Studies have shown the association between personal history of diabetes mellitus (DM type 1/2) and risk of colorectal cancer (CRC). This study aims to find the association between the family history of diabetes and CRC risk.

This large nationwide cohort study leveraged data from several Swedish nationwide registers (follow-up: 1964-2018) to compare the risk using standardized incidence ratio (SIR).

11,784,567 individuals (668,348 with DM) were included and followed for up to 54 years (median = 28 years). Those with a personal history of DM had a 1.4-fold increased risk of CRC compared to those without DM (95 % CI: 1.39-1.45). However, the addition of a family history of DM in 1 FDR or ≥ 2 FDRs did not significantly alter the increased risk of early-onset or late-onset CRC.

Leveraging one of the world's largest family-disease datasets, our cohort study confirmed that personal history of diabetes is associated with an increased risk of colorectal cancer, but we did not find an association between a family history of diabetes and risk of colorectal cancer.

Cathepsin D (CTSD) is a lysosomal aspartic protease with high expression in cancers. CTSD localized in different subcellular regions performs distinct roles. However, the precise regulation of its intracellular trafficking and extracellular secretion remains incompletely understood. This study showed that glycosylation modifications of CTSD determined its maturation and secretion in gastric cancer (GC) cells. Specifically, glycosylation at asparagine 134 (N134) dictated the intracellular trafficking and maturation of CTSD within lysosomes, through facilitating its sorting into COPII vesicles. Glycosylation at asparagine 263 (N263) was essential for the secretion of the proenzyme form of CTSD (pro-CTSD) via a novel pathway dependent on the small GTPase Rab3D. Notably, the extracellular release of pro-CTSD occurred more rapidly than its intracellular trafficking from the endoplasmic reticulum to lysosomes. This enhanced secretion speed may rapidly elevate the levels of pro-CTSD in the tumor microenvironment in response to extracellular stimuli. Ultimately, glycosylation at N134 and N263 regulated the autophagy and cell proliferation, respectively. These findings show the role of glycosylation in triggering the maturation and secretion of CTSD in GC cells. Through modulating its cellular trafficking, differential glycosylation modifications of CTSD defined the malignant behavior of GC cells.

This collaboration from the Obesity Medicine Association (OMA) and the American College of Osteopathic Family Physicians (ACOFP) examines obesity management from a primary care perspective.

This joint perspective is based upon scientific evidence, clinical experience of the authors, and peer review by the OMA and ACOFP leadership. The goal is to identify and answer sentinel questions about obesity management from a primary care perspective, utilizing evidence-based publications, and guided by expert clinical experience.

Obesity is a disease that contributes to both biomechanical complications and the most common cardiometabolic abnormalities encountered in primary care. Barriers that impede optimal care of patients with obesity in primary care include failure to recognize obesity as a disease, lack of accurate diagnosis, insufficient access to obesity treatment resources, inadequate training, insufficient time, lack of adequate reimbursement and the adverse impact of bias, stigma, and discrimination.

Family physicians are often the first line of treatment in the healthcare setting. This affords early intervention opportunities to prevent and/or treat overweight and/or obesity. Patient care is enhanced when primary care clinicians recognize the risks and benefits of anti-obesity medications and bariatric procedures, as well as long-term follow-up. Practical tools regarding the 4 pillars of nutrition therapy, physical activity, behavior modification, and medical interventions (anti-obesity medications and bariatric surgery) may assist primary care clinicians improve the health and lives of patients living with obesity.

Anthracycline-based chemotherapy is a vital treatment for various cancers but carries notable risks of cardiotoxicity. This study aimed to assess how different body mass index values and glycemic status influence the risk of major adverse cardiovascular events (MACE) in chemotherapy-naïve adult patients with cancer treated with anthracyclines.

This retrospective cohort included 11 393 chemotherapy-naïve patients who initiated anthracycline-based chemotherapy between 2000 and 2019. Follow-up began from the first anthracycline dose. Body mass index was categorized as underweight/normal weight (<25 kg/m2), overweight (25-29.9 kg/m2), and obese (≥30 kg/m2). Glycemic status was classified as normoglycemic or diabetes/prediabetes (diabetes: hemoglobin A1c ≥6.5% or fasting glucose ≥126 mg/dL; prediabetes: hemoglobin A1c 5.7%-6.4% or fasting glucose 100-125 mg/dL).

Over a median follow-up of 8.7 years, 985 (8.64%) patients experienced MACE. Obesity was significantly associated with an increased risk of MACE (hazard ratio [HR], 1.38 [95% CI, 1.10-1.73], reference: underweight/normal weight) and heart failure hospitalization, and diabetes/prediabetes also significantly predicted MACE (HR, 1.28 [95% CI, 1.10-1.50], reference: normoglycemic). Notably, overweight (HR, 0.85 [95% CI, 0.80-0.91]) and obesity (HR, 0.85 [95% CI, 0.74-0.96]) were associated with lower risk of all-cause mortality. Joint analysis revealed that patients with both obesity and diabetes/prediabetes had the highest risk of MACE (HR, 1.74 [95% CI, 1.28-2.37]) and heart failure hospitalization (HR, 1.99 [95% CI, 1.41-2.81]).

In patients with cancer undergoing anthracycline-based chemotherapy, both body mass index and glycemic status significantly affect cardiovascular risks, with the highest risk observed in those with concurrent obesity and diabetes/prediabetes, emphasizing the need for tailored risk assessment and management.

Obesity-related oesophageal adenocarcinoma (OAC), arising from Barrett's oesophagus (BO), incidence rates are rising coincident with high-fat diets. However, adipose tissue phenotype drives metabolic characteristics. Prior feeding studies demonstrated that obesogenic diets enriched in saturated fatty acids (SFA) induce a more adverse metabolic and pro-inflammatory adipose phenotype, compared to monounsaturated fatty acids (MUFA) enriched high-fat diets, despite equal obesity. We hypothesise that different fatty acids may alter the progression of BO to OAC, wherein SFA may be more pathogenic compared to MUFA. Proteomic analysis shows that SFA, not MUFA, increases fatty acid metabolism, oncogenic signalling, and mitochondrial respiratory chain to a greater extent in BO but not in OAC cells. Cellular metabolic analysis validated proteomic findings to show mitochondrial dysfunction in BO but showed an increase in glycolysis in OAC following SFA treatment compared to MUFA. Additionally, it showed a decrease in mitochondrial ATP production following treatment of SFA in BO and OAC cells. Reduction of SFA intake may be beneficial as a supplementary treatment approach to manage and/or prevent OAC progression.

