpressing PSMA on positron emission tomography (PET) imaging (uptake >liver in ≥1 lesion), ≥1 prior androgen receptor pathway inhibitor (ARPI) and (if eligible) 1 or 2 prior taxanes, and no prior radiopharmaceutical. 225 Ac-PSMA-Trillium was given intravenously every 6 weeks for up to 4 doses. Dose escalation used a 2-stage joint TITE-CRM design with ≥3 pts per dose level; ≤9 further pts could be added to any dose level considered tolerable with evidence of antitumor activity. The dose-escalation primary objectives were to determine the safety, tolerability and recommended dose for expansion (RDE) of 225 Ac-PSMA-Trillium. Dose-limiting toxicities (DLTs) were assessed in cycles 1–3. Exploratory analyses included baseline PSMA PET mean Standardized Uptake Value (SUVmean) and longitudinal circulating tumor DNA (ctDNA). Results: At data cut-off (18 Sept 2025), 50 patients had received ≥1 dose of 225 Ac-PSMA-Trillium (range: 75 to 150 kBq/kg; 12–13 pts/cohort). Median age was 71 years, 84% had bone metastases, 48% had measurable disease; 58% and 20% had received 1 or 2 prior taxanes, respectively; all received ≥1 prior ARPI. There were no DLTs or treatment-related deaths. Treatment-emergent adverse events (TEAEs) occurred in 98% of pts, most commonly dry mouth (76%; 52% grade [Gr] 1, 24% Gr 2, 0 Gr ≥3). Other common TEAEs were fatigue (48%) and nausea (44%). Overall, 38% had Gr ≥3 TEAEs, most commonly lymphopenia (20%), 16% had serious TEAEs and 4% discontinued treatment due to TEAEs. The overall response rate per PCWG3 criteria across all doses in pts with measurable disease at baseline (n=24) was 46% and the disease control rate was 83%. Based on safety and preliminary antitumor activity data, 125 kBq/kg was selected as the RDE. Respective PSA50 and PSA90 response rates were 58% and 36% overall, and 83% and 58% at the RDE. PSA responses were seen in 14 out of 15 pts with high PSMA expression at baseline (SUVmean >10). A dose-dependent trend in ctDNA clearance was seen up to the RDE by the start of the second cycle. Conclusions: 225 Ac-PSMA-Trillium was well-tolerated with no DLTs. PSA50 response rates were 83% at the RDE and 93% in all pts with SUVmean >10. These promising data support the further investigation of the molecule. Clinical trial information: NCT06217822 .

Cross institutional comparison of the miR-371a-3p assay in pre-surgical germ cell tumor (GCT) patients.

621 Background: miR-371a-3p (miR371) is a promising biomarker in GCTs. Diagnostic parameters of miR371 in the literature utilize different laboratory techniques, testing protocol, standards, and thresholds, potentially limiting cross-study comparison and generalized adoption. Establishing assay concordance and standardization is important before implementing the assay in clinical practice. Methods: The primary objective was to assess agreement between paired miR371 test results from the Memorial Sloan Kettering Cancer Center (MSK) and University of California San Diego (UCSD) assays, which differ in technique, testing protocol, analytical thresholds, and cutoff criteria, among chemotherapy naïve patients prior to orchiectomy or RPLND surgery. All samples were analyzed in CLIA-certified labs at both centers. An a piori sample size of 56 paired samples was determined to achieve 91% power to differentiate between 75% unacceptable agreement (null) versus 90% acceptable agreement (alternative) using a one-sided exact test with alpha 0.05. A minimum concordance of 48 of 56 paired test results was required to reject the null hypothesis of unacceptable agreement. Secondary objectives were to compare and quantify variation between paired Ct values and to assess assay performance characteristics in detecting active disease (defined as presence of non-teratomatous GCT [ntGCT] at surgery). Samples were randomly selected from those available at each institution, stratified to achieve approximately equal numbers of samples by site (MSK/UCSD), disease status (active/not active), and clinical setting (pre-orchiectomy/pre-RPLND). Results: Samples were categorized by clinical setting (pre-orchiectomy: n=27, pre-RPLND: n=29) and disease status (active: n=31, not active: n=25) and compared by institution. Assay agreement was 87.5% (95% CI: 75.9%, 94.8%), and the Spearman correlation coefficient between the two assays was 0.84 (95% CI: 0.74, 0.90). Forty nine of 56 samples demonstrated concordance allowing rejection of the null hypothesis. Both assays exhibited strong performance characteristics (Table). Conclusions: The primary objective of this cross-laboratory comparison was achieved, demonstrating concordance between the MSK and UCSD miR371 assays. Further cross-institutional comparisons in defined clinical settings will facilitate collaboration and widespread clinical adoption of the miR371 test. Additional clinical data will be presented. MSK ntGCT+ ntGCT- Total UCSD ntGCT+ ntGCT- Total miR371+ 29 3 32 miR371+ 30 3 33 miR371- 2 22 24 miR371- 1 22 23 Total 31 25 56 Total 31 25 56 Sensitivity 94 Sensitivity 97 Specificity 88 Specificity 88 PPV 91 PPV 91 NPV 92 NPV 96 AUC 92 AUC 98

