Diabetes has become a global health crisis, affecting over 800 million people, with serious complications such as vascular and neurological damage. While diabetes management has been extensively studied, the impact of environmental pollutants, particularly microplastics (PS), on diabetic health remains poorly understood. PS, defined as plastic particles smaller than 5 mm, are pervasive and can enter the body through inhalation or ingestion, posing potential risks. However, the effects of PS exposure, particularly in diabetes, have not been adequately explored. Most studies focus on high-concentration, long-term exposure, which does not reflect typical human exposure levels. This study investigates the effects of short-term PS exposure on diabetic SD rats, using histological, apoptotic, and omics techniques, including metabolomics, lipidomics, and 16S rDNA sequencing. Our results show that short-term PS exposure exacerbates lung and intestinal damage in diabetic rats, with significant alterations in the gut microbiome. We also observed correlations between differential metabolites and microbiota changes. These findings provide novel evidence that short-term PS exposure, at concentrations reflecting daily contact, worsens metabolic dysfunction and intestinal dysbiosis in diabetes. This study emphasizes the need to consider environmental pollutants in diabetes management and highlights potential strategies for prevention and therapy.

Keratins, as essential components of intermediate filaments in epithelial cells, play a crucial role in maintaining cell structure and function. In various malignant epithelial tumors, abnormal keratin expression is frequently observed and serves not only as a diagnostic marker but also closely correlates with tumor progression. Extensive research has demonstrated that keratins are pivotal in multiple stages of tumor metastasis, including responding to mechanical forces, evading the immune system, reprogramming metabolism, promoting angiogenesis, and resisting apoptosis. Here we emphasize that keratins significantly enhance the migratory and invasive capabilities of tumor cells, making them critical drivers of tumor metastasis. These findings highlight the importance of targeting keratins as a strategic approach to combat tumor metastasis, thereby advancing our understanding of their role in cancer progression and offering new therapeutic opportunities.

Epithelial ovarian cancer (EOC) progression is determined by numerous intracellular interactions and the interplay between malignant cells, normal cells, and the tumor acellular microenvironment, formed largely by the extracellular matrix (ECM). The structure and biochemical functioning of various ECM components, along with the activity of agents that regulate ECM remodeling, impact the disease's expansion (adhesion, proliferation, invasion), spread, and response to therapy. It is important to note that the involvement of ECM components and their regulators in the progression of EOC is bidirectional and distinctly depends on a particular tissue context. In certain situations, certain components of the ECM enhance the activity of cancer cells, but in other scenarios, they suppress it. In this review, we summarize the newest knowledge regarding diverse aspects of ECM engagement in EOC pathophysiology and chemotherapy. Moreover, we delineate conditions that exacerbate the pro-cancerous properties of ECM, including diabetes-associated glycation, aging, and cellular senescence. We also explore methods to therapeutically alter the properties of the ECM, which could be beneficial in ovarian cancer prevention and treatment.

The effect of metformin on postoperative delirium (POD) in patients with type 2 diabetes mellitus (T2DM) undergoing cardiovascular surgery remains unclear. This study aimed to evaluate whether metformin use reduces POD risk in this high-risk population by analyzing data from Taiwan's National Health Insurance Research Database using propensity score matching (PSM).

We included T2DM patients who underwent coronary artery bypass grafting (CABG) or valve replacement between 2015 and 2018. PSM was used to balance covariates between metformin users and non-users. Logistic regression and Kaplan-Meier analyses were performed to assess POD risk and its cumulative incidence.

Metformin use was associated with a significantly reduced risk of POD (adjusted odds ratio [aOR], 0.52; 95% confidence interval [CI], 0.40-0.67). A dose-response trend was observed, with decreasing aORs for higher cumulative metformin exposure. Protective factors included higher income, urban residency, and statin use; risk factors included older age, prolonged anesthesia, higher aDCSI, CCI scores, and depression.

Metformin significantly lowers the risk of POD in T2DM patients undergoing cardiovascular surgery, showing a clear dose-dependent protective effect. These findings highlight metformin's potential as a chemopreventive agent against post-surgical complications in this population.

Cancer is increasingly prevalent worldwide, often coexisting with type 2 diabetes (T2D). Recent breakthroughs reveal the immune system's pivotal role in eliminating tumors and how the metabolic environment, such as glucose availability, affects antitumor immunity. Diabetes is known to dysregulate both innate and adaptive immune responses, while cancer creates an immunosuppressive microenvironment. We hypothesize that diabetes in cancer subjects may exacerbate this immunosuppression. Here, we examine the current understanding of the interplay between T2D and solid tumors and the associated challenges. Despite inconsistencies in data from mouse models and human tissues, evidence suggests that T2D can impact the antitumor response. Possible mechanisms may involve myeloid cells, inducing local immunosuppression and impairing antigen presentation, and certain lymphoid cell populations, exhibiting exhaustion.

Colorectal cancer (CRC) is the third most common type of cancer worldwide, with Norwegian women having the highest incidence rate of colon cancer in 2022. The consumption of sweet beverages is a suggested modifiable risk factor for CRC; however, current evidence is limited and inconclusive.

To assess the associations between the intake of sugar-sweetened beverages (SSBs), artificially sweetened beverages (ASBs), and juice and the risk of overall and subsite-specific CRC among Norwegian women.

In this prospective cohort study, we included 73,921 participants aged 41-61 years at baseline. Information on sweet beverage consumption was collected using self-reported food frequency questionnaires at two time points between 1998 and 2014. We used Cox proportional hazards models to estimate hazard ratios (HRs) with corresponding 95% confidence intervals (CIs) for the associations between sweet beverage consumption and the risk of overall CRC, proximal colon cancer, distal colon cancer, and rectal cancer.

During a mean follow-up time of 16.5 years from baseline, 1,187 women were diagnosed with CRC. Compared to no consumption, juice consumption was inversely associated with overall CRC risk (HR≥ 7 glasses/wk = 0.81, 95% CI: 0.67-0.98; p-trend = 0.025), colon cancer (HR≥ 7 glasses/wk = 0.73, 95% CI: 0.58-0.94; p-trend = 0.015) and proximal colon cancer (HR≥ 7 glasses/wk = 0.71, 95% CI: 0.52-0.99; p-trend = 0.065) after adjusting for age, education, and diabetes status at baseline. No associations were observed between juice consumption and distal colon cancer or rectal cancer risk, or between the intake of SSBs or ASBs and CRC.

We observed no substantial association between the intake of SSBs or ASBs and the risk of CRC or cancer in colorectal subsites in our cohort of Norwegian women. Conversely, our results indicate that juice consumption is associated with a reduced risk of CRC, particularly in the colon. These results warrant further investigation in larger cohorts with power to detect possible differences in cancer risk across colorectal subsites, especially as patterns of sweet beverage consumption are changing.