DLK1, as a membrane-bound protein, has been extensively studied in the field of cancer research. As a ligand downstream of the Notch pathway, it broadly influences developmental and metabolic processes in the body. With deeper research, it has been found that DLK1 can induce the synthesis and secretion of insulin through the ERK and AKT pathways, playing a crucial role in the development of metabolic diseases. Diabetes mellitus (DM) is a chronic metabolic disorder characterized by insufficient insulin production by the pancreas or inadequate utilization of insulin by the body. This article aims to review the relationship between DLK1 and diabetes, recent research advancements, and to discuss future research directions and challenges.

Obesity and depression are major public health issues with a complex, bidirectional relationship potentially involving systemic inflammation.

Using a diverse sample from the National Health and Nutrition Examination Survey (NHANES) (n = 11,324; weighted population = 456,457,366), we examined the associations between obesity, systemic inflammation, and depression. Obesity was classified by Body Mass Index (BMI), depressive symptoms were assessed with the Patient Health Questionnaire-9 (PHQ-9), and systemic inflammation was measured using markers like Neutrophil-to-Lymphocyte Ratio (NLR), Systemic Inflammation Response Index (SIRI), and Systemic Immune-Inflammation Index (SII). Weighted logistic regression models were used to assess relationships between obesity, inflammation, and depression. Linear regression evaluated BMI's association with inflammation markers, and Restricted Cubic Spline (RCS) analysis explored their interrelationships. Subgroup analyses and interaction tests were conducted, and mediation analysis examined the role of inflammation markers in mediating the obesity-depression association.

Class III obesity was associated with higher inflammatory marker levels and increased depression risk. Mediation analysis showed NLR, SIRI, and SII mediated 5.2%, 5.9%, and 6.1% of the obesity-depression relationship.

Systemic inflammation partially mediates the relationship between obesity and depression.

Diabetes is one of the leading causes of death and disability worldwide. Developing earlier and more accurate diagnosis methods is crucial for clinical prevention and treatment of diabetes. Here, data on biochemical indicators and physiological characteristics of 4335 participants from the National Health and Nutrition Examination Survey (NHANES) database from 2017 to 2020 were collected. After data preprocessing, the dataset was randomly divided into a training set (70%) and a test set (30%); then the Boruta algorithm was used to screen feature indicators on the training set. Next, three machine learning algorithms, including Random Forest (RF), Multi-Layer Perceptron (MLP), and Extreme Gradient Boosting (XGBoost) were employed to build predictive models through 10-fold cross-validation on the training dataset, followed by performance evaluation on the test dataset. The RF model exhibited the best performance, with an area under the curve (AUC) of 0.958 (95% CI: 0.943-0.973), a recall of 0.897, a specificity and F1 score of 0.916 and 0.747, respectively, and an overall accuracy of 0.913. Moreover, SHapley Additive exPlanations (SHAP) and Partial Dependency Plots (PDP) were applied to interpret the RF model to analyze the risk factors for diabetes. Glycohemoglobin, glucose, fasting glucose, age, cholesterol, osmolality, BMI, blood urea nitrogen, and insulin were found to exert the greatest influence on the prevalence of diabetes. Collectively, the RF model has considerable application prospects for the diagnosis of diabetes and can serve as a valuable supplementary tool for clinical diagnosis and risk assessment in diabetes.

The white adipose tissue (WAT) expansion plays a significant role in the development of obesity. Cytoskeletal remodeling directly impacts adipogenic program, however, the precise mechanism remains poorly understood. Here, we identified a crucial role of Septin-7 (SEPT7), a cytoskeleton component, in the regulation of diet-induced processes of adipogenesis, lipogenesis, and lipolysis in WAT.

A high-fat diet (HFD)-induced obesity model was constructed using mice with inducible adipocyte-specific SEPT7 deficiency. The impact of SEPT7 on adipocyte morphology, cell number and metabolism capacity were evaluated with immunofluorescence, isoproterenol induced lipolysis assay, glucose tolerance test and insulin tolerance test. Adipocyte mTmG reporter line was established to trace in vivo adipogenesis. The preadipocyte 3T3-L1 cell was induced for exploring role of SEPT7 in adipocyte differentiation. qRT-PCR and Western-blot were used to investigate the expression of PPARγ, C/EBPα, and HSL in 3T3-L1 cell with siRNA-mediated SEPT7 knockdown.

SEPT7 expression was greatly induced in obesogenic human and murine adipocytes. Mice lacking SEPT7 in mature white adipocytes demonstrated defective differentiation of preadipocyte into mature adipocytes when fed HFD resulting in larger adipocytes, increased WAT inflammation and reduced lipolysis, which leading to increased WAT mass, liver fat accumulation and impaired glucose tolerance. Mechanistically, we identified SEPT7 restrains store-operated Ca2+ entry (SOCE) and regulates adipocyte adipogenesis and lipolysis by targeting PPARγ, C/EBPα and HSL.

We demonstrated that SEPT7 negatively regulates adipogenesis while promotes lipolysis and its repression drives WAT expansion and impaired metabolic health.

Background and Aims: Asthma, overweight/obesity, and cancer are closely related major public health problems. This study aimed to investigate the interaction between asthma and overweight/obesity on the cancer risk. Methods: We analyzed data from the National Health and Nutrition Examination Survey 2005-2018. Participants ages ≥ 20 years with information on asthma status, body mass index (BMI), and cancer diagnosis were included. Multivariate logistic regression models adjusted for relevant covariates were used to examine the associations among asthma, overweight/obesity, and cancer risk. In addition, we assessed the additive interaction between asthma and overweight/obesity on the cancer risk by using measures, including the relative excess risk due to interaction (RERI), attributable proportion of interaction (AP), and synergy index (S). Results: In total, 26,320 participants met the inclusion criteria. Asthma was associated with an increased risk of cancer (odds ratio [OR] 1.37 [95% confidence interval {CI}, 1.17-1.59]), whereas overweight/obesity (BMI ≥ 25 kg/m²) was also significantly associated with an elevated cancer risk (OR 1.97 [95% CI, 1.32-2.94]). Notably, a significant interaction between asthma and overweight/obesity was observed in relation to the cancer risk (RERI 0.49 [95% CI, 0.02-0.96]; AP 0.20 [95% CI, 0.04, 0.37]; S 1.53 [95% CI, 1.01-2.32]). Conclusion: Our findings demonstrated a synergistic interaction between asthma and overweight/obesity on the cancer risk. The combined effect of asthma and overweight/obesity on the cancer risk exceeded the sum of their individual effects.

