Immune checkpoint inhibitors (ICIs) improve cancer survival but can trigger immune-related adverse events. Among these, fulminant myocarditis is an often fatal complication with limited therapies. We developed a mouse model employing cardiomyocyte-restricted antigen expression to define how ICIs drive cardiac autoimmunity. Combined cytotoxic T cell antigen-4 (αCTLA-4) and programmed death-1 (αPD-1) blockade uniquely induced robust expansion of antigen-specific CD8 T cells, myocardial inflammation, and lethal arrhythmias. PD-1 blockade alone permitted the priming and effector differentiation of naive autoreactive CD8 T cells, whereas concomitant CTLA-4 inhibition amplified cardiac pathology. Unexpectedly, myocardial injury was independent of perforin-mediated cytotoxicity but critically depended on T cell-derived TNF, which promoted myeloid recruitment, cytokine production, and arrhythmogenesis. Genetic ablation of CD8 T cell-derived tumor necrosis factor (TNF) or TNF receptor 2 (TNFR2) blockade prevented cardiotoxicity while preserving antitumor efficacy. These findings establish a TNF-TNFR2-driven inflammatory circuit downstream of autoreactive CD8 T cells as a central mechanism of ICI myocarditis and a strategy to uncouple cardiotoxicity from immunotherapy benefits.

Perceptions of the term 'cancer survivor' among women with breast cancer: An interpretative phenomenological analysis.

The association between cancer history and long-term body composition based on a 10-year follow-up.

Adverse childhood experiences and cancer pain: A national cross-sectional analysis of survivors' pain outcomes.

Understanding the needs and preferences of oncology dietitians for mobile health apps.

As national cancer survival estimates in Italy date back to 2011, we provided updated figures using population-based cancer registries. Analyses by age and sex included 1.418.044 cancers diagnosed between 2013 and 2017 from 34 registries covering 48 million residents. The 2008-2017 period, with 20 registries covering 24 million residents, was used for trends and regional comparisons. Net survival was estimated by Pohar-Perme method with life tables by year, sex, residence and calculated using the international standard distribution. Five-year age-standardized net survival for all cancers combined was 66.7 % in females and 62.2 % in males. Females had better survival than males for most cancers, notably acute lymphatic leukaemia (+9 % points (pp)), upper respiratory/digestive (+9 pp), lung (+6 pp), CNS (+5 pp), and stomach (+4 pp). Males had a higher survival for bladder (+4 pp), kidney (+2 pp), and urinary cancers (+5 pp). Best outcomes (>75 %) were documented for prostate, testicular, breast, endometrial, thyroid, melanoma, Hodgkin lymphoma, bladder, and chronic lymphatic leukaemia. Poorest prognosis (<30 %) was for CNS, liver, lung, pancreas, and acute myeloid leukaemias. Survival was age-dependent, highest in younger and lowest in older patients, with > 40 % points gaps in some haematological cancers. From 2008-2017, net survival arose from 65.7 % to 70.7 % in men and from 69.9 % to 74.1 % in women. Improvements were seen for pancreas, lung, and acute leukaemias, mainly in women, while decreases affected bladder, cervical, chronic lymphatic leukaemia in men. Geographical disparities persisted, with higher survival in Northern-Central Italy (64.0 % for men and 68.3 % for women) than in Southern-Islands (58.1 % for men and 63.7 %, for women). Our findings confirmed a better prognosis for younger patients and females than male patients. Survival has continued to improve over time, even at a higher improving rate in the considered period than the past.

The cachexia index (CXI) demonstrates potential as both a diagnostic tool for cachexia and a prognostic tool for survival in cancer. However, CXI's predictive value has not been verified in cervical cancer. The purpose of this study is to investigate the prognostic value of the CXI in patients with cervical cancer treated with radiotherapy. We retrospectively screened patients diagnosed with cervical cancer who underwent radiotherapy in a single institution between September 2013 to September 2015. The CXI was calculated as the skeletal mass index (SMI) × albumin/neutrophil-to-lymphocyte ratio. SMI was measured by computed tomography using the muscles of the third lumbar vertebra. Survival times were evaluated using the Kaplan-Meier method and Cox proportional hazards regression. A nomogram for predicting survival was developed. A total of 81 patients with cervical cancer were included. The cutoff value of the CXI was set at 59.7 using receiver operating characteristic (ROC) analyses. According to this cutoff value, 47 patients were assigned to the high-CXI group, and 34 were assigned to the low-CXI group. The Cox regression analysis showed that a low CXI was associated with decreased overall survival (hazard ratio [HR]: 3.15; 95% confidence interval [CI]: 1.24-8.00; P = 0.016). Patients in the low-CXI group also had shorter progression-free survival than those in the high-CXI group, but the difference was of borderline significance (HR: 2.26; 95% CI: 1.00-5.11; P = 0.05). The pretreatment CXI is an independent prognostic factor in patients with FIGO II-III cervical cancer treated with radiotherapy.