The effect of medication use on chronic pruritus in patients with type 2 diabetes mellitus: a multicenter cross-sectional study

Pan-cancer assessment of deletions in COQ biosynthesis pathway genes associated with poor prognosis and potential benefit from BPM31510 intervention in kidney cancers.

500 Background: Defective energy metabolism has been established as a hallmark of cancer; however, the specific genetic basis underlying this relationship across cancers remains unclear. Ubiquinone (COQ10) plays an essential role in regulating efficient mitochondrial ATP generation and reactive species levels. Maintenance of CoQ10 levels is orchestrated by 13 CoQ10 biosynthetic genes that, when altered, results in severe metabolic dysfunction. However, the mutational, deletion/amplification, methylation, or mRNA expression status across cancers has not been thoroughly investigated. Methods: Towards this aim, we comprehensively molecularly analyzed 33 cancer types (n = 10535) from The Cancer Genome Atlas Program (TCGA) dataset to identify cancers that demonstrated poor prognosis associated with alterations in the COQ10 biosynthesis pathway. Pan-cancer in-silico analysis of expression, mutations, copy number alteration, and methylation of the COQ10 biosynthesis pathway genes, along with a subset of associated genes, was performed on the data. Across the 33 indications in TCGA, we identified Clear Cell Carcinoma (KIRC) (n = 530) and Papillary renal cell carcinoma (KIRP) (n = 288) as primary cancers that demonstrated a significantly poor prognosis with deletions in COQ10 biosynthesis genes. Results: Deletions in COQ2 (HR 2.35 (1.64 – 3.37); q-val = 0.0003), COQ4 (HR 1.76 (1.29 – 2.38); q-val = 0.009), and COQ6 (1.69 (1.25 – 2.28); q-val = 0.017) were associated with poor survival in KIRC. Deletions in these same genes were also associated with poor survival in KIRP, COQ2 (HR 5.86 (2.97 – 11.58); q-val = 0.00005), COQ4 (HR 3.27 (1.64 – 6.51); q-val = 0.018), and COQ6 (3.49 (1.83 – 6.65); q-val = 0.007). The incidence of one or more deletions was 63% in KIRC and 28% in KIRP cancers. Further, we investigated the association of several key proteins and their respective genes with known interaction with COQ10 for ATP generation in the mitochondrion relative to patient outcome. We observed 3 genes in KIRC and 6 genes in KIRP demonstrated an association with both poor survival and progression, with NDUFS7 (KIRC HR 4.45 q-val < 0.0001; KIRP HR 3.8 q-val = 0.032) and PRODH (KIRC HR 2.06 q-val = 0.029; KIRP HR 2.71 q-val = 0.032) demonstrating significance in both indications. Conclusions: This unbiased pan-cancer analysis clearly demonstrates that kidney cancers (KIRC/KIRP) may predominantly exhibit a genetic basis for altered mitochondrial metabolism due to a loss of ability to produce COQ10, further pushing the cells into glycolysis over aerobic respiration rendering them susceptible to metabolic interventions. Currently, we are developing a nanodispersion formulation of oxidized CoQ10 (BPM31510) that delivers supraphysiological levels of CoQ10 into circulation and into tumors, which is currently being investigated in Phase 2 clinical trials.

Base-edited CAR7 T cells are safe and efficacious in R/R T-ALL

Chiral Acoustic Phonon and Conservation of Pseudoangular Momentum in α‐Quartz (Adv. Mater. 16/2026)

Ultra‐Large‐Period Moiré Lattices in Twisted Trilayer MoS ₂ Induced by High‐Symmetry Sites