The incidence of Gastric cancer (GC) has shown a sharp upward trend, and patients with GC complicated by diabetes exhibit significantly worse clinical outcomes and prognosis compared to those without diabetes. Traditional Chinese medicine has played a crucial role in the treatment of both GC and diabetes. Currently, Banzhilian(Scutellaria barbata D. Don) is utilized in the treatment of GC; however, the specific small-molecule monomers it contains and their mechanisms of action have not yet been fully elucidated. This study aims to explore the mechanism of quercetin, a key component of Banzhilian, through network pharmacology, molecular docking, molecular dynamics (MD) simulation, bioinformatics, and in vitro and in vivo experiments. Initially, core targets and key pathways involved in the treatment of diabetes-associated GC (GC-diabetes) were identified using public databases. Subsequently, molecular docking, MD simulation, and survival analysis were performed. Experimental validation included CCK-8 assays, colony formation assays, apoptosis detection, cell cycle analysis, wound healing assays, Transwell migration assays, Western blotting, and mouse subcutaneous tumor formation experiments to evaluate the effects of quercetin, as an active monomer in Banzhilian, on Gastric cancer cells (HGC-27-HG cells) under high-glucose conditions. In this study, quercetin was identified as the key active component, with AKT1, TP53, JUN, MYC, and CCND1 recognized as the target genes, and the PI3K/AKT signaling pathway as the primary regulatory pathway. The results of the study indicate that the proliferation, migration, and invasion capabilities of HGC-27-HG cells are significantly higher than those of HGC-27 cells. However, quercetin inhibited the growth of HGC-27-HG cells, promoted apoptosis, induced cell cycle arrest at the G0/G1 phase, and reduced the cells' migration and invasion abilities. Furthermore, it downregulated the expression of target genes and their phosphorylation levels. The experimental findings confirmed that quercetin, as an active monomer in Banzhilian, suppresses the proliferation of HGC-27-HG cells by inhibiting the PI3K/AKT/MYC pathway, promoting apoptosis, blocking cell cycle progression, and inhibiting cell migration and invasion.

Although cancer chemopreventive agents have been confirmed to effectively protect high-risk populations from cancer invasion or recurrence, only over ten drugs have been approved by the U.S. Food and Drug Administration. Therefore, screening potent cancer chemopreventive agents is crucial to reduce the constantly increasing incidence and mortality rate of cancer. Considering the lengthy prevention process, an ideal chemopreventive agent should be nontoxic, inexpensive, and oral. Natural compounds have become a natural treasure reservoir for cancer chemoprevention because of their superior ease of availability, cost-effectiveness, and safety. The benefits of natural compounds as chemopreventive agents in cancer prevention have been confirmed in various studies. In light of this, the present review is intended to fully delineate the entire scope of cancer chemoprevention, and primarily focuses on various aspects of cancer chemoprevention based on natural compounds, specifically focusing on the mechanism of action of natural compounds in cancer prevention, and discussing in detail how they exert cancer prevention effects by affecting classical signaling pathways, immune checkpoints, and gut microbiome. We also introduce novel cancer chemoprevention strategies and summarize the role of natural compounds in improving chemotherapy regimens. Furthermore, we describe strategies for discovering anticancer compounds with low abundance and high activity, revealing the broad prospects of natural compounds in drug discovery for cancer chemoprevention. Moreover, we associate cancer chemoprevention with precision medicine, and discuss the challenges encountered in cancer chemoprevention. Finally, we emphasize the transformative potential of natural compounds in advancing the field of cancer chemoprevention and their ability to introduce more effective and less toxic preventive options for oncology.

Vitamin D plays a crucial role in the regulation of the immune system, with immunomodulatory effects that are key in the prevention of colorectal cancer (CRC). Over the past decades, research has shown that this steroid hormone impacts much more than bone health, significantly influencing immune responses. Vitamin D enhances immune organ functions such as the spleen and lymph nodes, and boosts T-cell activity, which is essential in defending the body against tumors. Additionally, vitamin D mitigates inflammatory responses closely linked to cancer development, reducing the inflammation that contributes to CRC. It acts via vitamin D receptors (VDRs) expressed on immune cells, modulating immune responses. Adequate vitamin D levels influence gene expression related to inflammation and cell proliferation, inhibiting tumor development. Vitamin D also activates mechanisms that suppress cancer cell survival, proliferation, migration, and metastasis. Low levels of vitamin D have been associated with an increased risk of CRC, with deficiency correlating with higher disease incidence. Lifestyle factors, such as a diet high in red meat and calories but low in fiber, fruits, and vegetables, as well as physical inactivity, contribute significantly to CRC risk. Insufficient calcium and vitamin D intake are also linked to disease occurrence and poorer clinical outcomes. Maintaining optimal vitamin D levels and adequate dietary intake is crucial in preventing CRC and improving patient prognosis. This review explores the role of vitamin D in immune regulation and summarizes findings from randomized clinical trials assessing the effects of vitamin D supplementation on CRC outcomes.

Colon cancer is one of the most prevalent malignancies globally. Anthropometric data are widely accessible. However, numerous anthropometric indicators exist, and no study has identified the most reliable predictor for colon cancer. This study aims to identify the most effective anthropometric indicators for predicting colon cancer.

Significant differences were observed in age, race, smoking, diabetes, hypertension, waist circumference, a body shape index (ABSI), Body Roundness Index (BRI), Conicity Index (ConI), Waist-to-Height Ratio(WHtR), and Weight-adjusted Waist Index(WWI) between colon cancer patients and controls (P < 0.05). ABSI (AUC: 0.68, 95% CI: 0.64-0.71), ConI (AUC: 0.68, 95% CI: 0.64-0.71), and WWI (AUC: 0.67, 95% CI: 0.63-0.70) were the most accurate anthropometric indices for predicting colon cancer. ABSI, ConI, and WWI demonstrated a strong correlation.

Analysis of NHANES data (2005-2018) identified ABSI, ConI, and WWI (AUC:0.67-0.68) as optimal anthropometric predictors of colon cancer, emphasizing abdominal obesity's clinical relevance. These cost-effective indices could enhance early screening in resource-limited settings.