Global breast cancer incidence, mortality, and survival among indigenous women: A systematic review and meta-analysis.

Associations between physical activity, body esteem, and self-esteem among women with breast and gynecological cancer.

A J-shaped relationship between Dietary Inflammatory Index and frailty risk among middle and old aged US cancer survivors.

Most young women who have survived childhood cancer express a desire to have children. Many of them are concerned about the potential adverse impact of pregnancy on their health, which has been affected by prior cancer treatment. The aim of this study was to determine whether motherhood increases the risk of developing subsequent malignant neoplasms. The study cohort consisted of 942 female childhood cancer survivors, median age at first cancer diagnosis 10.84 years (IQR 4.29-14.92), who had been treated at the Department of Pediatric Hematology and Oncology, Motol University Hospital, Prague, between 1965 and 2018. In this group, 363 women gave birth to 559 children. Seventy-three female childhood cancer survivors developed 80 subsequent malignant neoplasms. Of these, 40 subsequent malignant neoplasms occurred in women who had children. The median time from the end of primary cancer treatment to first subsequent malignant neoplasm development was 19.93 years (IQR 14.55-26.56). A comprehensive analysis revealed no difference in the risk of subsequent malignant neoplasms between mothers and "non-mothers". Only older age of the cancer survivors in follow-up and previous radiotherapy (p = 0.0133) were significant risk factors for subsequent malignant neoplasm development. This study revealed that motherhood does not increase the risk of subsequent malignant neoplasms. We confirmed a statistically significant increased risk of subsequent malignant neoplasms only for previous treatment modality, the length of follow-up and the age of the female childhood cancer survivors. These results are important for improving the quality of life of young cured women who are worried about a planned pregnancy. This study evaluated the long-term cancer risk among women treated for cancer during childhood, with particular focus on those who later gave birth. Among 942 participants, 363 had post-treatment pregnancies. Results indicate that childbearing does not increase the risk of subsequent malignant neoplasms in this population. Instead, elevated risk for subsequent malignant neoplasms was associated with older age at follow-up and prior exposure to radiotherapy. These findings provide evidence that pregnancy is safe for female childhood cancer survivors and support informed reproductive decision-making.

Quantifying cancer survival is a crucial component of cancer surveillance and control. Survival for all cancers combined is an overall summary to explore differences between population groups and over time. Net survival is the usual measure for reporting survival for all cancers combined. Differences in the cancer site distribution between groups can be adjusted for using standardization. We propose using individual weights incorporated into the Pohar Perme estimator of net survival for standardized all cancers combined survival estimates, rather than a weighted average of stratum specific estimates. This removes sparse data problems, where estimates are unobtainable for some strata. Extending to reference adjusted all-cause survival gives an alternative, interpretable measure, enabling partitioning of all-cause survival differences into those due to cancer site/age/sex distribution differences, other cause mortality differences and cancer mortality differences. We illustrate the methods using data on 749 889 individuals diagnosed with cancer in Norway 1986-2021. Using individual weights gives very similar estimates to traditional and model-based standardization and avoids using ad-hoc sparse data methods. Reference adjusted all-cause survival provides measures with simpler interpretation. For example, between 1986 and 1990 and 2016-2021 there was a 25.9 %age point improvement in 5-year all-cause survival. This improvement was partitioned into changes in the site/age/sex distribution (2.0), changes in other cause mortality rates (4.4) with the majority (19.6) due to improvements in cancer survival. Survival of all cancers combined is easily analyzed non-parametrically using individual weights. Reference adjusted all-cause survival gives a more interpretable measure improving understanding of differences over time/between groups.