Gastric cancer remains a significant global health concern. Radical gastrectomy is the primary curative treatment. Diabetes mellitus is a common comorbidity in patients undergoing surgery for gastric cancer, including radical gastrectomy. Previous studies have suggested that diabetes can negatively affect postoperative outcomes, such as wound healing, infection rates, and overall recovery. However, the specific impact of diabetes on recovery after radical gastrectomy for gastric cancer remains poorly understood. evaluate the influence of diabetes on postoperative recovery, including hospital stay duration, complications, and readmission rates, in patients undergoing gastrectomy for gastric cancer. Understanding these effects could help optimize perioperative management and improve patient outcomes.

To investigate the impact of diabetes on recovery after radical gastrectomy for gastric cancer and associated postoperative outcomes.

This retrospective cohort study was performed at the Endocrinology Department of Xuanwu Hospital, Capital Medical University, Beijing, China. We examined patients who underwent radical gastrectomy for cancer between January 2010 and December 2020. The patients were divided into the diabetes and non-diabetes groups. The main outcomes included length of hospital stay, postoperative complications, and 30-day readmission rate. Secondary outcomes included quality of life indicators. Propensity score matching was used to adjust for potential confounding factors.

A total of 1210 patients were included in the study, with 302 diabetic patients and 908 non-diabetic patients. After propensity score matching, 280 patients were included in each group. Diabetic patients demonstrated significantly longer hospital stays (mean difference 2.3 days, 95%CI: 1.7-2.9, P < 0.001) and higher rates of postoperative complications (OR 1.68, 95%CI: 1.32-2.14, P < 0.001). The 30-day readmission rate was also higher in the diabetic group as compared to the non-diabetic group (12.5% vs 7.8%, P = 0.02).

Patients with diabetes mellitus undergoing radical gastrectomy for gastric cancer experience prolonged hospital stay, increased postoperative complications, and higher readmission rates, thus requiring optimized perioperative management strategies.

The population of cancer survivors is increasing rapidly in the UK. Little is known about the variation in comorbidity and mortality by ethnicity and socio-economic condition in this population. This study explores these variations using primary care data from the Clinical Practice Research Datalink (CPRD) and linked secondary care data. The prevalence of multimorbidity and risk of mortality were calculated for Asian, Black, and Other ethnic and socio-economic groups in England, consisting of 333,226 cancer survivors across 28 cancer types. Odds ratios and hazard ratios were calculated using the White and most affluent groups as references and adjusted for age, sex, BMI, and smoking status. Stratified mortality analysis was conducted for survivors of the six common cancers in the UK: breast, prostate, colorectal, bladder, cervical, and lung. Compared to White cancer survivors, survivors of all other ethnic groups had a statistically significant higher prevalence of type 2 diabetes (Asian adjusted odds ratio (OR) 4.61 (4.02-5.28), Black OR 1.87 (1.52-2.30), and Other OR 2.06 (1.64-2.59)). However, they had lower prevalences of depression and anxiety. Asian survivors exhibited the highest overall prevalence of comorbidity. Black survivors had the worst survival (adjusted hazard ratio (HR) 1.48 (1.38-1.59)) for all cancers combined, as well as for breast, prostate, colorectal, and cervical cancers. Black breast cancer survivors face a particularly high mortality risk (HR 1.78 (1.52-2.10)) compared to Whites. Asian survivors had higher mortality for all cancers combined (HR 1.31 (1.23-1.39)) and specifically for lung cancer (HR 1.81 (1.44-2.28)). The Other ethnic group had a significantly increased risk of mortality in cervical cancer (HR 1.90 (1.19-3.03)). The risk of mortality increased with worse socio-economic conditions, regardless of ethnic group. Cancer survivors of non-White ethnicity and poorer socio-economic background in the UK have worse outcomes in terms of increased prevalence of multimorbidity and mortality compared to White survivors. These findings indicate the need to comprehend the underlying reasons for these disparities and to assess the implications for cancer services, patient experience, and overall outcomes.

Cancer patients are at an increased risk for the incidence and complications of acute myocardial infarction (AMI) due to shared risk factors and treatment-related adverse effects. Mortality trends for AMI-related deaths in adult cancer patients in the U.S. remain unexplored.

This study used CDC WONDER data for death certificates from 1999 to 2020, identifying U.S. adults (≥25 years) with cancer (ICD-10: C00-D49) who died of AMI (ICD-10: I21) as the underlying cause. Age-adjusted mortality rates (AAMRs) and annual percent changes (APCs) were calculated and stratified by gender, age, race, and geographic location.

Between 1999 and 2020, there were 109,462 AMI-related deaths in adult cancer patients. The AAMR decreased from 4.3 per 100,000 in 1999 to 1.4 in 2020. A significant decline occurred from 1999 to 2015 (APC: 6.65; 95 % CI: 6.95 to -6.40; p < 0.001), followed by a stable trend from 2015 to 2020 (APC: 1.36; 95 % CI: 2.69 to 0.91; p = 0.152). Men had higher AAMRs than women (3.5 vs. 1.5). AAMRs were highest in older adults (10.5) compared to middle-aged (0.7) and young adults (0.1). Racial disparities showed the highest AAMRs in non-Hispanic (NH) Black patients (2.7), followed by NH Whites (2.4), NH American Indian/Alaska Native (1.6), Hispanic/Latino (1.3), and NH Asian/Pacific Islander (1.1). Non-metropolitan areas had higher AAMRs than metropolitan areas (2.8 vs. 2.2).

This analysis highlights a significant decline in AMI-related mortality among cancer patients in the U.S., with persistent disparities by gender, age, race and geographical location.

This study investigates the potential of volatile organic compounds (VOCs) in breath as non-invasive biomarkers for monitoring blood glucose levels in individuals with Type 2 diabetes mellitus (T2DM). A pilot clinical study was conducted to explore the correlation between VOCs and blood glucose levels in six T2DM patients. Participants used a custom-developed sensor device to collect breath data at home, alongside finger-stick blood glucose readings. Breath data were transmitted to a cloud database, while blood glucose readings were recorded on paper charts. The sensor data from the device and the blood glucose readings from the charts were consolidated to create the study dataset. Support vector machine and random forest models were employed to analyze the dataset, which achieved accuracies of 85% and 82%, respectively. The results demonstrate the feasibility of at-home breath sensor data collection for clinical studies and suggest its potential as a viable alternative to traditional invasive glucose monitoring methods. Future studies will expand the dataset to include more participants and additional clinical variables to enhance model performance and predictive power. This research highlights the promise of non-invasive breath analysis for glucose monitoring, which could improve patient compliance and diabetes management.