The existing data on colon lesions in acromegaly is notably heterogeneous. This study aimed to analyze the endoscopic and histopathological characteristics of colon polyps and other colonic lesions in acromegaly patients.

This case-control study included 192 acromegaly patients and 256 controls. Colon polyps were categorized based on their size and histopathological classification. Colon malignancies and other colonic lesions, such as anal fissures, hemorrhoids, and diverticulosis, were also documented.

The prevalence of colon polyps was higher in the acromegaly group than in controls (p = 0.003), however, no differences were observed in the number, size, or histopathological subtypes of the polyps. Polyps in acromegaly patients were predominantly located in the distal colon and rectum. Multiple polyp locations and histopathological subtypes were more frequent in the control group (p = 0.042 and p = 0.018). Rates of low-grade dysplasia, high-grade dysplasia, and malignancy were similar between groups. Anal fissures were more common in the acromegaly group, whereas diverticulosis was less frequent (p = 0.001 and p < 0.001; respectively). Logistic regression analysis identified no significant clinical or laboratory predictors for colon polyps in acromegaly.

Patients with acromegaly exhibited a higher prevalence of colon polyps, predominantly located in the distal colon, which typically displayed a single histopathological subtype. No increased rates of colonic dysplasia, colon cancer, or other colonic lesions were observed in patients with acromegaly, except for an elevated prevalence of anal fissures.

Type 2 diabetes mellitus (T2DM) constitutes a significant risk factor for breast cancer (BC), with affected women exhibiting a two- to three-fold increased likelihood of developing BC. Furthermore, women diagnosed with both BC and T2DM tend to experience poorer prognoses and exhibit greater resistance to various treatments compared to their non-diabetic counterparts. Consequently, elucidating the comorbidities associated with T2DM and BC is instrumental in enhancing the diagnostic and therapeutic strategies for BC.

A series of bioinformatics methods including weighted gene co-expression network analysis (WGCNA), differentially expressed gene (DEG) analysis, machine learning, and single-cell sequencing analysis were used to identify the pathogenetic molecules of T2DM for BC. Biological experiments including CCK-8, colony formation, wound healing, transwell assay, immunohistochemistry, and immunofluorescence were performed to determine the molecule effect.

By conducting WGCNA and DEG analysis on the profiles of T2DM (GSE25724 and GSE20966) and the TCGA cohort of BC, we identified a total of 27 common hub genes shared between T2DM and BC. These genes were significantly enriched in pathways related to cell differentiation, cellular developmental processes, focal adhesion, and the MAPK signaling pathway. Notably, among these 27 genes, CCNB2, XRCC2, and CENPI were associated with poor prognosis in BC. Moreover, single-cell RNA sequencing analysis revealed that CCNB2, XRCC2, and CENPI are enriched in cancer cells within BC tissues. Additionally, we observed that CCNB2, XRCC2, and CENPI were elevated in BC tissues provided by patients with a diabetes history and associated with KI67 expression. Hyperglycemia treatment elevated the expression levels of CCNB2, XRCC2, and CENPI in BC cells, which correlated with increased cell proliferation and mobility. Conversely, the knockdown of these genes partially mitigated the pro-proliferative and pro-migratory effects induced by hyperglycemia in BC cells.

Our findings suggested that CCNB2, XRCC2, and CENPI may serve as key pathogenic mediators linking T2DM and BC. Targeting these molecules could potentially attenuate the adverse impacts of T2DM on BC progression.

The rising prevalence of obesity in the Kingdom of Saudi Arabia (KSA) poses a significant public health challenge. Estimates of the economic cost of obesity are crucial for prioritizing healthcare interventions, guiding policy choices, and justifying budget allocations aimed at reducing obesity prevalence. This study aimed to estimate the cost of obesity in the KSA in 2022.

A prevalence-based cost-of-illness approach was used to determine the cost of obesity. This analysis encompasses 29 diseases, namely obesity and twenty-eight diseases attributable to obesity. Both direct and indirect costs were considered. The annual cost of treatment for each obesity-attributable disease was obtained from the hospital records of one tertiary hospital in the KSA. Data on direct non-medical costs were obtained from the patient survey. The human capital approach was used to estimate the indirect costs of morbidity and mortality.

The total economic burden of obesity (2022 values) was estimated at US$116.85 billion from a societal perspective and US$109.67 billion from a healthcare system perspective. From a societal perspective, the total direct medical cost accounted for the largest portion of the total cost (94%). In terms of direct medical costs, the cost of treating diseases attributable to obesity was substantially greater than the cost of treating obesity itself. According to the sensitivity analysis, the total cost ranged from 3.4% of the country's Gross domestic product (GDP) when the unit cost of treatment was reduced by 74% to 9.5% of the country's GDP when the prevalence of obesity and its comorbidities was reduced by 5%.

Obesity imposes a substantial economic burden on the healthcare system and society in the KSA. Interventions aimed at promoting healthier lifestyles to reduce the prevalence and incidence of obesity and its comorbidities are highly warranted to alleviate the impact of obesity in the country.

Cancer and cardiovascular disease remain the leading causes of morbidity and mortality worldwide, and the two separate disease entities share several similarities and possible interactions. Patients with cancer may have underlying cardiovascular disease, which is often exacerbated by the stress of tumor growth or treatment. At the same time, cardiotoxicity induced by anti-cancer therapies or the malignant process itself can lead to new cardiovascular diseases. Efforts have been made to find a rational explanation for this phenomenon. As a classical tumor-promoting factor, we notice that SNAI2 simultaneously plays an important pathogenic role in cardiovascular diseases. Moreover, there are several striking parallels in the mechanisms of cancer and CVD, such as shared risk factors (e.g., smoking and diabetes), cellular phenotypic switching, and metabolic remodeling, all of which are mediated by SNAI2. This review aims to summarize SNAI2's role in the core mechanisms linking cancer and CVD, as well as explore therapeutic approaches targeting SNAI2 and also seeks to provide insights into the common mechanisms underlying both cancer and CVD.

