Prostate cancer is the most prevalent cancer among men within the U.S. and globally, with rising incidence, including advanced-staged disease. Risk factors for aggressive prostate cancer are not well defined. This systematic review and meta-analysis provide an overview of the relationship between cardiometabolic diseases (diabetes, dyslipidemia, obesity, and hypertension) and aggressive prostate cancer.

Aggressive prostate cancer was defined as disease that has spread or is at high risk of spreading: high-risk or very high-risk localized (T3-T4, Grade Group 4-5), node-positive (N1), or metastatic (M1). Using PRISMA guidelines, a total of 4,830 publications revealed 25 cohort studies of over 974,000 men. Following the systematic review of these prospective studies of men with prostate cancer, R was utilized to run a random effects model, yielding hazard ratios with 95% confidence intervals and generating forest plots with measures of heterogeneity.

Examination of these studies revealed that a positive association exists. Diabetes was associated with a significantly increased risk of aggressive prostate cancer (HR = 1.18; 95% CI: 1.07-1.30; p = 0.0008). Obesity also showed a significant association (HR = 1.15; 95% CI: 1.06-1.24; p = 0.0006), as did hypertension, though to a lesser degree (HR = 1.07; 95% CI: 1.00-1.14; p = 0.04). Dyslipidemia was not significantly associated with aggressive prostate cancer (HR = 1.03; 95% CI: 0.98-1.03; p = 0.26).

Three of the four cardiometabolic disease components (diabetes, obesity and hypertension) were shown to have statistical significance and offered intriguing evidence on their potential associations with aggressive prostate cancer. Dyslipidemia's association was not statistically significant, which could be attributed to variations in methods of assessment and differing mechanistic effects. High heterogeneity and limited study availability remain key limitations.

If such associations between cardiometabolic diseases and prostate cancer aggressiveness are shown to be cause and effect, such controllable and treatable conditions can allow oncologists to work alongside primary care physicians to improve patient outcomes and reduce the incidence of aggressive disease. Through the promotion of lifestyle modifications, tighter cardiometabolic control, and targeted interventions, public health efforts might improve prostate cancer outcomes.

In acute myeloid leukemia (AML), measurable residual disease (MRD) assessment is essential for predicting relapse and guiding therapy decision-making. Nucleophosmin 1 (NPM1) mutations are reliable MRD markers but apply to only ∼30% of patients with AML. Wilms tumor 1 (WT1) expression monitoring is applicable to a broader population but the European LeukemiaNet (ELN) threshold of 50 WT1 copies per 10⁴ ABL copies (0.5%) may be too high, which limits sensitivity.

With WT1 expression data from 100 healthy controls, this study established a revised WT1 threshold of seven copies per 10⁴ ABL copies (0.07%). Its performance was retrospectively validated against NPM1 in 308 paired follow-up samples from 63 patients with NPM1-mutated AML, and against the core binding factor (CBF) β-MYH11 fusion transcripts in 83 samples from 12 patients. Statistical analyses included concordance, sensitivity/specificity, survival estimates, and model comparison with the Akaike information criterion.

Compared to the ELN cutoff, the revised threshold showed higher concordance with NPM1 (78.6% vs. 73%) and sensitivity (54% vs. 24%; p < .0001) and acceptable specificity (91% vs. 98%; p = .002). In survival analyses, the seven-copy cutoff demonstrated stronger prognostic value than the ELN threshold, particularly after consolidation therapy. In the CBFB::MYH11 cohort, the two thresholds showed similar concordance but WT1 positivity with the revised cutoff preceded relapse in selected patients.

In AML, the revised WT1 threshold of seven copies per 10⁴ ABL copies enhanced MRD sensitivity while maintaining specificity, improving concordance with NPM1, and showing prognostic relevance. These findings support the clinical value of locally optimized WT1 thresholds, and highlight the need for prospective multicenter validation and harmonization of WT1-based MRD monitoring.

The high costs of cancer care may lead to medical debt for patients and families. This study examined the association of county-level medical debt and timely treatment initiation among individuals newly diagnosed with cancer.

Individuals aged 19 years and older who were newly diagnosed with acute leukemias, diffuse large B-cell lymphoma, Hodgkin lymphoma, female breast cancer, colorectal cancer, and lung cancer with consecutive enrollment in the same insurance type from the month of diagnosis through 90 days afterward were identified from the 2012-2021 Colorado Central Cancer Registry linked to the Colorado All-Payer Claims Database with information about county-level medical debt from the Urban Institute (N = 35,789). The exposure was the county-level share of adults with medical debt in collections, categorized in four quartiles (Q1-Q4). The outcome was timely treatment initiation-defined as the receipt of any cancer-directed treatment within 90 days after cancer diagnosis. The association of county-level medical debt and time to treatment initiation was examined by using multivariable Cox models.