KRAS mutations can cause metabolic reprogramming in ovarian cancer, leading to an increased metastatic capacity. This study investigated the metabolic reprogramming changes induced by KRAS mutations in ovarian cancer and the mechanism of action of metformin combined with a glutaminase 1 inhibitor (CB-839). KRAS-mutant ovarian cancer accounted for 14% of ovarian cancers. The expression of glucose metabolism-related (PFKFB3, HK2, GLUT1, and PDK2) and glutamine metabolism-related enzymes (GLS1 and ASCT2) was elevated in KRAS-mutant ovarian cancer cells compared with that in wild-type cells. KRAS-mutant cells had a higher aerobic oxidative capacity than did wild-type cells. Metformin inhibited proliferation, the expression of glucose metabolism-related enzymes, and the aerobic oxidative capacity of KRAS-mutant cells compared with those of control cells. Furthermore, it enhanced the expression of glutamine metabolism-related enzymes in KRAS-mutant cells. Metformin combined with CB-839 inhibited the proliferation and aerobic oxidation of KRAS-mutant cells to a greater extent than that observed in wild-type cells. Additionally, the inhibitory effects of metformin and CB-839 in the KRAS-mutant ovarian cancer NOD-SCID mouse model were significantly stronger than those in the drug-alone group. KRAS mutations lead to enhanced glucose and glutamine metabolism in ovarian cancer cells, which was inhibited by metformin combined with CB-839.

The incidence of gastric cancer (GC) shows strong geographic variation, with the highest incidence occurring in East Asia. Epidemiological studies have linked lifestyle, diet, and inflammatory factors to the risk of GC. However, their causal relationship is subject to debate due to the potential presence of bias. Addressing these uncertainties is vital for guiding effective preventive strategies.

We used genetic variants as instruments via two-sample univariate and multivariate Mendelian randomization analyses to examine the relationships between 40 potentially modifiable risk factors and gastric cancer in 6563 patients with gastric cancer and 195,745 controls. These population data came from a genome-wide association study of people of Asian ancestry and were obtained from BioBank Japan.

Our multivariable Mendelian randomization analyses provided suggestive evidence of a potential association between genetically predicted concentrations of serum hemoglobin (ORSD 0.62 [95% CI 0.41 ~ 0.93]; p = 0.02), lactate dehydrogenase (LDH) (ORSD 0.30 [95% CI 0.16 ~ 0.56]; p < 0.001) and alkaline phosphatase (ALP) (ORSD 0.80 [95% CI 0.73 ~ 0.88]; p < 0.001) and a decreased risk of GC. Furthermore, our study revealed a causal link between type 2 diabetes mellitus (T2DM) (ORSD 0.83, 95% CI = 0.73 ~ 0.93, p value = 0.002) and GC incidence.

This analysis identified several potential modifiable factors for gastric cancer, including hemoglobin, LDH, ALP and T2DM. These findings should be considered when formulating strategies for the primary prevention of GC, thereby informing evidence-based public health policies.

Small cell lung cancer (SCLC) is a therapeutically challenging disease. Metformin, an effective agent for the treatment of type 2 diabetes, has been shown to have antitumour effects on many cancers, including non-small cell lung cancer (NSCLC) and breast cancer. Currently, the antitumour effects of metformin on SCLC and the underlying molecular mechanisms remain unclear. CCK-8, EdU, colony formation, flow cytometry, immunofluorescence, molecular docking, western blotting, nude mouse transplanted tumour model, and immunohistochemistry experiments were conducted to analyse gene functions and the underlying mechanism involved. In vitro experiments demonstrated that metformin inhibited the growth of SCLC cells (H446, H526, H446/DDP and H526/DDP), which was confirmed in xenograft mouse models in vivo. Additionally, metformin induced cell cycle arrest, apoptosis, and autophagy in these SCLC cells. The molecular docking results indicated that metformin has a certain binding affinity for EGFR. The western blotting results revealed that metformin decreased the expression of EGFR, p-EGFR, AKT, and p-AKT, which could be reversed by EGF and SC79. Moreover, metformin activated AMPK and inactivated mTOR, and compound C and SC79 increased the levels of p-mTOR. Metformin can not only enhance the antitumour effect of cisplatin but also alleviate the toxic effects of cisplatin on the organs of xenograft model animals. In summary, the current study revealed that metformin inhibits the growth of SCLC by inducing autophagy and apoptosis via suppression of the EGFR/AKT/AMPK/mTOR pathway. Metformin might be a promising candidate drug for combination therapy of SCLC.

High fasting plasma glucose (HFPG) has been identified as one of the risk factors associated with the development of breast cancer. The worldwide distribution of breast cancer attributable to HFPG was not comprehensively investigated.

We utilized the data from the Global Burden of Disease Study 2021 to explore HFPG-related breast cancer deaths, disability adjusted life years (DALYs) and corresponding age-standardized rates (ASRs). The average annual percentage change (AAPC) and the estimated annual percentage change (EAPC) were employed to evaluate the temporal trend.

The global effect of HFPG resulted in nearly 30,570 breast cancer deaths and 819,550 DALYs in 2021, representing an age-standardized deaths rate (ASMR) of 0.66 (95% UI -0.19-1.57) and an age-standardized DALYs rate (ASDR) of 18.05 (95% UI -5.31-42.71). In the regions with low, low-middle, and middle SDI, the ASRs of HFPG-related breast cancer increased significantly over time. The highest ASMR and ASDR were observed in several countries, such as Palau, American Samoa, Cook Islands, Marshall Islands, and United Arab Emirates. There was a positive correlation between ASRs and Socio-Demographic Index (SDI) in countries where SDI was below 0.75. The escalation in death and DALYs was primarily driven by epidemiological change and population growth in low, low-middle, middle SDI regions.

Substantial disparities exist across diverse regions in breast cancer burden attributed to HFPG. It is urgent to regulate glycemic levels, improve healthcare infrastructures, and provide cost-effective care in less developed and developing countries that endure a disproportionately heavier health burden.

Comorbidities may complicate medical situations and have an impact on the treatment decisions and poor survival of cancer patients. How comorbidities cluster together and ultimately affect patients' outcomes in gastrointestinal tract cancer (GTC) is a poorly understood area.

In a multicenter prospective observational study from 2012 to 2021, we grouped the comorbidities of patients with GTC by latent class analysis, obtaining two comorbidity classes. Cox regression models were initially used to predict mortality. LASSO techniques were used to reduce the dimension. The final model included the comorbidity classes and nine more predictors. Additionally, the performance of different simple multimorbidity measures were compared using the Bayesian information criterion (BIC), ROC curves and C-index. Finally, the performance of the final model was analyzed using ROC curves, calibration curves and decision curves. The nomogram was drawn to evaluate the model.

