CT colonography (CTC) is a validated screening test for detection and prevention of colorectal cancer (CRC). In the United States, screening CTC has been covered for Medicare beneficiaries since 2025, elevating it to equal status with other reimbursed CRC screening tests and ending a 15-year policy stalemate. Screening CTC is a highly accurate examination with an immaculate safety record and equivalent sensitivity to colonoscopy for clinically significant polyps. Long-term observational CTC cohorts confirm safety for established polyp size thresholds in terms of test positivity and screening and surveillance intervals. Excellent technique with cathartic bowel preparation, stool tagging, and colonic distention is necessary for high-quality imaging and interpretation, particularly in detection of flat sessile serrated lesions (SSLs). Large SSLs and adenomatous polyps are the most relevant benign precursor lesions to CRC and are the main target of a primary prevention screening strategy. Only CTC and colonoscopy are sufficiently accurate for primary prevention, whereas stool-based and recently approved blood-based tests are limited to detection of cancer in a shorter screening window. CTC allows for selective polypectomy by risk-stratifying large polyps for removal, surveilling small polyps, and ignoring diminutive lesions. CTC is more efficient at identifying advanced neoplasia compared with a universal polypectomy strategy of colonoscopy only, which removes more pseudodisease and incurs excess risk of colonic perforation without benefit. Despite abundant evidence supporting CTC as an ideal screening test, it suffers from widespread and worsening underutilization due to barriers affecting radiology practice and physician support. Opportunistic screening and national trends in the CRC screening landscape will impact future uptake of CTC.

Gynecologic malignancies, including cervical, endometrial, and ovarian cancers (the most common), are a substantial cause of cancer-related morbidity and mortality worldwide, with the prognosis linked to the stage at diagnosis. The aim of screening is to help detect premalignant or early-stage malignant lesions to reduce mortality. Imaging has a limited role in primary screening for the most common gynecologic cancers and usually enters the patient care workflow after a positive screening test or abnormal laboratory results are obtained. Population-level screening for cervical cancer in individuals at average risk involves cytologic analysis and testing for high-risk human papillomavirus (HPV), with modified guidelines for patients at increased risk (ie, those with HIV infection, chronic immunosuppression, a history of high-grade cervical dysplasia, prior HPV-related lower genital tract malignancies, or in utero exposure to diethylstilbestrol [DES]). Routine population-level screening for endometrial and ovarian cancers in patients at average risk is not recommended; evaluation is driven by symptoms. Screening for endometrial cancer in patients at risk (eg, those with Lynch syndrome) includes clinical evaluation and assessment of endometrial thickness at transvaginal US. US-based screening for ovarian cancer in individuals at high risk (eg, those with BRCA gene mutations) is reserved for selected patients (eg, those who defer risk-reducing bilateral salpingo-oophorectomy), who undergo transvaginal US screening and serum biomarker level testing. When gynecologic malignancy is suspected based on symptoms, physical examination, or abnormal laboratory results, imaging aids in lesion detection and characterization, staging, treatment planning, and posttreatment surveillance. Imaging findings are increasingly integrated into formal staging systems, including the International Federation of Gynecology and Obstetrics classification system for cervical and endometrial cancer, which highlights the radiologist's role in multidisciplinary care. The authors summarize current and emerging screening strategies for cervical, endometrial, and ovarian cancers and the integration of imaging into the screening workflow. ^©RSNA, 2026 Supplemental material is available for this article.