Higher county-level medical debt was associated with lower likelihood of timely treatment initiation for all selected cancers combined (Q4 [counties with the highest medical debt rate; n = 8652] vs. Q1 [counties with the lowest medical debt rate; n = 9042]: hazard ratio [HR], 0.916; 95% confidence interval [CI], 0.871-0.963; p for trend = .001), for female breast cancer (Q4 vs. Q1: HR, 0.910; 95% CI, 0.847-0.978; p for trend = .011), and among individuals aged 19-64 years with private health maintenance organization plans (Q4 vs. Q1: HR, 0.790; 95% CI, 0.699-0.893; p for trend = .002) or Medicaid coverage (Q4 vs. Q1: HR, 0.869; 95% CI, 0.786-0.960; p for trend = .013).

Policies aimed at preventing and alleviating medical debt could be effective strategies for improving access to timely treatment.

Bladder cancer has notable heterogeneity. The urine-based fluorescence in situ hybridization (FISH) test can detect bladder cancer noninvasively. In this study, we aimed to construct a nomogram based on FISH results and clinical features (referred to as the FISH-clinical model) to predict the overall survival (OS) of bladder cancer patients following radical cystectomy (RC).

A total of 261 eligible patients were enrolled for this study. The SYSMH cohort was divided into training (n = 138) and internal validation (n = 70) sets; the SYSUTH cohort was used for external validation (n = 53). Multivariate Cox proportional hazards regression was applied for FISH-clinical model construction, and model performance was evaluated according to analyses of calibration, discrimination ability, and clinical usefulness.

FISH-identified chromosome 7 and 17 aneuploidies correlated significantly with increased pT stage; the former was associated with lymph node metastasis. Six variables, age, tumor size, pT stage, lymphovascular invasion, chromosome 7 aneuploidy, and p16 locus loss, were found to be independent predictors of OS and were incorporated into our FISH-clinical model. The model demonstrated good calibration and discrimination, with C-indexes (95% CIs) of 0.772 (0.693-0.851), 0.712 (0.605-0.819) and 0.705 (0.587-0.822), in the training, internal validation and external validation sets respectively. Decision curve analysis demonstrated the model's clinical utility. Furthermore, all enrolled patients were successfully categorized into high-, medium- or low-risk groups, and stratified analyses were performed.

Preoperative FISH has predictive value for OS, and we developed a FISH-clinical model for OS prediction in bladder cancer patients who have not received neoadjuvant chemotherapy or immunotherapy. This model showed favorable predictive efficacy with internal and external validation.

Pediatric posterior fossa tumor (PFT) resection is frequently complicated by postoperative hydrocephalus. Previous hydrocephalus risk stratification tools demonstrate limited performance in external validation and do not account for important intra- and post-operative variables. We aimed to evaluate additional risk factors for post-resection hydrocephalus to improve risk-stratification.

We conducted a retrospective analysis of pediatric patients who underwent resection of primary PFT's at our institution (January 2016-June 2024). We collected perioperative variables thought to influence hydrocephalus risk. The primary outcome was permanent CSF diversion within 6 months after resection. We used univariable and multivariable logistic regression with bidirectional stepwise selection to identify predictors of post-resection hydrocephalus.

A total of 112 patients were included. We identified age < 5 years, moderate/severe hydrocephalus, and subtotal resection (STR; ≥ 1.5 cm² residual tumor) as independent predictors of post-resection hydrocephalus on multivariable regression. STR exhibited an odds ratio of 8.25 (95% CI 2.72-26.84; p < 0.001), highlighting its strong association with the need for permanent CSF diversion. A scoring tool that incorporated STR and an age cutoff of < 5 years improved the discriminative performance (area under the ROC curve = 0.826) compared to the modified Canadian Preoperative Prediction Rule for Hydrocephalus (AUC = 0.720).

These findings suggest STR is associated with increased risk of persistent hydrocephalus and emphasize careful intraoperative decision-making when pursuing incomplete resection. Future multicenter studies will be necessary to validate this framework and to further elucidate how STR, in conjunction with age and hydrocephalus severity, can be leveraged to optimize treatment strategies in diverse healthcare settings.