We included 10,019 patients and obtained two comorbidity classes. Class 2 patients have a higher incidence of comorbidities, and a lower survival rate compared to Class 1 (P < 0.001). Compared to models containing the number of comorbidities or only a single comorbidity, the final model with the comorbidity classes has the highest AUC and C-index, as well as the lowest BIC, indicating this model has the best predictive performance.

We identified two classes of comorbidities that were associated with overall survival in patients with GTC. The combination of different comorbidities class plays a vital role in the prognosis of GTC.

Cancer and diabetes are increasingly prevalent, and it is not unusual for an individual to have both conditions at the same time. This occurrence has significant ramifications to the person, the clinical team providing care, and the broader health system.

For the period 2006-2019, we used national-level diabetes (Virtual Diabetes Register) and cancer (New Zealand Cancer Registry) data on nearly five million individuals over 44 million person-years of follow-up. We used cancer incidence among those with and without prevalent diabetes to project cancer incidence across the 2020-2044 period, using age-period-cohort modelling to account for factors driving trends in cancer incidence.

Cancer rates were highest among those with diabetes for 21 of the 24 most common cancers, and people with diabetes also have faster projected increases in cancer than those without diabetes. The greatest differences in cancer incidence by diabetes status were for uterine, liver, pancreatic and kidney cancers, which all have a strong relationship with obesity. In terms of projected burden, cancers in people with diabetes were projected to more than double from 20,243 to 48,773, a 141 % increase from 2015 to 19-2040-44. Age-standardised cancer incidence was projected to increase 2.4 times faster for people with diabetes.

Our findings reinforce the fact that diabetes prevention activities are also cancer prevention activities, and must therefore be prioritised and resourced in tandem. The projected volume of diabetes and cancer co-occurrence also has important policy implications in terms of workforce development, as well as service delivery.

In people living with HIV (PLWH) with hepatitis C virus (HCV) infection, liver and nonliver-related mortality significantly decreased after receiving direct acting antivirals (DAAs). We aimed to assess main causes and predictors of mortality after sustained virologic response induced by DAAs.

Retrospective study in antiretroviral treatment-experienced PLWH with HCV infection, followed at San Raffaele Hospital, Milan, Italy, who achieved sustained virologic response after DAAs. Kaplan-Meier analysis and log-rank test were used to estimate cumulative probability of death for any cause. Cox proportional hazards model was used to estimate adjusted hazard ratio (aHR) of death and the corresponding 95% confidence interval (95% CI); baseline variables included in the model were age, diabetes, hepatocellular carcinoma (HCC), α-fetoprotein (AFP), and albumin-bilirubin (ALBI) grade.

Among 663 people included with a median follow-up of 4.4 years (interquartile range = 3.5-5.5), 49 died. Overall 5-year cumulative probability of death was 8.0% (95% CI: 5.5% to 0.4%); 63.2% (n = 31/49) died from nonliver-related events [mainly nonliver malignancies (18/49) and cardiovascular events (7/49)]. At multivariate analysis, death was more likely in older people [aHR (5-year older) = 1.46, 95% CI: 1.16 to 1.83, P = 0.0009], and in people with diabetes (aHR = 2.98, 95% CI: 1.55 to 5.71, P = 0.001), ALBI grade ≥2 (aHR = 2.13, 95% CI: 1.17 to 3.90, P = 0.014), and AFP ≥3.4 ng/mL (aHR = 1.96, 95% CI: 1.01; 3.84, P = 0.049).

In our cohort, nonliver-related events and malignancies were the most common cause of death after HCV eradication. Diabetes, ALBI grade ≥2, and AFP ≥3.4 ng/L were associated with higher risk of death. In PLWH after HCV eradication, regardless of liver disease stage, surveillance of nonliver events, particularly malignancies, should be recommended.

A growing body of evidence emphasizes the role of glycemic variability (GV) in the development of conventional diabetes-related complications. Furthermore, advancements in diabetes management and increased life expectancy have led to the emergence of new complications, such as cancer, liver disease, fractures, infections, and cognitive dysfunction. GV is considered to exacerbate oxidative stress and inflammation, acting as a major mechanism underlying these complications. However, few reviews have synthesized the association between GV and these emerging complications or examined their underlying mechanisms. Hence, this narrative review provides a comprehensive discussion of the burden, risks, and mechanisms of GV in these complications, offering further evidence supporting GV as a potential therapeutic target for diabetes management.

Sodium glucose co-transporter 2 (SGLT2) inhibitors represent a novel class of hypoglycemic drugs that have emerged in recent years. These inhibitors function primarily by blocking the reabsorption of glucose in the kidneys, specifically targeting the SGLT2 proteins in the proximal convoluted tubules. This inhibition results in the reduction of blood glucose levels through increased glucose excretion in the urine. Recent studies have identified SGLT2 expression in various cancer types, suggesting that SGLT2 inhibition can potentially suppress tumor growth. This article provides a comprehensive review of the role of SGLT2 in tumorigenesis and tumor progression, and explores the underlying mechanisms and potential therapeutic applications of SGLT2 inhibitors as anticancer agents.

This article provides an overview of the current evidence on the epidemiology, overlapping risk factors, and pathophysiology of cardiovascular disease (CVD) in patients with cancer. It explores the cardiotoxic effects of anticancer therapy and their impact on prognosis. Although cancer survival rates have improved over the last two decades, the risk of CVD has risen over time in patients with cancer. CVD and cancer share similar risk factors and a common pathophysiology involving inflammation. Many chemotherapeutic agents used to treat cancer are associated with cardiovascular complications (such as heart failure, myocardial infarction, and thrombosis). Current evidence indicates a significant burden of CVD in patients with cancer, particularly in the first year following cancer diagnosis, with elevated risk persisting beyond this period. This short- and long-term risk of CVD may vary depending on the cancer type and treatment regimen. Early identification of potential cardiovascular risk in patients with cancer, can lead to more favorable clinical and survival outcomes. Given the acute and long-term consequences, patients with cancer require increased cardiovascular care and lifestyle optimization. This article offers valuable insights into the cardiovascular burden and needs of patients with cancer. It is intended for a general medical research readership interested in the intersection of cardiology and oncology.

Individuals with type 2 diabetes mellitus (T2DM) have increased colorectal cancer (CRC) risk, but it is unknown whether income dynamics are associated with CRC risk in these individuals. We examined whether persistent low- or high-income and income changes are associated with CRC risk in non-elderly adults with T2DM.