ABSTRACT Twisted trilayer (Tt) transition metal dichalcogenides with multiple rotational degrees of freedom offer unprecedented opportunities for constructing large‐wavelength moiré superlattices to maximize the effect of correlated behaviors. Precisely stacking trilayer structures to realize ultra‐large moiré superlattices remains a significant challenge, hindering investigations of moiré‐tuned excitonic properties. Here we fabricate Tt MoS 2 via chemical vapor deposition, in which two commensurate twists of 2.7° and 21.9° are sequentially introduced from the top to middle, and to bottom layers. An unprecedented super‐moiré structure with an ultra‐large periodicity of around 24 nm is achieved, 30 times larger than that of 21.9°‐bilayer MoS 2 , hierarchically composed of periodical mirror‐symmetric triangular tessellation patterns consisting of five kinds of high‐symmetric stacking registrations and the relaxation regions resulting from the interlayer gliding. This robust ultra‐large‐period superstructure generates a deep moiré potential to effectively suppress intralayer moiré excitons recombination and be against intervalley exchange interaction at the magnetic field up to 9T, associated with the enhanced layer‐valley‐locked polarization by two‐fold larger than that of the trilayer systems with incommensurate angles. Our work presents angle‐dependent super‐moiré architectures in Tt systems as a versatile platform for designing moiré quantum materials with tailored optoelectronic responses, advancing applications in valleytronic and excitonic devices.

Comprehensive genomic profiling in prostate cancer: Clinical relevance of BRCA1/2 pathogenic variants in the mCRPC.

210 Background: To delineate the genomic landscape of prostate cancer (PCa) and evaluate clinical outcomes of the PARP inhibitor olaparib in patients with pathogenic BRCA1/2 variants using a nationwide Japanese database. Methods: We conducted a retrospective cohort study of 5,893 patients with PCa registered in the Center for Cancer Genomics and Advanced Therapeutics (C-CAT) between June 2019 and June 2025. Comprehensive genomic profiling (CGP) was performed using five nationally approved assays, and results were reviewed by a Molecular Tumor Board (MTB). Clinical data were longitudinally collected. Overall survival (OS) was assessed from the initiation of first-line systemic therapy or from the start of olaparib. OS was compared according to homologous recombination repair (HRR) status and BRCA1/2 variant subtype. Results: Among 5,893 patients, 2,202 (37.4%) harbored ≥1 pathogenic HRR variant and 791 (13.4%) carried BRCA1/2 pathogenic variants. Olaparib was recommended for 792 patients, of whom 389 (49.1%) received it. Patients with HRR alterations had significantly shorter OS than those without (P = .021). BRCA1 variants were associated with worse OS compared with BRCA2 (P = .007). In BRCA2-mutated cases, those with BRCA2 loss demonstrated the most favorable survival (P < .001), whereas the I1859fs*3 variant showed a trend toward poorer outcomes. Multivariate analysis confirmed BRCA1 variants as independent adverse prognostic factors and BRCA2 loss as an independent predictor of improved outcomes. Conclusions: This nationwide analysis represents the largest real-world genomic cohort of PCa in Japan. Outcomes of olaparib varied by BRCA subtype: BRCA1 pathogenic variants were linked to poor prognosis, while BRCA2 loss predicted favorable response. These findings highlight the clinical importance of detailed genomic annotation to optimize precision oncology strategies in metastatic castration-resistant prostate cancer.

Contemporary patterns of treatment and outcomes in germ-cell tumors across a provincial cancer system: British Columbia Germ Cell Tumor Clinical Database.

603 Background: British Columbia (BC) provides centralized, province-wide management for germ-cell tumors (GCT) across a large, dispersed population of >5 million. Longstanding electronic record and recent data integration enabled a comprehensive, population-based GCT database. We describe real-world treatment patterns and outcomes and its potential as a North American platform for collaborative studies. Methods: Adult type II GCT diagnosed in BC, 2002–2022, were identified from linked oncology registries and pharmacy databases. Survival follow-up was censored July 31, 2025; systemic therapy through Dec 31, 2023. Primary outcome: overall survival (OS) from diagnosis by histology. Secondary: OS from first-line (1L), time to next therapy (TTNT) from 1L, and chemotherapy-free survival (CFS) from orchiectomy. Treatment patterns (1L regimen, salvage, radiotherapy [RT], surgery) were summarized by histology and era (2002–08, 2009–15, 2016–22). Results: Among 2,366 patients (seminoma 65%, non-seminoma 35%), median age was 38 [IQR 31–46] and 30 [24–36] years. Curative-intent systemic therapy was given to 682 patients (29%). BEP led 1L regimen in all eras (non-seminoma 56.4%→85.0%→78.9%; seminoma 25.7%→68.4%→76.1%), while VIP rose after 2016 mainly in non-seminoma (9.0%→16.4%) and remained rare in seminoma (≤2.5%). Salvage chemotherapy occurred in 5.1% overall, chiefly TIP. RT decreased and was largely confined to seminoma (11.9% vs 2.5%; predominantly adjuvant); in non-seminoma it was largely palliative. Surgical management in non-seminoma was marked by RPLND (20.9%) and lung resections (4.7%). OS from diagnosis (3y/5y): seminoma 98.0/97.2%; non-seminoma 96.5/95.8%. OS from 1L: 95.4/94.7% (seminoma) vs 94.2/93.6% (non-seminoma). TTNT (1y/3y): 88.1/86.2% vs 87.1/84.4%. By era, 5y OS from diagnosis improved 96.2%→97.4%; 5y OS from 1L 90.5%→95.7%; 3y TTNT 83.1%→84.2%. CFS (1y/3y) after orchiectomy: 79.6/73.3% (seminoma) vs 59.2/55.2% (non-seminoma). Conclusions: Across two decades, outcomes for GCT in BC remain outstanding within a publicly funded, multidisciplinary hub-and-spoke system. Practice patterns reflect centralized, expert-guided care with low adjuvant use, BEP-dominant 1L regimens, and appropriate surgical consolidation in non-seminoma. The population-based BCGCT database with validated longitudinal data enables secondary analyses, data sharing, and linkage with emerging biobanks and datasets.