While computed tomography (CT) imaging is commonly used to evaluate canine nasal tumors, the ability to differentiate tumor types based on imaging features remains limited. This retrospective study examined dogs with confirmed nasal neoplasia to determine whether CT characteristics differ between epithelial and mesenchymal tumors. Cases from a single institution (2013-2022) were reviewed, and the frequency of CT features between epithelial and mesenchymal tumors was compared using Fisher's exact test. Also, CT features of less commonly reported nasal neoplasms, including squamous cell carcinomas, polyps, and osteosarcomas, were described. Sixty-seven dogs with nasal neoplasia were identified; 48 (72%) had a type of epithelial neoplasia, and 19 (28%) had mesenchymal neoplasia. Dogs with epithelial neoplasia were more likely to show intracranial mass extension (p = 0.04; OR 5.1; 95% CI 1.1-23.9), cribriform plate lysis (p = 0.03; OR 4.5; 95% CI 1.2-15.8), lysis of ipsilateral sphenoid sinus (p < 0.0001; OR 18.7; 95% CI 3.9-85.9), mass extension into ipsilateral sphenoid sinus (p = 0.01; OR 5.8; 95% CI 1.6-20.2), and frontal sinus fluid (p = 0.05; OR 4.7; 95% CI 1.3-16.2) than dogs with mesenchymal neoplasia. Dogs with mesenchymal neoplasia were more likely to show fluid in the ipsilateral maxillary recess (p = 0.01; OR 5.3; 95% CI 1.4-18.6). Squamous cell carcinoma patients had two distinct presentation patterns: either a small nodule centered on the nasal planum with no associated lysis and mass extension, or a mass centered on and causing lysis of the maxillary or nasal bone. This investigation provides the first comprehensive comparison of CT characteristics between different canine nasal tumor types, offering potential prebiopsy diagnostic indicators.

BACKGROUND Abemaciclib is a selective cyclin-dependent kinase inhibitor that has been approved as an adjuvant treatment for advanced hormone-positive, human epidermal growth factor receptor-2 (HER2)-negative breast cancer and is usually used in combination with an aromatase inhibitor. This report describes the case of a 43-year-old man with a grade 2, stage IIIc, hormone receptor-positive, HER2-negative, invasive ductal carcinoma of the left breast successfully managed with left mastectomy, radiation therapy, and postoperative oral tamoxifen and abemaciclib. CASE REPORT A 43-year-old man presented to our Dermatology Department with a primary concern of non-healing erosion in the left areola that persisted despite 3 months of topical ointment application. Tissue diagnosis confirmed breast cancer, and the patient was referred to the Breast Surgery Department. Imaging studies and detailed tissue analysis revealed a grade 2, hormone receptor-positive, HER2-negative, invasive ductal carcinoma of the left breast. The preoperative stage was cT4bN1aM0 (tumor with skin involvement, limited axillary node metastases, no distant spread), corresponding to stage IIIB. The patient underwent surgery (left mastectomy with axillary lymph node dissection; levels I-III). The pathological stage was IIIC (pT4bN3aM0: skin involvement with extensive nodal metastases and no distant disease). We administered postoperative adjuvant chemotherapy with sequential administration of anthracycline and taxane, and postoperative radiation therapy, followed by postoperative adjuvant endocrine therapy with tamoxifen and abemaciclib. To date, no signs of recurrence have been observed. CONCLUSIONS This report describes a rare case of advanced male breast cancer and a successful outcome following postoperative treatment that included abemaciclib.

Acute myeloid leukemia (AML) exhibits pronounced heterogeneity, necessitating deep molecular characterization for precision therapy. Lactate metabolism and histone lactylation, influencing tumor biology via epigenetic regulation and immune microenvironment remodeling, represent an emerging focus. This study combines single-cell RNA sequencing (scRNA-seq) and bulk RNA sequencing (bulk RNA-seq) data to investigate the prognostic value of lactate/lactylation-associated genes (LL-genes, defined as genes involved in lactate metabolism and histone lactylation regulation) in AML. Specifically, Seurat was utilized for scRNA-seq clustering with cell annotation/validation via the TISCH2 database. Gene Set Variation Analysis (GSVA) assessed lactate/lactylation pathway activity. In bulk RNA-seq, ConsensusClusterPlus enabled molecular subtyping, while ten machine learning algorithms constructed a prognostic model. scRNA-seq revealed specific LL-gene overexpression in malignant progenitors, concomitant with elevated lactate metabolism-lactylation activity (LML-CAS; Lactate Metabolism-Lactylation Modification Combined Activity Score), enhanced metabolic-inflammatory synergy, and immunosuppression (increased Tregs/M2 macrophages). Molecular subtyping identified two clusters (A/B) exhibiting divergent survival outcomes (Cluster A: poorer prognosis). An optimized 7-gene prognostic model demonstrated high accuracy, predicting reduced chemotherapy response among high-risk patients. Transcriptomic profiling indicated lactylation-associated immunosuppression (e.g., downregulated CXCL9/10-CXCR3 axis, enrichment of T cell exhaustion markers) and heightened in silico-predicted sensitivity to BCL-2/FGFR inhibitors (ABT-737/AZD4547) in high-risk patients. qRT-PCR confirmed RNA-level dysregulation of key LL-genes (IFI16, THOC2, HIST1H2BD, ARPP19), aligning with bioinformatic predictions. Western blot analysis further validated aberrant protein expression of IFI16 and THOC2 in AML specimens, reinforcing their dysregulation. Collectively, integrated analyses uncovered lactate/lactylation-associated heterogeneity in AML. Our machine learning-based prognostic model predicts survival, therapeutic response, and drug sensitivity, suggesting a potential strategy for precision therapeutics in AML.