Using nationally representative data from the Korean Health Insurance Service database, 1,909,492 adults aged 30 to 64 years with T2DM and no history of cancer were included between 2009 and 2012 (median follow-up of 7.8 years). We determined income levels based on health insurance premiums and assessed annual income quartiles for the baseline year and the four preceding years. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated after adjusting for sociodemographic factors, CRC risk factors, and diabetes duration and treatment.

Persistent low income (ie, lowest income quartile) was associated with increased CRC risk (HR5 years vs 0 years 1.11; 95% CI, 1.04-1.18; P for trend = 0.004). Income declines (ie, a decrease ≥25% in income quantile) were also associated with increased CRC risk (HR≥2 vs 0 declines 1.10; 95% CI, 1.05-1.16; P for trend = 0.001). In contrast, persistent high income (ie, highest income quartile) was associated with decreased CRC risk (HR5 years vs 0 years 0.81; 95% CI, 0.73-0.89; P for trend < 0.0001), which was more pronounced for rectal cancer (HR 0.64; 95% CI, 0.53-0.78) and distal colon cancer (HR 0.70; 95% CI, 0.57-0.86).

Our findings underscore the need for increased public policy awareness of the association between income dynamics and CRC risk in adults with T2DM.

With the rising prevalence of type 2 diabetes mellitus (T2DM) and obesity, several previously under-recognised complications associated with T2DM are becoming more evident. The most common of these emerging complications are metabolic dysfunction-associated steatotic liver disease (MASLD), cancer, dementia, sarcopenia, and frailty, as well as other conditions involving the lung, heart, and intestinal tract. Likely causative factors are chronic inflammation and insulin resistance, whereas blood glucose levels appear to play a lesser role. We discuss these complications and the new approaches being developed to prevent and manage them, especially incretin-based therapies. We argue that these new interventions may work in a complementary way to other proven cardiorenal protective therapies to reduce the burden of T2DM complications.

Cigarette smoking and diabetes mellitus (DM) increase risks of cardiovascular diseases and all-cause mortality in cancer survivors. An increased risk of DM incidence in cancer survivors has been observed and smoking is an important modifiable risk factor for DM development in the general population. Thus, we investigated the association between smoking behavior change after cancer diagnosis and DM incidence in cancer survivors.

This retrospective cohort study using the Korean National Health Insurance System database included patients with newly diagnosed cancers between 2010 and 2016. Smoking behavior changes after cancer diagnosis were categorized as never smoker, ex-smoker, quitter, smoking starter, and persistent smoker. The associations between smoking behavior changes and DM incidence in overall and specific cancers were investigated using Cox regression analyses.

Of the 263,940 cancer survivors, 67.6 % were never smokers, 16.0 % were ex-smokers, 9.3 % were quitters, 1.0 % were smoking starters, and 6.2 % were persistent smokers. During a mean follow-up of 4.0 years, 12,175 patients were diagnosed with DM after cancer development. Compared to the never smokers, the adjusted hazard ratios (95 % confidential interval) of DM incidence were 1.06 (1.00-1.13) for ex-smokers, 1.45 (1.35-1.54) for quitters, 1.46 (1.25-1.71) for starters, and 1.57 (1.45-1.69) for persistent smokers.

Compared with never smokers, cancer survivors who engaged smoking at any point before or after cancer diagnosis showed an increased risk of DM incidence after cancer diagnosis. Cancer survivors should be advised to quit smoking promptly and to maintain abstinence throughout cancer survivorship.

Studies show that new onset diabetes mellitus (DM) (NOD) predates the diagnosis of PDAC by up to 2 years. Two tumor-intrinsic molecular subtypes of PDAC that are prognostic and predictive of chemotherapy response have been described and validated. We hypothesize that patients with NOD may have different molecular subtypes and prognoses.

This is a single-institution study of patients who underwent resection for PDAC from 2009 to 2022 with de-identified samples available for sequencing. Demographic and clinical factors were examined using bivariate and multivariate analysis.

A total of 97 patients met inclusion criteria: 70 with no history of DM, 11 with longstanding DM (> 2 years), and 16 with NOD. The demographics between groups were overall similar. After controlling for age, sex, race, BMI, and tobacco history, NOD was not a significant predictor of PDAC subtype. There were no survival differences between groups. Transcriptomic analysis suggests the upregulation of inflammatory and immune activation and regulation pathways in NOD.

As continued interest in NOD and PDAC mounts, we are the first to examine if NOD may be associated with molecular subtypes and outcomes. Further investigation into the underlying pathophysiology of the NOD group is still needed.

In the dose titration of transdermal fentanyl to prevent unrelieved pain, it is important to consider not only dose adjustment, but also the titration period, which is influenced by the time required to reach the steady state. Many patients with cancer pain experience comorbidities that might affect the skin properties and influence transdermal absorption. We hypothesized that skin changes due to diabetes mellitus (DM) would affect the titration period of transdermal fentanyl. We conducted a retrospective study and diabetic animal model study to test this hypothesis.

In the retrospective study, the titration period was defined in terms of "dose change" and "number of rescue opioids" in patients initiated on transdermal fentanyl. Multiple logistic regression analysis was performed to analyze the relation between the titration period and comorbidities, including DM. In the diabetic animal model study, intercellular lipids of stratum corneum (SC) were analyzed in Goto-Kakizaki (GK) rats, a model of DM, and the pharmacokinetics of intravenously or transdermally administered fentanyl was examined.

In the retrospective study, the titration period ranged from 5 to 39 days (n = 387), and the patients taking a longer period (6 days or more) was significantly related to in patients with unspecified DM: AOR (95% confidence interval), 0.438 (0.217-0.884). In the diabetic animal model study, the ceramides (CERs) content in the SC was decreased by approximately 30% in GK rats compared to Wistar rats. The absorption rate constant (ka) of fentanyl administered transdermally was increased approximately 1.4-fold in GK rats, though there was no difference in transdermal bioavailability (F) or systemic clearance (CLtot).

Our results suggest that the steady state of transdermally administered fentanyl is reached sooner in cancer patients with DM as a comorbidity. Earlier pain assessment and dose adjustment may be possible in these patients.

