Cancer epidemiology cohorts (CECs) provide key insights into genetic, environmental, lifestyle, and clinical factors influencing cancer development, progression and outcomes. Engaging communities impacted by research and participants in cohort studies is essential for building trust and ensuring the success of these studies. While the concept of engagement in cancer research is not new, the practice of engagement is evolving towards more rigorous, bidirectional relationships between researchers and communities. Here, we discuss some goals of engagement in CECs supported by the National Cancer Institute (NCI), Division of Cancer Control and Population Sciences (DCCPS), Epidemiology and Genomics Research Program (EGRP), which include: (1) involving community and participant voices in study design and implementation, (2) providing updates on study progress, (3) returning value to communities and participants, and (4) demonstrating appreciation to study participants. This paper also outlines opportunities to enhance engagement activities across cohorts such as expanding the use of digital technologies, continuing to share lessons learned, and supporting report back of findings. Additionally, strengthening evidence base on how to engage communities at all stages of research can foster more meaningful partnerships and ultimately lead to more impactful research and better health outcomes.
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Incidence of common cancers has been rising in the U.S., with strong geographic variation in risk factors and incidence, particularly in the Southeast and in rural and high-poverty areas. Elevated cancer risk may translate into higher geographic concentrations of cancer survivors who require surveillance, follow-up care, and supportive services. Local geospatial assessment of cancer burden may inform both cancer prevention and survivorship planning. We utilized adult (≥ 18 years) incident cases of colorectal, prostate, breast, and lung cancers from the 2010-2019 Alabama Statewide Cancer Registry data. We performed Bayesian disease mapping to estimate census tract-level relative risks (RRs) and classified tracts as hot and cold spots at 99% credible intervals (CrIs). Stratified analyses examined median RR differences by 2010 Rural-Urban Commuting Area codes and 2010-2019 Area Deprivation Index (ADI) quartiles. We identified 7, 9, 3, and 83 hot-spot tracts for colorectal, prostate, breast, and lung cancer incidence, respectively. Colorectal hot spots were concentrated in rural southwestern Alabama; prostate cancer hot spots formed a band across south-central Alabama; breast cancer hot spots were localized to Huntsville and Birmingham; and lung cancer hot spots were widespread across rural areas. Increasing rurality was associated with higher median RRs for colorectal, prostate, and lung cancers. Neighborhood-level geographic disparities in cancer risk highlight areas with higher concentrations of cancer survivors with survivorship care needs. Linking geospatial incidence patterns with survivorship planning could support targeted strategies for surveillance, symptom management, psychosocial care, and health maintenance in high risk communities in the Deep South.
Type 2 diabetes mellitus (T2DM) and cancer are both major global public health concerns; however, their causal relationship remains unclear. This study aims to quantitatively investigate the potential causal associations between T2DM and 17 site-specific cancers through a systematic review and meta-analysis of Mendelian randomization (MR) studies. We systematically searched Scopus, PubMed, the Cochrane Library, Web of Science, Embase, and Ovid MEDLINE to identify MR studies investigating the association between T2DM and cancer published up to June 2025. A meta-analysis was performed on extracted data, accompanied by heterogeneity testing, sensitivity analysis, and publication bias assessment. The initial search yielded 1,143 articles. After multi-level screening, 44 articles were ultimately included, with 42 articles (comprising 131 MR studies) eligible for meta-analysis. The pooled results demonstrated that T2DM was significantly associated with an increased risk of pancreatic cancer (OR = 1.09, 95% CI: 1.04-1.15, P = 0.0007) and endometrial cancer (OR = 1.07, 95% CI: 1.04-1.09, P < 0.00001). Conversely, T2DM was significantly associated with a decreased risk of gastric cancer (OR = 0.90, 95% CI: 0.85-0.93, P < 0.00001), melanoma (OR = 0.97, 95% CI: 0.95-0.99, P = 0.009), and esophageal cancer (OR = 0.86, 95% CI: 0.79-0.93, P = 0.0002). The effect sizes for T2DM's associations with thyroid and breast cancers were modest, with no clinical significance. No significant causal association was identified between T2DM and the remaining ten cancer types. The causal relationship between T2DM and cancer appears to be tissue-specific. T2DM significantly increases the risk of pancreatic and endometrial cancers while demonstrating a negative association with gastric cancer, melanoma, and esophageal cancer. https://www.crd.york.ac.uk/PROSPERO/, identifier CRD420251066404.