Costs of maternal care revealed through body condition in Northern Resident killer whales (Orcinus orca)

Histologic predictors of clinically significant biochemical recurrence and PSA kinetics after radical prostatectomy.

398 Background: Radical prostatectomy (RP) is a key treatment for localized prostate cancer. However, 20–40% of patients experience biochemical recurrence (BCR)—defined as a PSA rise >0.2 ng/mL after surgery—indicating disease progression. Unfavorable histologic features, such as cribriform and intraductal carcinoma, have been shown to predict adverse oncologic outcomes and long-term disease progression following RP. We investigated whether these features can provide insight into the risk of BCR, PSA kinetics, and the risk of metastasis or cancer-related death after BCR. Methods: We retrospectively analyzed a post-RP group from one institution with a median follow-up of 13.5 years (7.9–17.8). Pathology specimens were re-reviewed by a blinded GU pathologist and classified as containing favorable (FH) or unfavorable (UH) histology. Outcomes included BCR, PSA doubling time (PSADT), and development of metastasis or cancer-specific death following BCR. Group differences were assessed using Wilcoxon rank-sum tests and Chi-squared or Fisher’s exact. Multivariable Cox regression or Logistic regression evaluated associations between histology type, BCR risk, and PSADT. Results: A total of 844 subjects met the inclusion criteria. BCR occurred in 33.8% (285/844), and 61.8% (123/199) had a PSADT ≤1 year. Patients with UH had higher rates of BCR (52% vs. 10%, p < 0.001), earlier BCR (26 vs. 60 months, p = 0.005), and more frequently had a PSADT ≤1 year (65% vs. 40%, p = 0.016). Among UH patients with BCR, metastatic progression (39% vs. 0%, p < 0.001) and cancer-specific death (20% vs. 0%, p < 0.001) were more common. On multivariable analysis, UH (HR 3.47, p < 0.001), initial PSA (HR 1.02, p <0.001), positive margins (HR 1.48, p = 0.002), and grade group (HR 1.56, p < 0.001) were independently associated with BCR, while age and pathologic T stage were not. UH (OR 2.77, p = 0.044) and positive margins (OR 1.86, p = 0.047) were also associated with PSADT ≤1 year, while age, initial PSA, and pathologic T stage were not. Conclusions: UH features were associated with higher rates of clinically-significant BCR resulting in adverse cancer outcomes, underscoring their value as predictors of prostate cancer progression. Notably, those with UH experienced earlier BCR and had a faster PSADT, which raises possible differences in post-RP follow-up and management. Clinical characteristics by histology type. Characteristic Overall n = 844 Favorable Histology n = 361 Unfavorable Histology n = 483 p-value Age at surgery (yrs) 61 (57, 66) 60 (56, 64) 63 (58, 67) <0.001 Initial PSA before surgery (ng/mL) 6.0 (4.5, 9.2) 5.2 (4.2, 6.7) 6.9 (4.9, 11.0) <0.001 Margin Status <0.001 Positive 301 (37%) 96 (28%) 205 (44%) Pathological T Stage <0.001 T2 434 (51%) 267 (74%) 167 (35%) T3 410 (49%) 94 (26%) 316 (65%) Grade Group <0.001 0-1 15 (1.8%) 15 (4.2%) 0 (0%) 2 545 (65%) 337 (93%) 208 (43%) 3 162 (19%) 9 (2.5%) 153 (32%) 4-5 122 (14%) 0 (0%) 122 (25%)

Discovery of predictive biomarkers for cancer therapy through computational approaches

Modulating Ultraviolet‐Visible‐Near Infrared Emission in Hybrid Metal Halides via ns ² Ion Doping (Adv. Mater. 15/2026)