IntroductionLymph node (LN) metastasis of lung adenocarcinoma, particularly occult lymph node metastasis (OLNM), remains difficult to predict using conventional imaging and basic positional parameters, adversely affecting prognosis. This study aimed to: (1) evaluate a new CT index (a/A + b/B) for predicting OLNM in cN0 patients, and (2) create and validate a nomogram for predicting LN metastasis probability in CT-suspected cases.MethodsThis single-center retrospective study involved 387 lung adenocarcinoma patients (225 non-LN, 84 OLNM, and 78 with CT-suspected/pathologically confirmed LN metastasis) who had surgery from 2016 to 2024. A spatial index (a/A + b/B) was developed to combine two perpendicular anatomical axes, vertical proximity to the interlobar fissure and horizontal proximity to the mediastinum/hilum, into one standardized metric.ResultsThe combined ratio a/A + b/B was significantly lower in the OLNM and metastatic groups. A lower a/A + b/B was significantly associated with OLNM (OR = 0.175, 95% CI: 0.048-0.638, P = 0.007), suggesting a 0.1-unit decrease in the a/A + b/B ratio increased OLNM risk by 19%. A nomogram utilizing a/A + b/B differentiates CT-suspected LN metastasis from node-negative cases, showing AUCs of 0.83 (95% CI: 0.76-0.90) in training, 0.85(95% CI: 0.76-0.94) in internal validation, and 0.70(95% CI: 0.50-0.91) in external validation.ConclusionA ratio of a/A + b/B < 0.6 indicates a high OLNM risk in cN0 patients. This index can predict OLNM when LNs are small on CT, and a nomogram can differentiate CT-suspected LN metastasis from node-negative cases, meriting further study.

Medical debt affects millions of US residents and has been associated with higher cancer mortality. Whether medical debt burden is associated with incidence of advanced stage cancer, a key determinant of survival, remains unclear.

To examine the association between medical debt and cancer incidence in the US.

This cross-sectional study used ecological county-level data linking 2016 medical debt with age-adjusted incidence rates of 9 cancers from January 1, 2017, to December 31, 2021. The study included 2958 US counties with available data on medical debt in collections and cancer incidence rates. Population-based data were obtained and analyzed from January 11, 2025, to February 15, 2026.

Percentage of residents with any medical debt in collections in 2016.

Age-adjusted all-stage and late-stage (regional or distant) cancer incidence rates per 100 000 person-years from 2017 to 2021. Multivariable models adjusted for urban-rural status, Social Vulnerability Index (SVI), primary care physician density, and states were used to estimate differences in age-adjusted incidence rates of cancer associated with county-level medical debt burden.

Among the 2958 US counties included in the analysis, 1154 (39.0%) were urban and 1804 (61.0%) were rural. The mean (SD) prevalence of medical debt in collections was 21.1% (9.6%), with a mean (SD) primary care physician density of 0.54 (0.35) physicians per 1000 population. The prevalence of medical debt ranged from 1.2% to 51.8%. The mean (SD) medical debt prevalence was higher in rural than urban counties (21.5% [10.0%] vs 20.5% [8.9%]; P = .007) and in counties in the highest vs lowest SVI quartile (27.4% [9.0%] vs 13.9% [6.9%]; P < .001). After adjustment, each 10percentage point increase in county-level medical debt was associated with a higher incidence of late-stage lung cancer (5.15 [95% CI, 4.62-5.68] additional cases per 100 000 person-years), colorectal cancer (0.69 [95% CI, 0.44-0.94] additional cases per 100 000 person-years), cervical cancer (0.39 [95% CI, 0.23-0.55] additional cases per 100 000 person-years), melanoma (0.59 [95% CI, 0.48-0.70] additional cases per 100 000 person-years), kidney and renal pelvis cancer (0.38 [95% CI, 0.27-0.49] additional cases per 100 000 person-years), bladder cancer (0.24 [95% CI, 0.16-0.32] additional cases per 100 000 person-years), and head and neck cancer (0.92 [95% CI, 0.77-1.07] additional cases per 100 000 person-years). Similar patterns were observed for overall cancer incidence.

In this cross-sectional study of US counties, higher medical debt burden was associated with higher incidence rates of late-stage and overall cancer across multiple cancer types. These findings suggest that medical debt may reflect structural and financial barriers associated with cancer diagnosis and outcomes at the population level.

Diffuse lower-grade glioma (DLGG), i.e. WHO grade 2 and 3 tumors, frequently manifests with epileptic seizures, significantly affecting quality of life. While [¹⁸F]FET PET is routinely used to assess glioma metabolism, differences between patients with and without glioma-related epilepsy have not yet been assessed systematically. The objective of this study was to assess whether preoperative [¹⁸F]FET PET uptake is associated with epileptic seizures at initial presentation in patients with DLGG.