Purpose To determine the interval cancer rate (ICR) after negative screening contrast-enhanced mammography (CEM) and compare the characteristics of interval cancers (ICs) with those of CEM screen-detected cancers. Materials and Methods This retrospective, single-institution study included consecutive screening CEM examinations performed from January 2015 through December 2021. ICs diagnosed within 1 year of a negative screening CEM and all CEM screen-detected cancers were identified. Two breast radiologists independently reviewed prior negative CEM examinations to classify ICs as missed, misinterpreted, or occult. Patient- and lesion-level characteristics were compared between ICs and screen-detected cancers using the Wilcoxon rank sum test for continuous variables and the Fisher exact or χ2 tests for categorical variables. Results The study included 6911 screening CEM examinations in 2756 female patients (median age, 53 years; IQR, 47-60 years). Among 6120 negative screening examinations, 14 ICs were diagnosed in 14 patients. The overall ICR was 2.29 cancers per 1000 examinations, and the symptomatic ICR was 0.82 per 1000 examinations (five of 6120). ICs accounted for 13% (14 of 106) of all cancers diagnosed (interval and screen detected). Invasive ICs occurred more frequently in the setting of moderate or marked background parenchymal enhancement than screen-detected cancers (six of eight, 75% vs 17 of 57, 30%; P = .02). Most ICs (10 of 14, 71%) were occult on prior screening CEM. Conclusion The ICR after CEM was 2.29 cancers per 1000 examinations, representing 13% of all cancers diagnosed. Most ICs were occult at prior CEM, and invasive ICs were more frequently associated with moderate or marked background parenchymal enhancement when compared with CEM screen-detected cancers. Keywords: Mammography, Breast, Interval Cancers Supplemental material is available for this article. © RSNA, 2026.
Cancer-associated thrombosis (CAT) is a leading cause of morbidity and mortality among cancer patients. While venous thromboembolic events have been extensively studied due to their higher incidence, arterial thrombosis in cancer patients-referred to as cancer-associated arterial thromboembolism (CA-ATE)-is less well understood but may pose a greater danger. The pathophysiology of CA-ATE involves complex interactions between the tumor microenvironment, cancer cells, patient-related factors, and cancer therapies. Some chemotherapeutic agents, particularly platinum-based compounds (cisplatin, oxaliplatin), gemcitabine, taxanes, and targeted therapies such as tyrosine kinase inhibitors (TKIs), have been associated with an increased risk of arterial thrombosis. In certain patient populations, hormonal therapy and selective estrogen receptor modulators may also contribute to this risk. Additionally, factors such as patient age, cancer type, and stage contribute to an increased risk of arterial thrombosis in this population. Key mechanisms driving CA-ATE include endothelial injury, hypercoagulability, and platelet activation. Certain malignancies, notably lung and pancreatic cancers, are associated with a higher incidence of arterial thrombotic events. The aim of this review is to enhance understanding of the underlying mechanisms of cancer-related arterial thromboembolism and to highlight the various therapeutic, cancer-related, and patient-related factors that contribute to the occurrence of cancer-associated arterial thrombotic events.