Thyroid carcinoma is the most common malignant endocrine tumour, and its prevalence has been on the rise in recent years. However, mechanisms underlying the metastasis of thyroid carcinoma and candidate biomarkers remain elusive. In this study, we screened genes involved in the virulence and metastasis of papillary thyroid carcinoma (PTC).

Oxford Nanopore Technology full-length transcriptome sequencing and bioinformatic analyses were performed to analyse differentially expressed genes (DEGs) in PTC. We collected 15 cancerous and paracancerous tissue pairs from patients with PTC for RNA sequencing. The significance thresholds for DEGs were |log2(fold change)| ≥ 1 and false discovery rate (FDR) < 0.01. Gene Ontology and Kyoto Encyclopaedia Gene and Genome pathway enrichment analyses of the 50 most significant DEGs were performed. Immunohistochemistry was used to evaluate LAMB3 expression in tissue microarrays (58 pairs of PTC samples) and its correlation with clinicopathological parameters. Differences in gene expression between cancerous and paracancerous tissues were analysed using the Wilcoxon test. The correlation between gene expression and clinical variables was assessed using Fisher's exact test.

Transcriptomic analysis revealed the presence of 1,687 DEGs in PTC, and the expression of 804 and 883 genes was found to be upregulated and downregulated, respectively. LAMB3 expression was significantly elevated in cancerous tissues when compared to that in paracancerous tissues (p < 0.001). LAMB3 expression was significantly positively associated with PTC tumour tissue size (p = 0.001, r = 0.49) and T stage (p = 0.017, r = 0.339).

Our findings suggest that LAMB3 expression significantly increases in PTC and it is associated with tumor size and T stage.

To compare the metabolomic profile differences between ILD (interstitial lung disease) and chronic obstructive pulmonary disease (COPD) controls, and to distinguish profiles between progressive and stable idiopathic pulmonary fibrosis (IPF)/ILD subjects.

This single-center prospective study enrolled n = 71 (progressive IPF/ILD: n = 33, stable IPF/ILD: n = 27, COPD: n = 11) participants between December 2021 and October 2022. Metabolite quantification was performed using the liquid chromatography-mass spectrometry (LC-MS platform), and nuclear magnetic resonance spectroscopy (¹H NMR). Further, pathway enrichment analysis was performed to identify biochemical pathways associated with the disease.

715 metabolites were accurately quantified to investigate (a) differences between the combined groups of stable and progressive idiopathic pulmonary fibrosis IPF/ILD and COPD controls, and (b) differences between progressive IPF/ILD and stable IPF/ILD controls. The most notable metabolites distinguishing fibrotic lung disease (both stable and progressive IPF/ILD) from COPD were glycerolipids (GL). Enrichment analysis of IPF/ILD versus COPD revealed significant disruptions in lipid metabolic pathways, particularly glycerophospholipids, and sphingolipids (false discovery rate FDR q-value < 0.05). In addition, significant disruptions in TG species were found in progressive IPF/ILD with enrichment analysis revealing dysregulation of metabolic pathways associated with glycerophospholipids (FDR q-value < 0.05).

These findings emphasize the dysregulation of lipid metabolism in fibrotic lung diseases, involving glycerolipids, glycerophospholipids, and sphingolipids. The distinct lipid alterations identified through metabolomic profiling provide valuable insight into lipid metabolism in IPF/ILD, warranting further research to explore their potential as biomarkers.