This retrospective study included 121 patients with DLGG with preoperative [¹⁸F]FET PET (2015-2025). [¹⁸F]FET uptake parameters were determined in patients with measurable disease according to PET RANO 1.0 criteria. Seizure status was assessed exclusively for seizures occurring before surgery. Statistical analyses included Fisher's exact test, Mann-Whitney U test, and multivariable logistic regression.

Seventy-eight patients (64%) demonstrated measurable disease in [¹⁸F]FET, of whom 57 (73%) presented with epileptic seizures compared to 17 (40%) in the no-uptake group (p < 0.001). In the measurable disease group, those with seizures exhibited significantly higher median TBR_max (3.02; IQR 2.35-4.00) and TBR_mean (2.2; IQR 1.8-2.5) values than those without seizures (TBR_max 2.4; IQR 2.00-3.16, TBR_mean 1.9; IQR 1.7-2.2). The tumor location did not account for the observed association between [¹⁸F]FET uptake and seizures (p > 0.05). In multivariable analyses, [¹⁸F]FET uptake remained independently associated with preoperative seizures (adjusted OR 2.86, 95% CI 1.18-7.07; p = 0.020).

These findings demonstrate an association between [¹⁸F]FET uptake and glioma-related epilepsy in DLGG. Further research on amino acid transporter expression and glutamatergic pathways may elucidate underlying mechanisms.

The nationwide registry analysis by Beck et al. provides valuable insights into treatment patterns for retroperitoneal sarcoma in Germany over two decades, highlighting increasing use of multivisceral resection and improved survival analyses. While the study establishes an important framework for evaluating rare cancers using registry data, several methodological issues may influence the interpretation of the reported temporal trends and clinical conclusions. First, the observed increase in multivisceral resection may partly reflect progressive improvements in registry documentation and procedure coding rather than a true change in surgical practice. Second, substantial missing data for tumor grade and metastatic status raise concerns regarding potential selection bias in survival analyses performed on complete cases without sensitivity analyses. Addressing documentation completeness and the impact of missing data would strengthen confidence in the reported findings and improve the applicability of registry-based evidence for clinical decision-making and future rare cancer research.

Parental cancer can disrupt family dynamics, particularly in families with adolescent and young adult (AYA) children. While strong family functioning supports better psychosocial outcomes, factors that influence this functioning remain underexplored. This study examined correlates and trajectories of family functioning among AYA and their parents following a cancer diagnosis.

In this longitudinal study, quantitative surveys were completed by parents diagnosed with cancer and their AYA offspring at two timepoints: within 12 months of diagnosis (T1) and 6 months later (T2). Outcomes included perceived family functioning, family resilience, communication avoidance about cancer, individual distress, parental self-efficacy, and AYA support needs.

At T1, 55 AYA (aged 12-24 years) and 71 parents (aged 32-62 years), both predominantly female, participated; 31 AYA and 52 parents completed both timepoints. When controlling for age and gender, T1 better family functioning (low scores) was associated with greater family resilience (high scores, AYA: β = -0.57, p < .001; parents: β = -0.21, p = .035) and lower communication avoidance about cancer (low scores, AYA: β = 0.29, p = .04; parents: β = 0.39, p < .001). T2 family functioning was associated with T1 family functioning (AYA: β = 0.75, p < .001; parents: β = 0.67, p < .001), with higher T1 AYA distress additionally being associated with poorer AYA family functioning (β = 0.42, p = .001). Most participants maintained high family functioning over time (parents: 78%; AYA: 71%), while 16-19% showed persistent low functioning.

Family resilience and open communication about cancer facilitate adaptation 0-12 months after a parental cancer diagnosis in both parents and their AYA children. While initial T1 parent and AYA perceived family functioning was associated with family functioning 12-18 months post-diagnosis, initial distress was associated with T2 functioning only among AYA. Although most participants show stable, high family functioning post-diagnosis, targeted support is essential for those at risk. Findings underscore the importance of early psychosocial interventions to promote healthy family dynamics in the context of parental cancer.