Men who have sex with men (MSM) are disproportionately affected by human papillomavirus (HPV)-associated anal cancer. Prior to national anal cancer screening guidelines, literature suggested that the overall utilization of screening was low, with slightly higher uptake in MSM living with human immunodeficiency virus (HIV). The objective of this study was to report the recency of anal cancer screening by various screening methods and describe differences in self-reported screening histories by HIV status in MSM. We also aimed to comment on the use of cross-sectional methods for research on anal cancer screening utilization in MSM. This cross-sectional survey recruited MSM in Minnesota from two online dating sites to participate in a single survey on anal cancer screening experiences. Fisher's exact tests and t-tests were used to examine differences in demographics and screening experiences by HIV status. A total of 52 MSM participated in the survey, and 38 provided data on previous anal cancer screening experiences. Most participants were white (65.4%), gay (88.5%), and HIV-negative (69.8%). Approximately 57% of MSM living with HIV self-reported an experience with anal cancer screening in the last year compared to 37.5% of MSM living without HIV (p = 0.32). Screening was often recommended by HIV providers for MSM living with HIV (66.7%) versus primary care providers for HIV-negative MSM (47.2%, p < 0.01). MSM living with HIV more often reported a history of an abnormal result compared to HIV-negative MSM (71.4% vs. 29.2%, p = 0.018). Our findings suggest that MSM in Minnesota are utilizing anal cancer screenings in accordance with current recommendations. MSM living with HIV were more likely to report a history of HPV-related infections and abnormal results, supporting continued prioritization of screening in this population. The differences in recommending providers by HIV status highlight the need for additional training to support equitable and consistent practices. Finally, we suggest the use of alternative methods to document future anal cancer screening utilization in MSM.
The link between salt intake and the risk of gastric cancer remains uncertain, and a causal relationship has not been established. Therefore, clarifying the causal effect of salt intake on the risk of gastric cancer using reliable causal inference methods is necessary. The aim of this study was to assess the causal association between salt intake and cancer by integrating summary-level genome-wide association study (GWAS) data. Two-sample Mendelian randomization (MR) analyses were performed using summary statistics from a GWAS. Inverse-variance weighted (IVW) regression, Mendelian randomization-Egger (MR-Egger) regression, and weighted median analyses were used to evaluate the causal relationship between salt intake and gastric cancer. Moreover, Mendelian Randomization Pleiotropy RESidual Sum of Squares and Outliers and MR-Egger analyses were used to evaluate the level of multipotency, and "leave-one-out" sensitivity analysis was assessed. The IVW method estimate indicated that salt intake was not correlated with gastric cancer incidence. The IVW (β = 0.1008, standard error [SE] = 0.1510, odds ratio [OR] = 1.1061, 95% confidence interval [CI], 0.82-1.48, P = .5042), MR-Egger regression (β = 0.059, SE = 0.5318, OR = 1.0612, 95% CI, 0.37-3.01, P = .9111), and weighted median (β = 0.2639, SE = 0.2298, OR = 1.3020, 95% CI, 0.82-2.04, P = .2508) analyses revealed no causal relationship between salt intake and gastric cancer risk (P > .05). In addition, the funnel plot and MR-Egger analysis (P = .6694 > .05) did not indicate horizontal pleiotropy or heterogeneity. GWAS data from public databases were used in this study, and the causal relationship between salt intake and gastric cancer risk was analyzed via a two-sample MR method. The results revealed no genetic causal relationship between salt intake and gastric cancer.
Recent advances in computational pathology enables AI-assisted diagnosis and risk stratification of breast cancer. This advance in technology will reduce the inconsistent reporting of breast cancer grading using Nottingham Histologic grading system. This study evaluated the implementation of the DeepGrade model for breast cancer grading using H&E-stained slides from breast cancer patients in Ethiopia. To assess the accuracy, specificity, and sensitivity of the DeepGrade model in distinguishing between grade 1 and grade 3 tumours. Additionally, the study aimed to explore the model's ability to further classify Nottingham Histologic Grade 2 tumours into two distinct risk categories. A retrospective analysis was conducted using data from 200 tumour samples from the Department of Pathology, Tikur Anbessa Specialized Hospital, Addis Ababa, Ethiopia. The performance of the DeepGrade model was compared with three pathologists' diagnosis using metrics such as specificity, sensitivity, area under the curve and agreement level. The DeepGrade model reached a 100% specificity for low-grade tumours and an 82.05% sensitivity for high-grade tumours, with an AUC of 0.914 and an agreement level of 86.79%. Our findings illustrated the model's strong agreement with the pathologist, and a Kappa coefficient of 0.71 (95% CI: 0.51-0.90). The study showed the potential significance of DeepGrade model utilization in enhancing breast cancer grading practices in resource-limited settings. By adopting this model, a consistent and standardized grading system for breast cancer can be established, significantly enhancing the effectiveness of breast cancer management.