Introduction: The incidence of breast cancer, as well as diabetes mellitus (DM), has continuously increased in recent years. The concurrent study of these diseases is particularly important, as there is a strong correlation between them due to hormonal, biochemical, and environmental factors. Moreover, the underlying metabolic dysfunction in this case could affect the treatment of breast cancer, as well as overall survival. In addition, the relationship of these two diseases with depression is not well studied. Patients with DM and cancer patients both experience depressive symptoms that have an impact on their mental health, as well as their quality of life. Personalized medicine offers a potential solution to these challenges by tailoring treatments to individual patient profiles. The present study will attempt to fill a gap in the existing literature regarding the relationship of patients with concurrent breast cancer and DM experiencing depression. More specifically, it will attempt to answer the question of whether there is a strong correlation between breast cancer, DM, and mental health in patients from a large geographical division of the country. Methodology: This was a cross-sectional study. A total of 120 female patients participated in the research, 60 with type 2 diabetes mellitus (T2DM) (group B) and 60 with T2DM and breast cancer (group A). The DASS-21 questionnaire was used to determine their levels of anxiety and depression, and ADDQoL-19 was used to measure the patients' quality of life. Results: Regarding quality of life, women with T2DM and breast cancer showed a better quality of life (QoL) than women with T2DM. Women who were retired (p = 0.025) and consequently postmenopausal (p = 0.035) demonstrated the highest levels of QoL, while stage III cancer patients had lower ADDQoL-19 scores. Regarding mental health, in the women from group A, a positive correlation of treatment with the occurrence of anxiety and depression (p = 0.034) and a negative correlation of cancer stage with mental health was observed. The women in group B (those with T2DM only) showed better mental health outcomes related to their treatment (p = 0.009). However, both married and unmarried women in this study experienced mental health burdens, with no significant difference between the two groups in terms of mental health impact. These findings suggest that marital status did not significantly influence the mental health of the participants in this study. Conclusions: Women with T2DM and breast cancer generally presented a better clinical picture than women with T2DM alone. Therefore, the comorbidity of these two diseases did not seem to negatively affect the quality of life and mental health of these women.

To examine the characteristics of patients with pancreatic cancer with long-term survival.

Although pancreatic cancer is a highly lethal malignancy, a minority of patients experience long-term survival. The characteristics of these patients remain largely unidentified.

An indolent subgroup was established using carbohydrate antigen 19-9 (CA19-9), which is the best-validated biomarker for pancreatic cancer. Of 1558 patients, 13.9% were included in the CA19-9-normal (≤37 U/mL) subgroup.

A normal CA19-9 level was an independent variable for overall survival (median survival, 18.1 vs 9.7 months, hazard ratio = 0.53, P < 0.001). The 5-year survival of patients with stage IV CA19-9-normal cancer was higher than that of patients with stage I-IV CA19-9-high cancer (22.4% vs 6.8%, P = 0.034). The CA19-9-normal subgroup exhibited reduced levels of circulating glucose ( P < 0.001) and increased expression of insulin ( P < 0.001) compared with the CA19-9-high subgroup. Glucose was a substrate for CA19-9 biosynthesis through the hexosamine biosynthesis pathway. In addition, in pancreatic cancer animal models of diabetes, glucose control decreased CA19-9 levels and improved overall survival. In a clinical trial (NCT05306028) of patients before undergoing major anticancer treatments, glucose control decreased CA19-9 levels in 90.9% of the patients.

CA19-9-normal pancreatic cancer is a strikingly indolent subgroup with low glucose and high insulin. Glucose control is a promising therapeutic strategy for pancreatic cancer.

Thyroid dysfunction is more common in other endocrine disorders such as diabetes mellitus (DM). Carcinoembryonic antigen (CEA), a common tumor biomarker, is found elevated in patients with thyroid dysfunction. However, the relationship between thyroid hormone levels and CEA levels remains unclear.

In total, 663 patients with type 2 diabetes at the Tongzhou Branch of Dongzhimen Hospital were enrolled in this retrospective study. Data were collected from inpatient electronic files between December 2011 and December 2019. Laboratory indices were statistically analyzed using logistic regression and Spearman correlation analyses.

In our study, total triiodothyronine (TT3), free triiodothyronine (FT3), serum albumin(ALB), total protein (TP), and triglyceride (TG) levels were significantly higher in the T2DM patients with normal values of CEA than T2DM patients who had abnormal values of CEA, whereas alkaline phosphatase (ALP), Glucose (GLU), and HbA1c levels were significantly increased in the T2DM patients with abnormal CEA level. Binary logistic regression analysis demonstrated that FT3, GLU, HbA1c, and TG levels remained as independent risk factors for CEA in patients with T2DM (β=-0.907, P =0.004; β =-1.009, P=0.004; β =0.090, P = 0001; β= 0.336, P <0.001; β= -0.293, P =0.009, resp). Spearman correlation analysis showed that CEA level was significantly positively correlated with HbA1c and GLU (rs value: 0.265, P <0.001; rs value: 0.270, P <0.001, resp.) and negatively correlated with FT3 and TG levels (rs value: -0.139, P <0.001; rs value: -0.103 P =0.008, resp). Furthermore, multivariate logistic regression analysis indicated that the FT3 quartiles were significantly associated with CEA levels before and after adjusting for confounding factors.

Our study determined that FT3 remained an independent risk factor for CEA in patients with T2DM and was significantly negatively correlated with CEA levels.

This study explored the influence of type 2 diabetes and impaired glucose tolerance (IGT) on the risk of the multimorbidity cluster of cardiovascular disease (CVD) and cancer.

A total of 1629 participants in the Da Qing Diabetes Prevention Outcome Study were recruited in the present analysis, including normal glucose tolerance (NGT, N = 492), IGT (N = 540), and newly diagnosed type 2 diabetes (N = 597) groups. Cox proportional hazards analyses were performed to assess the relationship between NGT, IGT, and newly diagnosed type 2 diabetes and the risk of the multimorbidity cluster of CVD and cancer.

The incidence rates for multimorbidity cluster CVD and cancer were 1.25, 3.17, and 3.23 per 1000 person-years in people with NGT, IGT, and the newly diagnosed type 2 diabetes groups, respectively, over 34-year follow-up. Cox analysis revealed that diabetes status (as time-dependent variable) was significantly associated with the subsequent increased risk of multimorbidity cluster of CVD and cancer compared with non-diabetes (hazard ratios [HR] = 2.55, 95% confidence interval [CI] 1.51-4.31) after adjustment of potential confounders. Similar analysis showed that this risk was significantly higher in the IGT and newly diagnosed type 2 diabetes groups compared with NGT, with HR of 3.28 (95% CI 1.83-5.87) and HR of 3.90 (95% CI 2.14-7.09), respectively. Whereas compared diabetes with IGT group, this risk was not significantly different.

Similar to newly diagnosed type 2 diabetes, IGT is significantly associated with an increased risk of the multimorbidity cluster of CVD and cancer compared with NGT. This finding highlights the urgent need for an active detection of IGT and effective prevention and management of diabetes.

The onset of colorectal cancer (CRC) in patients younger than 50 continues to rapidly increase. This study highlights the epidemiologic changes, risk factors, clinical characteristics, and molecular profiles prevalent in early onset CRC patients, and identifies key areas for future research. It has been noted that only a small fraction of early onset CRC cases is attributed to known hereditary mutations and fit the canonical pathway of late-onset colorectal cancer development. To highlight this, we review the genetic and epigenetic modifications specific to early onset CRC. We also discuss the synergetic effect of single-nucleotide polymorphisms and environmental factors on the early onset of CRC. Additionally, we discuss the potential of noninvasive biomarker assays to enhance early detection, screening, diagnosis, and prognostic outcome predictions.