Food intake is an essential contributor to both health and disease. Nutrients contribute to a beneficial metabolic equilibrium at the cellular level, preventing or delaying disease onset. Dietary intake contributes to obesity, and obesity supports further cancer and metastasis. Metastasis, a multifactorial and multistep process, is supported by the systemic inflammation of obesity. Spreading of the cancer cells requires the presence of a plethora of recruiter and regulator molecules. Molecules such as chemokines are provided at high levels by obesity-associated fat depots. Chemokine up-regulation in adipose tissue of obese individuals has been associated with different types of cancers such as breast, prostate, colon, liver, and stomach. Chemokines support all metastasis steps from invasion/migration to intravasation, circulation, extravasation, and ending with colonization. The obesity pool of chemokines supporting these processes includes CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL11, CCL18, CCL19, CCL20, CXCL1, CXCL5, CXCL 8, CXCL10, and CXCL12. Keeping obesity under control can be beneficial in reducing the levels of pro-inflammatory chemokines and the risk of poor cancer outcome. Nutrients can help, support, and boost cancer treatment effects or jeopardize the treatment. Constituents with anti-inflammatory and anti-obesity properties such as polyphenols, organosulfur components, fatty acids, curcumin, and vitamin E have a proven beneficial effect in lowering obesity and its contribution to metastasis.

Acromegaly is associated with a possible increased risk of neoplasias, like colorectal cancer (CRC), although magnitude of this risk is unclear.

Evaluate frequency of colonic adenomatous polyps and CRC in patients with acromegaly at first and subsequent colonoscopies; correlate risk factors of CRC and disease activity of acromegaly with colonoscopy findings and analyze relationship of acromegaly as a risk factor for CRC and the best period for screening this neoplasia.

Patients ≥18 years-old with acromegaly were included. A questionnaire involving characteristics of follow-up of acromegaly and risk factors of CRC was created. Biochemical and colonoscopic data were collected through medical records. Only full-length colonoscopies with satisfactory colonic preparation were included.

123 patients (77 women) were included (mean age at diagnosis of 43.1 years and mean follow-up of 13.7 years). In baseline colonoscopy, 80.5% had non-neoplastic findings, 14.6% non-advanced adenomas, 3.3% advanced adenomas and 1.6% CRC. At end of the study, 3 (2.4%) patients were diagnosed with CRC. No patient under 50 years had a neoplastic lesion on colonoscopy. We observed a positive statistically significant relationship between smoking (p = 0.026), age at diagnosis of acromegaly (p < 0.001), age at baseline colonoscopy (p = 0.002), and risk of adenomas and/or CRC at initial colonoscopy.

Smoking and advanced age were positively related to a higher risk of developing premalignant/malignant colonic lesions. Age ( > 50 years) was the most robust variable. Our data suggest that screening age for CRC in acromegaly should be reviewed.

To evaluate the correlation between serum glycosylated hemoglobin (HbA1c) levels and the risk of prostate cancer incidence and mortality, providing a comprehensive analysis to inform preventative and clinical strategies.

A systematic review and meta-analysis was conducted including studies based on their documentation of prostate cancer incidence and mortality related to HbA1c levels, with a minimum of 3 risk-related data levels. The Newcastle-Ottawa Quality Assessment Scale (NOQAS) was used for quality assessment and risk of bias evaluation. We employed generalized least squares (GLS) to assess the linear trend within individual studies and combined these estimates using a random effects model. Additionally, we utilized a restricted cubic spline (RCS) model to investigate potential nonlinear trends.

A total of 13 studies were included in the quantitative synthesis ultimately. The quantitative analysis did not find a significant association between HbA1c levels and prostate cancer incidence. However, a significant positive correlation was revealed between HbA1c levels and both cancer-specific mortality (CSM) and all-cause mortality (ACM), with a 1% increase in HbA1c levels associated with a 26% increase in CSM and a 21% increase in ACM.

The HbA1c level is significantly associated with increased prostate cancer mortality. The results highlight the importance of considering blood sugar control in the comprehensive risk assessment for prostate cancer, particularly among the nondiabetic population.

Obesity due to excessive fat accumulation, affects health and quality of life and increases the risk of diseases such as type 2 diabetes and cardiovascular conditions. Traditional causes, such as calorie excess and sedentary behavior, do not fully explain the obesity epidemic, leading to the hypothesis that endocrine-disrupting chemicals or obesogens contribute to obesity. The obesogenic mechanisms of representative obesogenic substances, such as bisphenols, have been discussed, mainly focusing on their interactions with estrogen receptors. Based on several studies showing that obesogens induce obesity by mimicking glucocorticoids, this review focused on the role of the glucocorticoid receptor pathway. In addition, the anti-obesogenic bioactive substances that have been studied to this date along with their inhibitory mechanisms were discussed.

Cancer and cancer treatments can weaken the body's immune system, making cancer patients particularly vulnerable to COVID-19. While evidence suggests that cancer patients may be at increased risk for severe outcomes after COVID-19 infection, there is a lack of population-based studies comparing long COVID prevalence between cancer survivors and non-cancer individuals.

We utilized data from the 2022 Behavioral Risk Factor Surveillance System (BRFSS), analyzing a sample of 120,658 U.S. adults who had tested positive for COVID-19. Long COVID was defined as the presence of COVID-19 symptoms lasting three months or longer. The weighted prevalence of long COVID was compared between cancer survivors and non-cancer individuals. Crude and adjusted odds ratios (ORs) with 95 % confidence intervals (CIs) were calculated. Multiple imputation was employed to address missing data on COVID-19 vaccination.

Among 17,362 cancer survivors who tested positive for COVID-19, 4009 reported having long COVID (weighted prevalence = 24.0 %), compared to a weighted prevalence of 21.6 % in non-cancer individuals (p < 0.001). After controlling for covariates and accounting for the complex sampling design, the adjusted OR was 1.17 (95 % CI = 1.06-1.30, p = 0.002). In participants under 45 years old, cancer survivors had a notably higher prevalence of long COVID compared to non-cancer individuals (32.1 % vs. 21.3 %, p < 0.001), with an adjusted OR of 1.33 (95 % CI = 1.07-1.66, p = 0.012). In participants aged 45 and above, the prevalence difference was not significant (22.7 % vs. 21.9 %, p = 0.324), with an adjusted OR of 1.14 (95 % CI = 1.02-1.27, p = 0.024). Regarding the association of COVID-19 vaccination with long COVID, four or more doses were linked to a significant reduced odds of long COVID among cancer survivors (adjusted OR=0.55, 95 %CI = 0.34-0.88, p = 0.013).

Cancer survivors are observed to have higher odds of developing long COVID, particularly younger survivors. The association of COVID-19 vaccination with long COVID varies between cancer survivors and non-cancer individuals, with cancer survivors requiring more doses to achieve significant reduction in the odds of long COVID.