Implementation of prehabilitation for patients undergoing surgical treatment for colon cancer has proven effective in reducing the risk of postoperative complications. Currently the recommended maximal treatment interval has limited span for implementation of a prehabilitation program. The aim of the current study was to determine the association between advised treatment interval and (cancer-free) survival, while stratifying for the risk of postoperative complications. This retrospective multicenter study included patients who underwent elective surgical treatment for colon cancer between 2010 and 2016. Patients were stratified based on risk of postoperative complications (high-risk and non-high-risk). Treatment interval was defined as time between diagnosis and surgery, divided into three categories (≤35 days, 36-49 days, and > 49 days). Primary endpoints were overall survival and cancer-free survival, assessed by multivariate Cox proportional hazard regression analysis. A total of 3376 patients were included, of whom 60% were considered non-high-risk and 40% high-risk, with a median age of 72 years (IQR 64-78). Of the included patients, 862 (26%) had tumor stage I, 1353 (40%) had tumor stage II, and 1160 (34%) had tumor stage III colon cancer. Treatment interval was not associated with cancer-free survival (36-49 days [non-high-risk p = 0.77; high-risk p = 0.56] or > 49 days [non-high-risk p = 0.46; high-risk p = 0.13]). A treatment interval > 49 days was associated with poorer five-year overall survival in non-high-risk patients (HR = 1.35, p < 0.05), but not in high-risk patients (p = 0.69). A treatment interval of 36-49 days was not associated with five-year overall survival (non-high-risk p = 0.24; high-risk p = 0.98). Extending the treatment interval in curative treatment of colon cancer up to 49 days appears safe for both high-risk and non-high-risk patients. For high-risk patients, the expected benefits of longer treatment interval including prehabilitation should be balanced with the medical urgency to operate.
Identifying robust biomarkers for early cancer detection remains challenging, particularly when working with limited or heterogeneous datasets. Here, we present a proof-of-concept deep learning framework for cancer classification using blood-based proteomic profiles. Our approach leverages sample type transfer and synthetic data augmentation to improve performance and generalization across sample types. Models were trained on plasma proteome data from 13,208 pan-cancer cases and 39,806 controls in the UK Biobank. To address class imbalance and enrich the feature space, a convolutional neural network (CNN-Synth) was trained to detect cancer cases using data augmented with synthetic pan-cancer samples generated via a variational autoencoder. Performance was evaluated in an independent saliva-based dataset from a head and neck cancer case-control study (n = 156). CNN-Synth (AUC = 0.88) surpassed models trained without synthetic data (AUC ≤ 0.77). SHapley Additive explanations identified well-known cancer markers as key features. These results highlight the use of sample type transfer and synthetic data augmentation, with further validation needed.
Survival rates for childhood cancer remain far lower in low- and middle-income countries (LMICs) compared to high-income countries (HICs). In Tanzania, challenges in cancer care for children are driven by shortages of trained providers, limited infrastructure, and constrained access to essential medications. This study evaluates pediatric oncology capacity and infrastructure in Northern Tanzania to identify system gaps and opportunities for improvement. A cross-sectional survey of capacity for pediatric cancer care was conducted at 25 hospitals across the Kilimanjaro, Arusha, Manyara, and Tanga regions in Tanzania. Facilities included health centers, district hospitals, regional hospitals, and one zonal referral hospital. Using a tool adapted from the International Society of Paediatric Oncology (SIOP) Global Mapping Survey, the World Health Organization Essential Medicines List, and the Global Initiative for Childhood Cancer, we collected data on hospital infrastructure from hospital leaders and staff. Key indicators included diagnostic imaging, pathology services, oncology workforce, medicine availability, treatment modalities, and cancer case volumes. Descriptive statistics were summarized using R. Of the facilities surveyed, only one hospital (Kilimanjaro Christian Medical Centre) had a dedicated pediatric oncology ward and subspecialized staff. Although all facilities reported access to basic imaging such as x-ray and ultrasound, advanced imaging modalities (CT, MRI, specialized imaging) were confined to higher-level hospitals. Only 1 out of 25 hospitals offered pathology and pediatric surgical services. Among 20 essential pediatric oncology medicines assessed, only dexamethasone was universally available. District hospitals, despite serving the largest pediatric catchment areas and recording the highest admissions for children, lacked dedicated pediatric oncology wards. Pediatric oncology services in Northern Tanzania are constrained by shortages in infrastructure, personnel, diagnostics, and medications. District hospitals have limited capacity to treat childhood cancer, resulting in critical delays in diagnosis and treatment. Strengthening infrastructure at the district level, creating efficient referral systems, and embedding pediatric oncology care into broader health systems may improve survival outcomes for children with cancer.