Growing epidemiological evidence indicates an association between obesity, type 2 diabetes, and certain cancers, suggesting the existence of common underlying mechanisms in these diseases. Frequent hyperglycemias in type 2 diabetes promote pro-inflammatory responses and stimulate intracellular metabolic flux which rewires signaling pathways and influences the onset and advancement of different types of cancers. Here, we review the provocative impact of hyperglycemia on a subset of interconnected signalling pathways that regulate (i) cell growth and survival, (ii) metabolism adjustments, (iii) protein function modulation in response to nutrient availability (iv) and cell fate and proliferation and which are driven respectively by PI3K (Phosphoinositide 3-kinase), AMPK (AMP-activated protein kinase), O-GlcNAc (O-linked N-acetylglucosamine) and Wnt/β-catenin. Specifically, we will elaborate on their involvement in glucose metabolism, inflammation, and cell proliferation, highlighting their interplay in the pathogenesis of diabetes and cancer. Furthermore, the influence of antineoplastic and antidiabetic drugs on the unbridled cellular pathways will be examined. This review aims to inspire the next molecular studies to understand how type 2 diabetes may lead to certain cancers. This will contribute to personalized medicine and direct better prevention strategies.

The prevalence of Alzheimer's disease and other forms of dementia is increasing worldwide, and finding effective treatments for these conditions is a major public health challenge. Natural bioactive drugs have been identified as a promising source of potential treatments, due to their ability to target multiple pathways and their low toxicity. This paper reviews the current state of research on natural bioactive drugs used in the treatment of Alzheimer's disease and other dementias. The paper summarizes the findings of studies on various natural compounds, including curcumin, resveratrol, caffeine, genistein, quercetin, GinkoBiloba, Withaniasomnifera, Ginseng Brahmi, Giloy, and huperzine, and their effects on cognitive function, neuroinflammation, and amyloid-beta accumulation. In this review, we discuss the mechanism of action involved in the treatment of Alzheimer's disease. The paper also discusses the challenges associated with developing natural bioactive drugs for dementia treatment, including issues related to bioavailability and standardization. Finally, the paper suggests directions for future research in this area, including the need for more rigorous clinical trials and the development of novel delivery systems to improve the efficacy of natural bioactive drugs. Overall, this review highlights the potential of natural bioactive drugs as a promising avenue for the development of safe and effective treatments for Alzheimer's disease and other dementias.

The aim of this study was to determine the association between insulin glargine usage and the potential increase in cancer risk among the Lithuanian population diagnosed with type 2 diabetes mellitus (T2DM).

A retrospective cohort study was conducted. The cohort of insulin users was established by identifying all male and female patients diagnosed with T2DM, as recorded in the National Health Insurance Fund database between 1 January 2000 and 31 December 2012. The risk of cancer among insulin glargine users was compared with the risk in non-glargine insulin users. Cox proportional hazard models were used to estimate hazard ratios (HR) and their 95% confidence intervals (CI).

The overall cancer risk for all sites combined showed no significant difference (HR 0.84, 95% CI 0.67-1.05). Although a general decrease in the risk of cancers was observed at most sites for glargine users, the use of insulin glargine was associated with a non-significant increase in the risk of mouth and pharynx, stomach, non-melanoma skin, breast, cervical, ovarian, and central nervous system cancers. There was a tendency for a lower risk of colon, rectum, rectosigmoid, and anus cancer among glargine users (HR 0.45, 95% CI 0.18-1.12, p = 0.09).

Our research contributes to the growing body of evidence showing that insulin glargine is not associated with an increased risk of all cancers or specific types of cancer.

Diabetes greatly reduces the survival rates in breast cancer patients due to chemoresistance and metastasis. Reorganization of the cytoskeleton is crucial to cell migration and metastasis. Regulatory cytoskeletal protein kinases such as the Rho kinase (ROCK) and focal adhesion kinase (FAK) play a key role in cell mobility and have been shown to be affected in cancer. It is hypothesized that diabetes/high-glucose conditions alter the cytoskeletal structure and, thus, the elasticity of breast cancer cells through the ROCK and FAK pathway, which can cause rapid metastasis of cancer. The aim of the study was to investigate the role of potential mediators that affect the morphology of cancer cells in diabetes, thus leading to aggressive cancer. Breast cancer cells (MDA-MB-231 and MCF-7) were treated with 5 mM glucose (low glucose) or 25 mM glucose (high glucose) in the presence of Rho kinase inhibitor (Y-27632, 10 mM) or FAK inhibitor (10 mM). Cell morphology and elasticity were monitored using atomic force microscopy (AFM), and actin staining was performed by fluorescence microscopy. For comparative study, normal mammary breast epithelial cells (MCF-10A) were used. It was observed that high-glucose treatments modified the cytoskeleton of the cells, as observed through AFM and fluorescence microscopy, and significantly reduced the elasticity of the cells. Blocking the ROCK or FAK pathway diminished the high-glucose effects. These changes were more evident in the breast cancer cells as compared to the normal cells. This study improves the knowledge on the cytoarchitecture properties of diabetic breast cancer cells and provides potential pathways that can be targeted to prevent such effects.

Evidence on type 2 diabetes onset age and duration on mortality risk has been limited by short follow-up, inadequate control for confounding, missing repeated measurements, and inability to cover the full range of onset age, duration, and major causes of death. Moreover, scarce data dissect how type 2 diabetes onset age and duration shape life expectancy.

We evaluate prospectively these topics based on 270,075 eligible participants in the Nurses' Health Studies and Health Professionals Follow-up Study, leveraging repeated measurements throughout up to 40 years of follow-up. Cox models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs).

In fully adjusted analyses, incident early onset type 2 diabetes (diagnosed <40 years of age) was associated with significantly higher mortality from all-causes (HR, 95% CI was 3.16, 2.64-3.79; vs. individuals without type 2 diabetes), cardiovascular disease (6.56, 4.27-10.1), respiratory disease (3.43, 1.38-8.51), neurodegenerative disease (5.13, 2.09-12.6), and kidney disease (8.55, 1.98-36.9). The relative risk elevations declined dramatically with each higher decade of age at diagnosis for deaths from most of these causes, though the absolute risk difference increased continuously. A substantially higher cumulative incidence of mortality and a greater loss in life expectancy were associated with younger age at type 2 diabetes diagnosis. Longer disease duration was associated with generally higher relative and absolute risk of mortality.