It is widely acknowledged that dietary habits have profound impacts on human health and diseases. As the most important sweeteners and energy sources in human diets, hexoses take part in a broad range of physiopathological processes. In recent years, emerging evidence has uncovered the crucial roles of hexoses, such as glucose, fructose, mannose, and galactose, in controlling the differentiation or function of immune cells.

Herein, we reviewed the latest research progresses in the hexose-mediated modulation of immune responses, provided in-depth analyses of the underlying mechanisms, and discussed the unresolved issues in this field.

Owing to their immunoregulatory effects, hexoses affect the onset and progression of various types of immune disorders, including inflammatory diseases, autoimmune diseases, and tumor immune evasion. Thus, targeting hexose metabolism is becoming a promising strategy for reversing immune abnormalities in diseases.

Long-term exposure to air pollutants and diabetes are both linked to cancer development. However, their combined effect remains unclear. This study examined the relationship between air pollutants and cancer incidence, with diabetes as a potential mediator. Data from 10,590 participants in the 2015 China Health and Retirement Longitudinal Study (CHARLS) were analyzed. Participants were grouped based on cancer diagnosis, and air pollutant exposure levels were estimated using satellite-based spatiotemporal models. Generalized linear regression and restricted cubic spline (RCS) analysis were used to assess the impact of air pollutants and diabetes in covariates-adjusted models. Further analyses, including conditional independence test, mediation effect and sensitivity analysis based on Bayesian networks, were performed to further analyze specific air pollutants. After adjusting for covariates, particulate matter (PM) (PM ≤ 1 μm in aerodynamic diameter [PM1], PM2.5, ammonium (NH4), nitrate (NO3) and diabetes showed significant associations with cancer incidence. RCS analysis confirmed significant direct effects of PM2.5 and PM10 on cancer and the mediated effects of diabetes. The interaction between diabetes and both PM2.5 and PM10 was further supported by conditional independence tests, highlighting diabetes as a significant mediator in the PM2.5-cancer relationship. This study offers a novel perspective by identifying diabetes as a key intermediary in the association between PM2.5 exposure and cancer risk, providing evidence that diabetes plays a significant mediating role in air pollutant-related cancer development.

Alzheimer's disease is linked with diabetes and cancer, emphasising the need for effective treatments. Plantago lanceolata, recognised as safe by various pharmacopeias, was investigated in this study for therapeutic potential. We examined the effects of its leaf extracts and sub-extracts (methanol, hexane, dichloromethane, ethyl acetate, butanol, aqueous) on AChE, BChE, α-amylase, α-glucosidase enzymes, as well as their impact on HDF-a and U87-MG cancer cells. The phytochemical characterisation was performed using ICP-MS and LC-MS/MS. Cytotoxic effects were evaluated on HDF-a and U87-MG cell lines, along with assessments for nuclear abnormalities. Na and K were detected in extracts, with isoleucine and cyanidin-3-O-glucoside being the most concentrated compounds. Extracts at concentrations exceeding 25 µg/mL significantly increased cytotoxicity in HDF-a cell lines compared to the control group, without inducing nuclear abnormalities. Methanol extract demonstrated moderate inhibition against AChE and BChE at concentrations of 100 µg/mL and 500 µg/mL, respectively. These findings suggest that extracts exhibit potential therapeutic effects.

Colorectal cancer (CRC) poses a significant health burden in Europe, but comprehensive studies on this region are limited.

Using data from the Global Burden of Diseases (GBD), Injuries, and Risk Factors Study 2021, we analyzed the regional distribution and temporal trends of the CRC and early-onset CRC burden in Europe from 1990 to 2021. Decomposition analysis was applied to quantify the contributions of population growth, aging, and epidemiological changes. The research also evaluated major risk factors associated with CRC and early-onset CRC.

The burden of CRC in Europe was found to be higher than the global average. While the age-standardized incidence rate (ASIR) increased, both the age-standardized mortality rate (ASMR) and age-standardized disability-adjusted life years rate (ASDR) decreased. Early-onset CRC exhibits similar distribution characteristics and patterns of change. Males had a significantly higher CRC burden than females. Population aging was the primary driver of increased burden in Europe. Risk factor analysis revealed that low whole grain intake and high red meat consumption were the primary contributors to the elevated ASMR and ASDR of CRC and early-onset CRC. Additionally, the CRC and early-onset CRC burden associated with high BMI and high fasting plasma glucose showed an increasing trend.

The overall burden of CRC and early-onset CRC in Europe remains higher than the global level, with increasing ASIR and decreasing ASMR and ASDR. Targeted prevention and control strategies should be developed based on the major risk factors for CRC. Older adults and men should be prioritized for interventions.

Overweight is thought to affect the outcome of minimally invasive surgery. There is still a lack of controlled studies of laparoscopic pancreaticoduodenectomy (LPD) versus open pancreaticoduodenectomy (OPD) in overweight patients. This study was designed to compare short-term and long-term outcomes in overweight patients treated with LPD and OPD.

Clinical and follow-up data on overweight patients who received LPD or OPD at Shandong Provincial Hospital from January 2015 to December 2022 were analyzed retrospectively. The bias between groups were balanced by 1:1 propensity score matching (PSM). Kaplan-Meier survival curves described long-term survival outcomes in overweight pancreatic ductal adenocarcinoma (PDAC) patients.

A total of 502 overweight patients were enrolled in the study. There were 276 patients in the LPD group and 226 in the OPD group. After matching, 196 patients were enrolled in each group. Compared with the OPD group, the LPD group had fewer estimated blood loss (EBL) (140 vs. 200 mL, P < 0.001), more lymph node dissection (14 vs. 12, P = 0.010), and shorter postoperative length of stay (LOS) (13 vs. 16 days, P < 0.001). There were no significant differences in severe complications, 90-day readmission and mortality rates (all P > 0.05). The subgroup analysis of obese patients also showed that the LPD group had fewer intraoperative EBL, more lymph node dissection, and shorter LOS. The survival analysis showed that overweight patients with PDAC who underwent LPD or OPD had similar overall survival (OS) (23.8 vs.25.7 months, P = 0.963) after PSM.

It is safe and feasible for overweight patients undergoing LPD to have less EBL, more lymph node harvesting, and a shorter LOS. There was no statistically significant difference in long-term survival outcomes among overweight PDAC patients between the two approaches.