Early-onset (<50 years) and never-smoker lung cancers are increasing global concerns. The emerging trends challenge current screening guidelines, which focus on adults aged >50 years with heavy smoking histories. We applied the US Preventive Services Task Force (USPSTF) 2021 screening criteria as the primary definition of high-risk individuals eligible for lung cancer screening and assessed the potential optimization of these criteria using real-world lung cancer data in China. In this nationwide, multicenter, hospital-based observational study, we enrolled asymptomatic patients with surgically resected primary lung cancer across 26 tertiary hospitals from January 1, 2014 to December 31, 2021. Screening eligibility was classified using USPSTF 2021 criteria (aged 50-80 years, ≥20 pack-year smoking history, and ≤15 quit-years for former smokers). Temporal trends in eligibility, screening utilization, and mortality risks were assessed through joinpoint regression and Cox proportional hazards models. A total of 106,266 asymptomatic patients with lung cancer were enrolled. Among the 102,555 patients with complete age and smoking information, only 8.8% (8985/102,555) met the USPSTF 2021 eligibility criteria. The eligibility proportion declined sharply from 21.6% (350/1617) in 2014 to 6.1% (1737/28,582) in 2021, with the annual percentage change being -17.4% [95% confidence interval (CI) -19.1 to -15.9]. Patients with screening utilization, irrespective of eligibility status, demonstrated a higher proportion of stage Ia diagnoses compared with those who were not screened. Screening- ineligible group exhibited 40% lower mortality risk overall [adjusted hazard ratio (HR)=0.60, 95% CI 0.55-0.66], with consistent survival advantages across stage I (adjusted HR=0.63, 95% CI 0.54-0.74) and stage III (adjusted HR=0.76, 95% CI 0.64-0.90) subgroups. Rigid age- and smoking-based criteria overlook substantial at-risk populations in China. Implementing individualized risk stratification is essential to advance equitable lung cancer screening.
The incidence of lung cancer increases with age. On average, patients diagnosed with lung cancer are about 70 years. It is known that older patients are more prone to complications after major lung resection due to physiological changes; however, there is still a lack of knowledge of predictive factors associated with a higher complication risk. In this study the association of age and postoperative complication rates in lung cancer patients is analyzed. Further, predictors of postoperative complications in the era of minimally invasive surgery in older patients are identified. We retrospectively analyzed 180 consecutive patients with pathologically proven lung adenocarcinoma and squamous cell carcinoma. Patients were categorized into septuagenarians and octogenarians. Univariate and multivariate analyses were conducted to detect risk factors of postoperative morbidity. There were 141 (78.33%) and 39 patients (21.67%) in the septuagenarian group and octogenarian group, respectively. 67 (37.2%) patients experienced postoperative complications. The thirty-day mortality rate was 1.6%. The groups did not differ in terms of postoperative complications. Upon multivariate analysis, ECOG score ≥ 1 (p = 0.032), lowered FEV1/FVC (p = 0.029), and hypoalbuminemia (p = 0.027) were significant predictors for the development of major complications after lung cancer surgery. Age over 80 years was not found to be an independent risk factor for the complication rates after lung cancer surgery. However, ECOG performance status ≥ 1, reduced FEV1/FVC, and lower serum albumin levels were independently associated with major postoperative complications.