Early onset of type 2 diabetes and longer disease duration are associated with substantially increased risk of all-cause and cause-specific mortality and greater loss in life expectancy.

Prediabetes, which is a precedent of overt diabetes, is a known risk factor for adverse cardiovascular outcomes. Its impact on adverse cardiovascular outcomes in patients with cancer who are prescribed anthracycline-containing chemotherapy (ACT) is uncertain. The objective of this study was to evaluate the association of prediabetes with cardiovascular events in patients with cancer who are prescribed ACT.

The authors identified patients with cancer who received ACT from 2000 to 2019 from Clinical Data Analysis Reporting System of Hong Kong. Patients were divided into diabetes, prediabetes, and normoglycemia groups based on their baseline glycemic profile. The Primary outcome, a major adverse cardiovascular event (MACE), was the composite event of hospitalization for heart failure and cardiovascular death.

Among 12,649 patients at baseline, 3997 had prediabetes, and 5622 had diabetes. Over median follow-up of 8.7 years, the incidence of MACE was 211 (7.0%) in the normoglycemia group, 358 (9.0%) in the prediabetes group, and 728 (12.9%) in the diabetes group. Compared with normoglycemia, prediabetes (adjusted hazard ratio [HR], 1.20; 95% confidence interval [CI], 1.01-1.43) and diabetes (adjusted HR, 1.46; 95% CI, 1.24-1.70) were associated with an increased risk of MACE. In the prediabetes group, 475 patients (18%) progressed to overt diabetes and exhibited a greater risk of MACE (adjusted HR, 1.76; 95% CI, 1.31-2.36) compared with patients who remained prediabetic.

In patients with cancer who received ACT, those who had prediabetes at baseline and those who progressed to diabetes at follow-up had an increased risk of MACE. The optimization of cardiovascular risk factor management, including prediabetes, should be considered in patients with cancer who are treated before and during ACT to reduce cardiovascular risk.

Patients with cancer who have preexisting diabetes have a higher risk of cardiovascular events, and prediabetes is often overlooked. In this study of 12,649 patients with cancer identified in the Clinical Data Analysis Reporting System of Hong Kong who were receiving treatment with anthracycline drugs, prediabetes was correlated with increased deaths from cardiovascular disease and/or hospitalizations for heart failure. Patients who progressed from prediabetes to diabetes within 2 years had an increased risk of combined hospitalization for heart failure and death from cardiovascular disease. These findings indicate the importance of paying greater attention to cardiovascular risk factors, including how prediabetes is managed, in patients who have cancer and are receiving chemotherapy with anthracyclines, emphasizing the need for surveillance, follow-up strategies, and consideration of prediabetes management in cancer care.

Both diabetes and cancer are major global health issues that are among the leading causes of morbidity and mortality. There is a high prevalence of diabetes among cancer patients, many of whom require a surgical procedure. This review focuses on the operative complications in patients with diabetes and cancer, and the perioperative management of diabetes in cancer patients.

A literature search of articles in English-published between January 2010 and May 2024-was carried out using the databases PubMed, MEDLINE, Google Scholar, and the Cochrane Database of Systematic Reviews. The search primarily focused on the operative complications in patients with diabetes and cancer, and perioperative management strategies.

The relationship between cancer and diabetes is complex; cancer patients have a high risk of developing diabetes, while diabetes is a risk factor for certain cancers. In addition, various cancer therapies can induce or worsen diabetes in susceptible patients. Many individuals with cancer and diabetes require surgery, and due to underlying diabetes, they may have elevated risks for operative complications. Optimal perioperative management for these patients includes managing perioperative glycemia and other comorbid illnesses, adjusting diabetic and cancer treatments, optimizing nutrition, minimizing the duration of fasting, supporting early mobilization, and providing patient education to enable self-management.

While evidence is limited, optimal perioperative management for patients with both diabetes and cancer is necessary in order to reduce surgical complications. Future studies are needed to develop evidence-informed perioperative strategies and improve outcomes for these patients.

Bladder cancer (BC) and Renal cell carcinoma (RCC) are the most common urogenital cancers among both sexes, with a yearly global incidence of around 500 000 each. Both BC and RCC have been linked to diabetes. Poor glycemic control (malglycemia) is a serious consequence of diabetes and a possible consequence of systemic treatments used in BC and RCC. The objective of this study was to investigate the prevalence of diabetes and use of hospital-based care for malglycemia in people with BC or RCC.

This Swedish retrospective population-based register study used national health-data registers for longitudinal data on cancer incidence covering 15 years, use of hospital-based health care, and filled prescriptions of outpatient medications. Study endpoints included co-prevalence of diabetes in individuals with BC/RCC, healthcare resource utilization due to malglycemia, use of systemic corticosteroids, and changes in diabetes management for people with concomitant type 2 diabetes.

We identified 36,620 and 15,581 individuals diagnosed with BC and RCC, respectively, between 2006 and 2019. The proportion of individuals registered with diabetes was 24% in BC and 23% in RCC. An association between BC/RCC and poor glycemic control was found, although the number of malglycemic events in hospital-based care were few (65/59 per 1000 individuals with diabetes and BC/RCC respectively with at least one event). An earlier switch to insulin-based diabetes management was observed in BC/RCC compared to matched individuals with type 2 diabetes but no cancer. The results also indicated an association between steroid treatment and poor glycemic control, and that systemic corticosteroids were more common among people with BC/RCC compared to diabetes controls.

The high prevalence of diabetes and increased use of systemic corticosteroid treatment observed in this large national study highlights the need for specific clinical management, risk-assessment, and monitoring of individuals with BC/RCC and diabetes.

This retrospective cohort study explores the relationship between vitamin D levels and 5-year mortality risk among 1,549 colon cancer patients seen at University of California health centers between 2012 and 2019, with a particular focus on the mediating role of comorbidities. Methods leveraged structural equation modeling to assess both direct and indirect pathways linking vitamin D to mortality risk. This analysis revealed a protective direct effect of higher vitamin D levels against mortality risk. Additionally, this study uncovered an indirect pathway, demonstrating that vitamin D lowers mortality risk by mitigating comorbidity, which subsequently influence mortality risk. Study results indicate that approximately 9.2% of the beneficial effect of vitamin D on mortality risk is attributable to its capacity to reduce comorbidity burden. In disaggregated and confounder-adjusted structural modeling, there were significant indirect effects for 25(OH)D on mortality risk through its effects on depression and obesity but not on anxiety, diabetes, or chronic kidney disease. These results suggest that the protective effects of vitamin D in colon cancer etiology appear to be through direct action on cancer progression, though patients who also suffer from depression and obesity would especially benefit from achieving adequate levels of serum vitamin D.