The potential impact of one-carbon metabolism (OCM)-related B vitamins (vitamin B2, B6, B12, and folate) on colorectal cancer survival warrants investigation but research is sparse. This cohort study examined the association between the prediagnostic dietary intakes of OCM-related B vitamins and colorectal cancer survival. A total of 2799 colorectal cancer patients from the Guangdong Colorectal Cancer Cohort, enrolled at baseline in 2010, were followed for mortality outcomes through 2023. Dietary data were collected from patients using a food frequency questionnaire for the year prior to their diagnosis. Multivariable Cox proportional hazards regression models were applied to calculate hazard ratios (HR) and 95% confidence intervals (95% CI) to examine the association between OCM-related B vitamins and colorectal cancer survival. Restricted cubic spline analyses and stratified analysis were performed. During the follow-up period of approximately 60.33 months, 639 deaths were documented, of which 574 were colorectal cancer-specific deaths. Dietary vitamin B2 and B6 intake was significantly associated with survivals. The adjusted HRs in the highest versus the lowest quartile of vitamin B2 intake were 0.77 (0.62-0.97) for overall survival and 0.71 (0.55-0.90) for colorectal cancer-specific survival, and vitamin B6 intake were 0.79 (0.64-0.99) for overall survival and 0.75 (0.59-0.94) for colorectal cancer-specific survival. Nonlinear associations were observed between vitamin B6 intake and both overall survival and colorectal cancer-specific survival. However, no significant association was found between vitamin B12 or folate intake and survivals. These results suggest that high prediagnostic intake of vitamin B2 and B6 may be associated with improved survivals in colorectal cancer patients.

A decade after the term 'trained immunity' (TRIM) was coined to reflect the long-lasting hyper-responsiveness of innate immune cells with an epigenetically imprinted 'memory' of earlier stimuli, our understanding has broadened to include the potential implications of TRIM in health and disease. Here, after summarizing the well-documented beneficial effects of TRIM against infections, we discuss emerging evidence that TRIM is also a major underlying mechanism in chronic inflammation-related disorders such as periodontitis, rheumatoid arthritis and cardiovascular disease. Furthermore, mounting evidence indicates that the induction of TRIM by certain agonists confers protective antitumour responses. Although the mechanisms underlying TRIM require further study, the current knowledge enables the experimental development of innovative therapeutic approaches to stimulate or inhibit TRIM in a context-appropriate manner, such as the stimulation of TRIM in cancer or its inhibition in inflammatory disorders.

Malic enzyme 1 (ME1) plays a key role in promoting malignant phenotypes in various types of cancer. ME1 promotes epithelial-mesenchymal transition (EMT) and enhances stemness via glutaminolysis, energy metabolism reprogramming from oxidative phosphorylation to glycolysis. As a result, ME1 promotes the malignant phenotypes of cancer cells and poor patient prognosis. In particular, ME1 expression is promoted in hypoxic environments associated with hypoxia-inducible factor (HIF1) α. ME1 is overexpressed in budding cells at the cancer invasive front, promoting cancer invasion and metastasis. ME1 also generates nicotinamide adenine dinucleotide (NADPH), which, together with glucose-6-phosphate dehydrogenase (G6PD) and isocitrate dehydrogenase (IDH1), expands the NADPH pool, maintaining the redox balance in cancer cells, suppressing cell death by neutralizing mitochondrial reactive oxygen species (ROS), and promoting stemness. This review summarizes the latest research insights into the mechanisms by which ME1 contributes to cancer progression. Because ME1 is involved in various aspects of cancer and promotes many of its malignant phenotypes, it is expected that ME1 will become a novel drug target in the near future.

Chronic diseases such as diabetes and cancer are the leading causes of mortality worldwide. Receptors for Advanced Glycation End products (RAGEs) are ubiquitous factors that catalyse Advanced Glycation End products (AGEs), proteins, and lipids that become glycated from sugar ingestion. RAGEs are cell surface receptor proteins and play a broad role in mediating the effects of AGEs on cells, contributing to modifying biological macromolecules like proteins and lipids, which can cause Reactive Oxygen Species (ROS) generation, inflammation, and cancer. We targeted RAGE inhibition analysis and screening of United States Food and Drug Administration (FDA) libraries through molecular docking studies that identified the four most suitable FDA compounds: Zytiga, Paliperidone, Targretin, and Irinotecan. We compared them with the control substrate, Carboxymethyllysine, which showed good binding interaction through hydrogen bonding, hydrophobic interactions, and π-stacking at active site residues of the target protein. Following a 100 ns simulation run, the docked complex revealed that the Root Mean Square Deviation (RMSD) values of two drugs, Irinotecan (1.3 ± 0.2 nm) and Paliperidone (1.2 ± 0.3 nm), were relatively stable. Subsequently, the Molecular Mechanics Poisson-Boltzmann Surface Area (MMPBSA) determined that the Paliperidone molecule had a high negative energy of -13.49 kcal/mol, and the Absorption, Distribution, Metabolism, and Excretion (ADME) properties were in control for use in the mentioned cases. We extended this with many in vitro studies, including an immunoblotting assay, which revealed that RAGEs with High Mobility Group Box 1 (HMGB1) showed higher expression, while RAGEs with Paliperidone showed lower expressions. Furthermore, cell proliferation assay and Apoptosis assay (Annexin-V/PI staining) results revealed that Paliperidone was an effective anti-glycation and anti-apoptotic drug-however, more extensive in vivo studies are needed before its use.

Metabolic syndrome (Mets) in adolescents is a growing public health issue linked to obesity, hypertension, and insulin resistance, increasing risks of cardiovascular disease and mental health problems. Early detection and intervention are crucial but often hindered by complex diagnostic requirements. This study aims to develop a predictive model using NHANES data, excluding biochemical indicators, to provide a simple, cost-effective tool for large-scale, non-medical screening and early prevention of adolescent MetS. After excluding adolescents with missing diagnostic variables, the dataset included 2,459 adolescents via NHANES data from 2007-2016. We used LASSO regression and 20-fold cross-validation to screen for the variables with the greatest predictive value. The dataset was divided into training and validation sets in a 7:3 ratio, and SMOTE was used to expand the training set with a ratio of 1:1. Based on the training set, we built eight machine learning models and a multifactor logistic regression model, evaluating nine predictive models in total. After evaluating all models using the confusion matrix, calibration curves and decision curves, the LGB model had the best predictive performance, with an AUC of 0.969, a Youden index of 0.923, accuracy of 0.978, F1 score of 0.989, and Kappa value of 0.800. We further interpreted the LGB model using SHAP, the SHAP hive plot showed that the predictor variables were, in descending order of importance, BMI age sex-specific percentage, weight, upper arm circumference, thigh length, and race. Finally, we deployed it online for broader accessibility. The predictive models we developed and validated demonstrated high performance, making them suitable for large-scale, non-medical primary screening and early warning of adolescent Metabolic syndrome. The online deployment of the model allows for practical use in community and school settings, promoting early intervention and public health improvement.