Neurocognitive deficits in adult survivors of childhood cancer are well established, but less is known about developmental disorders (DD) arising shortly after cancer diagnosis. Using 2016-2019 linked Ohio cancer registry and Medicaid data, we compared DD among 324 children with cancer and 606,913 cancer-free controls. Pre-diagnosis, DD prevalence was similar (16% vs. 16.9%). However, post-diagnosis, children with cancer had over twice the risk of DD (ARR 2.09, 95% CI 1.55-2.83) across developmental domains. These findings reveal that DD emerges soon after cancer diagnosis, potentially related to treatment and/or secondary toxicities and highlight the need for early screening and rehabilitative intervention.

Effects of exercise on health-related fitness and patient-reported outcomes in survivors of head and neck cancer: a systematic review and meta-analysis.

Association of social isolation and loneliness with cancer prognosis: an analysis of the UK Biobank.

Assessment of survival and clinicopathologic characteristics associated with lymph node isolated tumor cells in epithelial ovarian cancer.

Understanding the changing burden of head and neck cancers (HNC) is essential to guide public health interventions and inform cancer care strategies. We conducted a cohort study using routinely collected primary care data Clinical Practice Research Datalink (CPRD) GOLD from the United Kingdom. Adults aged ≥ 18 years with ≥ 1 year of prior history were included. We estimated crude and age-standardised incidence rates (IRs) and one-, five-, and ten-year survival from 2000 to 2021, stratified by age and calendar year. Findings from CPRD GOLD were compared with primary care data from CPRD Aurum (England only). There were 12,455 patients with a diagnosis of HNC from CPRD GOLD (69.2 % male; median age 64 years). Crude incidence in GOLD increased from 9.08 (95 % CI: 7.88-10.42) per 100,000 person-years in 2000-15.59 (14.07-17.23) in 2021, with similar trends observed in CPRD Aurum. Age-standardised incidence trends were attenuated overall but remained elevated for oropharyngeal and tongue cancers. Five-year survival improved modestly, from 53.8 % (95 % CI: 51.4-56.3 %) in 2000-2004-58.7 % (56.5-60.9 %) in 2015-2019. Incidence increases for HNC were attenuated after age standardisation, suggesting a contribution of demographic ageing, although elevations persisted for specific subsites. Small improvements in long term survival highlights more research is needed to improve earlier diagnosis which will lead to better patient outcomes.

Changing landscape in stage, treatment and survival of gastric cancer in China 1998-2022: Insights of 40,158 patients from the National Gastric Cancer Cohort.

Large-scale DNA organization analysis of primary breast cancers for prediction of axillary lymph node metastases.

Chronological age is an imperfect proxy for risk assessment in geriatric oncology. There is an urgent need for an objective, easily measurable biological aging signature to refine patient stratification and personalize therapeutic decisions. We analyzed a panel of seven aging-related biomarkers (including markers of inflammation, anabolic reserve, and telomere status) in 244 nonmetastatic breast cancer patients from two age groups ("Old", ≥70 years, N = 162; "Young", ≤60 years, N = 82). We used Latent Class Analysis (LCA) to integrate these markers and identify distinct biological risk profiles. These profiles were then evaluated for their association with Overall Survival (OS) and Cancer-Specific Death (CSD) via Competing Risk Analysis. LCA identified two patient profiles. The Unfavorable Biologic Profile (56.1% of the cohort) was defined by a triad of high MCP-1, high Chitinase activity, and low IGF-1. This profile was strongly associated with poorer OS (Age-adjusted HR=1.82, p = 0.018). Crucially, 15% of chronologically "Young" patients were assigned to this high-risk profile, while 23% of "Old" patients were assigned to the Favorable Profile. Furthermore, the Unfavorable Profile was more strongly and specifically associated with CSD (Subdistribution HR: 2.05, p = 0.012) than with Non-Cancer Death. Our results delineate an unfavorable, trans-chronological biological profile that identifies patients with low host reserve, largely driven by inflammaging and catabolism. This integrated signature provides a robust, objective screening tool to identify biologically frail patients, validating the need for Comprehensive Geriatric Assessment (CGA) and biomarker-guided therapeutic de-escalation (e.g., avoiding adjuvant chemotherapy) to improve individualized outcomes in oncology. BS32220096117.