Skin cancer remains one of the most significant global health issues due to its high prevalence and wide range of clinical outcomes. The management of skin cancer has changed as a result of recent developments in theranostics and nanotheranostics, which combine therapeutic and diagnostic modalities into single platforms to enable precision medicine and customized treatment. Current developments in molecular biomarkers, diagnostic technologies, epidemiology, and therapeutic approaches-such as immunotherapy and nanocarrier-based methods-are summarized in this review. Multimodal imaging, AI-powered diagnostic models, targeted molecular medicines, and risk assessment tools are some of the major advancements that have improved early identification, individualized care, and monitoring. Obstacles include tumor heterogeneity, safety issues, and regulatory restrictions that prevent widespread clinical translation still exist despite the success of preclinical and a few clinical uses. To further improve the efficacy of skin cancer diagnosis and treatment, future directions suggest the use of multiomics, consumer-driven digital health technologies, sophisticated nanomaterials, and AI-powered customisation. If remaining scientific and practical concerns are resolved, theranostics and nanotheranostics present intriguing opportunities for attaining high degrees of personalization, efficacy, and safety in the treatment of skin cancer.
ObjectiveOccupational exposure to carcinogens significantly contributes to the global burden of tracheal, bronchial, and lung (TBL) cancers. This study aims to quantify the global, regional, and national burden of TBL cancers attributable to occupational carcinogens using Global Burden of Disease (GBD) 2021 data and project trends to 2050. Additionally, we employ Mendelian Randomization (MR) to explore potential causal relationships between modifiable risk factors and TBL cancers.MethodsWe extracted mortality and Disability-Adjusted Life Year (DALY) data for TBL cancers caused by occupational carcinogens from the GBD 2021 database. Exponential smoothing and autoregressive integrated moving average (ARIMA) models projected the burden to 2050. Two-sample MR analysis utilized genome-wide association study (GWAS) data, primarily from individuals of European ancestry, to investigate causal links.ResultsIn 2021, occupational carcinogens caused 285,628 deaths and 6.12 million DALYs globally. While age-standardized mortality and DALY rates declined in some high-income countries, low- and middle-income countries (LMICs) showed rising trends. Projections indicate a potential shift, with some regions plateauing while others face increasing burdens due to persistent exposure. MR analysis confirmed significant causal relationships, identifying higher BMI, smoking, visceral adiposity, and waist circumference as risk factors, while coffee consumption, dried fruit intake, physical activity, and education were protective.ConclusionDespite progress, the burden of occupational TBL cancers remains substantial, particularly in LMICs. The discordance between declining rates in high-income nations and rising burdens elsewhere highlights the need for targeted interventions and stricter regulations. Integrating genetic evidence supports precision prevention strategies focusing on both occupational safety and modifiable lifestyle factors.
Cancer therapy-related cardiac dysfunction (CTRCD) is a significant complication of contemporary oncologic treatment and a key contributor to incident heart failure (HF) in cancer survivors. Although certain potentially cardiotoxic cancer therapies are known to increase risk, contemporary population-based estimates in large, diverse, and contemporary cohorts remain limited. The aim of the Kaiser Permanente Cardiovascular Health Enhancement and Monitoring for Oncology (KP CHEMO) study was to determine the incidence, timing, and treatment-specific variation in CTRCD among adults receiving potentially cardiotoxic cancer therapies within an integrated United States (U.S.) health system. We conducted a retrospective cohort study of adult Kaiser Permanente Northern California (KPNC) members diagnosed with malignant tumors between 2012 and 2022 who received anthracyclines, human epidermal growth factor receptor (HER2) inhibitors, immune checkpoint inhibitors (ICIs), or tyrosine kinase inhibitors (TKIs). CTRCD was defined as a >10% decline in left ventricular ejection fraction (LVEF) to <53% or incident HF identified by natural language processing. Crude and cumulative incidence rates were calculated overall and by drug class. Early CTRCD was ≤12 months; late was >12 months. Among 26,646 patients (mean age 62±14 years; 64% women; 57% non-Hispanic White), the cumulative incidence of CTRCD was 8.4% (95% CI 7.7-9.1). Incidence was highest with HER2 inhibitors (10.7%) and lowest with ICIs (5.2%) (P<0.001). Nearly half of all events occurred within the first year. CTRCD was common and occurred predominantly within the first year after therapy initiation, potentially reflecting both early susceptibility and more intensive early surveillance. Variation across drug classes highlights differing cardiotoxic risk profiles. These findings support early risk prediction models and targeted surveillance strategies to reduce downstream HF risk.