The incidence of lung cancer is closely associated with diabetes; however, it remains unclear whether diabetes influences the genetic mutations present in lung cancer. Therefore, we will compare the genetic mutations in patients with lung adenocarcinoma (ADC) who have diabetes against those who do not.

We included 279 patients diagnosed with lung adenocarcinoma (143 with diabetes and 136 without diabetes) at the Second Affiliated Hospital of Chongqing Medical University between 2016 and 2023, and analyzed the clinical characteristics and genetic mutation profiles of all participants.

In comparison to ADC patients without diabetes, those with diabetes exhibited a lower overall gene mutation rate (49.7% vs. 65.4%, P = 0.008). Female ADC patients demonstrated a higher total gene mutation rate and EGFR gene mutation rate than their male counterparts (49.3% vs. 66.9%, P = 0.003; 27.6% vs. 58.3%, P < 0.001, respectively), although their TP53 gene mutation rate was lower (8.6% vs. 2.4%, P = 0.027). ADC patients without a smoking history had a higher gene mutation rate and EGFR gene mutation rate than those with a smoking history (62.6% vs. 47.4%, P = 0.014; 51.6% vs. 22.7%, P < 0.001, respectively), but a lower KRAS gene mutation rate (4.4% vs. 14.4%, P = 0.003). Conversely, ADC patients with a drinking history had a lower EGFR gene mutation rate than those without (48% vs. 62.6%, P = 0.018; 31.0% vs. 47.5%, P = 0.007), yet a higher KRAS gene mutation rate (14.0% vs. 4.5%, P = 0.005). Univariate and multivariate linear regression analyses revealed that being female, having no smoking history, and being in phase II or IV of tumor stage were associated with gene mutation. Subgroup analysis indicated that the rate of gene mutation in male smoking lung adenocarcinoma patients with diabetes was significantly lower than in those without diabetes.

This retrospective study of real-world data suggests that patients with lung adenocarcinoma and diabetes may have a reduced likelihood of developing genetic mutations, particularly among male smokers. Furthermore, gender, smoking history, and tumor stage may be correlated with the presence of gene mutations.

Endometrial cancer (EC) is a common malignant tumor that is closely associated with metabolic disorders such as diabetes and obesity. Advanced glycation end products (AGEs) are complex polymers formed by the reaction of reducing sugars with the amino groups of biomacromolecules, mediating the occurrence and development of many chronic metabolic diseases. Recent research has demonstrated that the accumulation of AGEs can affect the tumor microenvironment, metabolism, and signaling pathways, thereby affecting the malignant progression of tumors. However, the mechanism by which AGEs affect EC is unclear. Our research aimed to investigate how AGEs promote the development of EC through metabolic pathways and to explore their potential underlying mechanisms. Our experimental results demonstrated that AGEs upregulated the choline metabolism mediated by choline kinase alpha (CHKA) through the receptor for advanced glycation end products, activating the PI3K/AKT pathway and enhancing the malignant biological behavior of EC cells. Virtual screening and molecular dynamics simulation revealed that timosaponin A3 could target CHKA to inhibit AGE-induced progression of EC and that a newly discovered CHKA inhibitor could be a novel targeted inhibitor for the treatment of EC. This study provides new therapeutic strategies and contributes to the treatment of EC.

Abnormalities of carbohydrate antigen 19 - 9 (CA19-9) are common in patients with type 2 diabetes mellitus (T2DM), and in some patients, CA19-9 returns to normal level after glycemic control. The aim of this study was to investigate the factors associated with CA19-9 levels in patients with T2DM and the associated influences on the degree of reduction of CA19-9 levels after antidiabetic therapy (AT). This study was an observational cross-sectional study. A total of 213 patients with T2DM were enrolled in this study, of whom 105 with abnormal CA19-9 and 108 with normal CA19-9. Socio-demographic information, complete blood counts, biochemical indicators, thyroid function indicators, and CA19-9 level were collected separately for each subject. Levels of glycosylated hemoglobin, type A1C (HbA1c), fasting blood glucose (FBG) were significantly higher in T2DM patients with abnormal CA19-9 compared to patients with normal CA19-9 (both FDR < 0.001). CA19-9 level was significantly and positively correlated with neutrophil/lymphocyte ratio (NLR) (r = 0.16, P = 0.02), monocyte/lymphocyte ratio (MLR) (r = 0.16, P = 0.02), and FBG (r = 0.38, P < 0.001), while significantly and negatively correlated with free triiodothyronine (FT3) (r=-0.22, P = 0.002) and albumin count (r=-0.18, P = 0.007). After AT, the degree of decrease in CA19-9 level in T2DM patients with abnormal CA19-9 was significantly positively correlated with degree of decrease in FBG (r = 0.33, P < 0.001), as well as CA19-9 level before AT (r = 0.73, P < 0.001), NLR (r = 0.20, P = 0.04), and MLR (r = 0.25, P = 0.01). In this study, we investigated the influencing factors associated with CA19-9 level and the factors influencing degree of CA19-9 reduction after AT in T2DM patients with abnormal CA19-9.

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.

To investigate the spatiotemporal variations in body mass index among Han adolescents aged 18 years across 27 provinces of China from 1985 to 2019.

Cross-sectional epidemiological study.

A total of 141,406 adolescents aged 18 years were included from eight Chinese National Surveillance on Students' Constitution and Health from 1985 to 2019. Body mass index data were extracted from 27 provinces in each CNSSCH. All provinces were categorized into seven regions. Linear regression was used to assess the trends.

The population-based national body mass index of boys and girls aged 18 years from 27 provinces increased by 2.35 kg/m2 and 1.40 kg/m2, respectively (all p < 0.001). Body mass index has been greater and the increase was larger in North China and East China during the 34-year period. Body mass index has been smaller and the increase was smaller in South China and Southwest China. The Northeast China had the largest increase in body mass index, becoming the region with the largest body mass index through 2019.

The body mass index among Chinese adolescents aged 18 years across provinces increased from 1985 to 2019. Further national and local efforts are needed to address spatiotemporal variations in body mass index.