This single-center, cross-sectional case-control study aimed to characterize the gut microbiome profiles of patients with advanced colorectal cancer (CRC), identify candidate microbial features, and explore how well these features distinguished advanced CRC cases from healthy controls within the study dataset. Fecal samples were collected from 72 treatment-naïve patients with advanced CRC and 61 healthy controls. Microbial community structure was profiled using high-throughput sequencing of the V3-V4 region of the 16 S rRNA gene. The analytical pipeline included α/β-diversity analysis, multilevel taxonomic analysis, LEfSe, and machine-learning algorithms, including random forest (RF), gradient boosting machine (GBM), and LASSO, to identify key Amplicon Sequence Variants (ASVs) and evaluate their ability to discriminate between the two groups. Results showed significantly reduced α-diversity and distinct β-diversity in the CRC group. Key SCFA-producing genera (Faecalibacterium, Agathobacter, Roseburia) were consistently depleted. The RF feature-prioritization model achieved an out-of-bag (OOB) accuracy of 0.850 and an OOB AUC of 0.899. Nested five-fold cross-validation based on the prioritized ASVs yielded AUCs of 0.891, 0.900, and 0.891 for RF, GBM, and LASSO, respectively. These findings show internally reproducible case-control discriminatory patterns within the present cohort and support further evaluation of the prioritized microbial features in independent, clinically representative populations.

Ormeloxifene (ORM), a selective estrogen receptor modulator with a non-steroidal structure, exhibits mild estrogenic activity in bone and anti-estrogenic activity in uterine and breast tissues. ORM induces cell-cycle arrest and exhibits antineoplastic activity in breast cancer. However, its direct effect on the cellular senescence phenotype has not been documented.

Two-dimensional gel electrophoresis (2DE)-based proteomic analysis of ORM-treated MDA-MB-231 cells identified differentially regulated proteins by MALDI-TOF/TOF mass spectrometry. Functional categorization and pathway-level integration of these proteins suggested a coordinated cellular response converging on stress-induced cellular senescence. MTT, colony formation, cell-cycle, β-galactosidase and Sudan Black B staining, and immunoblotting were performed to investigate ORM-induced senescence. ORM inhibited viability of MCF7 and MDA-MB-231 cells, with IC₅₀ values ranging from 7 to 9 µM, and reduced their colony-forming ability, with a greater effect in MCF7 cells. ORM induced G0/G1 growth arrest in MCF7 cells by decreasing CDK4/CDK6 and increasing CDK inhibitors p21Cip1/p27Kip1. Furthermore, ORM induced irreversible senescence in a time-dependent manner, as evidenced by β-galactosidase and Sudan Black B staining and increased expression of established senescence markers. Interestingly, ORM enhanced the sensitivity of MCF7 cells to tamoxifen.

Collectively, these findings suggest that ORM restrains tumor progression by promoting irreversible senescence. The combination of ORM and tamoxifen may represent a potential therapeutic strategy for tamoxifen-resistant breast tumors.

To explore the clinical patterns of nivolumab-induced cytokine release syndrome (CRS), and to provide a basis for diagnosis, treatment and prognosis.

Clinical reports of nivolumab-induced CRS before March 31, 2026 were collected, and clinical data were extracted for retrospective analysis.

Thirty-five patients were included, with a median age of 55 years (range 3, 86). The median time for the appearance of CRS was 54.5 days (range 0.2, 391) and the median number of cycles was 3 (range 1, 17). Fever (85.7%), hypotension (57.1%), tachycardia (42.9%), fatigue (25.7%), rash (25.7%) and impaired consciousness (25.7%) were the main symptoms of patients. Laboratory tests may reveal liver injury, renal injury, elevated C-reactive protein, elevated ferritin, and elevated interleukin-6. After discontinuing nivolumab and receiving treatment with glucocorticoids and tocilizumab, 71.4% of the patients showed improvement in symptoms and clinical markers, while 28.6% of the patients died.

Nivolumab-induced CRS can lead to multi-organ functional impairment and even be fatal. During the administration of nivolumab, the possibility of CRS should be taken into consideration. Glucocorticoids and tocilizumab are widely utilized as primary therapeutic approaches for the management of CRS in clinical practice. However, given the limited available evidence and inherent clinical confounders, the standardized and optimal treatment strategy for nivolumab-induced CRS remains undefined and requires further exploration.