This chapter will thoroughly examine how the landscape of skin cancer therapeutics is changing with a particular focus on the fact that nanotechnology has resulted in a transformative advancement in drug delivery systems. It starts by providing a summary of the epidemiology of skin cancer, and the treatment difficulties that are associated with conventional modalities, including surgery, radiotherapy, and topical chemotherapy, and their shortcomings. The wide variety of nanocarriers, including lipid-based systems, polymeric nanoparticles, micelles, dendrimers, and inorganic platforms like gold nanoparticles and quantum dots, are then discussed along with their physicochemical properties, the mechanism of improved drug solubility, stability, bioavailability, and targeted activity. The hybrid and stimuli-sensitive delivery systems that are intended to be delivered on the site of action in response to internal (pH, redox, enzyme) or exterior (light, temperature, magnetic field) stimuli receive particular attention. The efforts to optimize therapeutic utility and reduce toxicity in the off-target tissues through enhanced permeability and retention (EPR) impact and ligand-based targeting are among the passive and active tumor targeting mechanisms that are taken into consideration.The chapter ends with a discussion on the recent research, combination therapies, theranostics, and future on clinical translation of nanotechnology-based methods in managing skin cancer.
Patients with ulcerative colitis (UC) have an increased risk of developing colorectal cancer through inflammation-driven carcinogenesis distinct from sporadic disease. Although the relative risk remains elevated, contemporary population-based studies indicate a substantial decline in absolute incidence, likely reflecting improved disease control, biologic therapies and structured surveillance colonoscopy. This review synthesizes current evidence on the epidemiology and determinants of colitis-associated colorectal cancer (CAC), highlighting key risk modifiers such as disease extent and duration, persistent inflammation, family history, and primary sclerosing cholangitis. We further summarize advances in understanding the molecular and immunologic mechanisms underlying CAC, including genomic instability, immune dysregulation, oxidative stress, microbiome alterations, and tumor microenvironment remodeling. Emerging molecular and histologic biomarkers that may enhance risk stratification and guide precision surveillance are discussed. In addition, contemporary surveillance approaches and evolving chemoprevention strategies are critically evaluated. Collectively, this review outlines current challenges and future directions for individualized CRC prevention in patients with UC.
Hepatocyte growth factor activator inhibitor type-1 (HAI-1) plays pivotal roles in epithelial integrity and tumour biology. Although implicated in various malignancies, its expression profile and prognostic value in bladder cancer (BC) remain incompletely defined. High levels of HAI-1 ectodomain in urine have previously been reported to be associated with poor prognosis in BC patients. This study aimed to determine the relationships between tissue and urine levels of HAI-1 and clinical outcomes in BC. This study used immunohistochemistry to measure HAI-1 expression across 770 BCs of all stages and grades. HAI-1 expression was scored on the basis of the percentage of positive cancer cells, subcellular localisation, and staining intensity. Additionally, HAI-1 (SPINT1) mRNA expression was compared with protein levels in tissue and urine. HAI-1 was highly expressed in low-grade, early-stage disease with strong membranous staining. Reduced overall HAI-1 expression, loss of membranous staining and increased cytoplasmic staining correlated with higher stage and grade and shorter survival. SPINT1 mRNA levels were positively correlated with membranous HAI-1 staining intensity (p = 0.005). Urinary levels of HAI-1 were negatively associated with the fraction of HAI-1 positive cancer cells and membranous staining intensity (p < 0.05). A positive correlation was observed between SPINT1 expression and urinary HAI-1 levels (p < 0.05). The Urobasal A subtype had lower urinary HAI-1 ectodomain levels than other subtypes. HAI-1 expression may serve as a biomarker of tumour differentiation and prognosis in BC. Increased ectodomain shedding into the urine, rather than increased expression, likely explains the higher urine HAI-1 levels seen in more aggressive tumours.