Several studies have indicated that the dysregulation of microbial metabolites and the inflammatory environment resulting from microbial dysbiosis may contribute to the occurrence and progression of cardiovascular diseases. Therefore, restoring the disordered gut microbiota in patients with colorectal cancer by fecal microbiota transplantation (FMT) has the potential to reduce the incidence of cardiac disease. In this study, we identified cardiac dysfunction in azomethane and dextran sodium sulfate-induced colorectal cancer mice. Intestinal microbes from healthy mice were transferred to colorectal cancer mice, which vastly reversed the disorder of the gut microbiota and effectively alleviated cardiac dysfunction. Moreover, FMT regulated the expression of serum metabolites such as uridine triphosphate (UTP), tiamulin, andrographolide, and N-Acetyl-D-glucosamine, as well as cytokines like TGF-β, IRF5, and β-MHC in the heart. These findings uncover that the disturbed gut microbiota causes cardiac dysfunction in colorectal cancer mice by modulating the expression of serum metabolites and cytokines, which could be alleviated by treatment with FMT.

Descriptions of the effect of chemotherapy on all the electrocardiographic parameters in breast cancer women during chemotherapy are limited.

A retrospective and within-subject longitudinal study of the effect of chemotherapeutics and different chemotherapeutic regimens on electrocardiographic parameters was conducted in 948 breast cancer women who had completed chemotherapy with ECG recording at initial diagnosis and before each cycle of chemotherpy. Heart rate (HR), QRS interval, P-R interval, QRS axis, QT interval, QTc interval, and the incidence of QTc interval prolongation were analyzed. Age, body mass index (BMI), history of hypertension, diabetes, and coronary heart disease were also collected for further stratified study.

Compared to initial diagnosis, changes in HR [74 (67, 82) bpm vs. 79 (73, 87)bpm], P-R interval [148 (136, 160) ms vs. 150 (138, 162) ms], QRS axis [41° (19.25°°, 60°) vs. 33° (15°, 53.75°)], QT interval [376 (358, 394) ms vs. 372 (354, 386) ms], QTc interval [417 (404, 431) ms vs. 426 (414, 436) ms], and incidence of QTc interval prolongation (9.6% vs. 15.8%) were all significant after chemotherapy, P < 0.001. There were statistically differences in HR, QRS axis, QTc interval, and the incidence of QTc interval prolongation between initial diagnosis and prechemotherapy of the last cycle under different age strata (≤ 45 years, 45 ~ 55 years, ≥ 55 years), different BMI range groups (18.5-22.9 kg/m2, 23-24.9 kg/m2, and 25-29.9 kg/m2), and even in patients without history of hypertension, diabetes, or coronary heart disease, respectively, P < 0.05. Resting HR, QRS axis, and QTc interval between each cycle of TEC regimen were different, P < 0.001. Resting HR and QTc interval between different cycles of EC-T(H) regimen were different, P < 0.05. Compared to initial diagnosis, a longer QTc interval occurred from the third to the last cycle of TEC regimen, P < 0.05. Only QTc interval before the fifth cycle of EC-T(H) regimen was statistically different from that at initial diagnosis, P = 0.012.

Chemotherapy affects the ECG parameters of HR, P-R interval, QRS axis, QT interval, QTc interval, and QTc interval prolongation in early-stage breast cancer women during chemotherapy. Electrocardiographic parameters may be affected significantly by TEC regimen than by EC-T(H) or TC regimen. Trial registration Retrospectively registered.

Evidence on the association between the neutrophil-to-lymphocyte ratio (NLR) and all-cause and cardiovascular disease (CVD) mortality in adults with cancer is limited.

This study aimed to examine the relationship between NLR and all-cause and CVD mortality in adults with cancer.

A retrospective cohort study included 2,639 cancer patients in the U.S. from the NHANES dataset (2005-2018), collecting demographic, laboratory, and mortality data. Multivariable Cox regression analysis, subgroup analysis and restricted cubic spline analyses assessed the associations between NLR and mortality outcomes.

During a median follow-up of 77 months, 713 (27.0%) deaths occurred, including 149 (5.6%) from CVD. Multivariable Cox regression analysis revealed that a high NLR, treated as a continuous variable, was significantly correlated with increased all-cause mortality (HR, 1.09; 95% CI, 1.05-1.12; p < 0.001) and CVD mortality (HR, 1.12; 95% CI, 1.05-1.19; p < 0.001). Meanwhile, when evaluating NLR as a categorical variable, the adjusted hazard ratios (HR) for NLR and all-cause mortality in quartiles Q2 (1.6-2.2), Q3 (2.2-3), and Q4 (>3) were 1.06 (95% CI: 0.83-1.34, p = 0.062), 1.12 (95% CI: 0.89-1.42, p = 0.334), and 1.30 (95% CI: 1.04-1.63, p = 0.021), respectively, when compared with individuals in the lower quartile Q1 (≤1.6). In terms of CVD mortality, the adjusted HR values for NLR in Q2, Q3, and Q4 were 0.92 (95% CI: 0.50-1.69, p = 0.062), 1.24 (95% CI: 0.71-12.19, p = 0.334), and 1.76 (95% CI: 1.04-2.97, p = 0.034), respectively, compared to those in the lower NLR quartile Q1 (≤1.6). Subgroup analysis showed similar patterns (all p-values for interaction > 0.05). Kaplan-Meier analysis indicated lower survival rates for individuals with higher NLR, and RCS analysis suggested a positive linear relationship between NLR and all-cause and CVD mortality.

Elevated NLR is linked to higher all-cause and CVD mortality risks among adults with cancer.

Cardiovascular diseases and cancer are leading global causes of morbidity and mortality, necessitating advances in diagnosis and treatment. Doxorubicin (Doxo), a potent chemotherapy drug, causes long-term heart damage due to cardiotoxicity. Small extracellular vesicles (sEVs) carry bioactive molecules-such as proteins, lipids, and nucleic acids-that can modulate gene expression and signaling pathways in recipient cells, including cardiomyocytes. Through the delivery of cytokines, microRNAs, and growth factors, sEVs can influence cell survival, which plays a critical role in the development of cardiotoxicity. This study investigates the role of sEVs derived from breast cancer cells treated or not with Doxo and their potential to induce cardiomyocyte damage, thereby contributing to cardiotoxicity. We isolated sEVs from MCF-7 cells treated or not to Doxo using ultracentrifugation and characterized them through Nanoparticle Tracking Analysis (NTA), Scanning Electron Microscopy (SEM), and Western Blotting (WB) for the markers CD63, CD81, and TSG101. We analyzed cytokine profiles using a Multiplex Assay and Cytokine Membrane Array. We exposed Guinea pig cardiomyocytes to different concentrations of sEVs. We assessed their viability (MTT assay), shortening, reactive oxygen species (ROS-DHE dye) production, mitochondrial membrane potential (JC-1 dye), and calcium dynamics (FLUO-4 dye). We performed statistical analyses, including t-tests, ANOVA, Cohen's d, and η2 to validate the robustness of the results. Treatment of MCF-7 cells with 0.01 μM Doxorubicin resulted in increased sEVs production, particularly after 48 h of exposure (~1.79 × 108 ± 2.77 × 107 vs. ~5.1 × 107 ± 1.28 × 107 particles/mL, n = 3, p = 0.0019). These sEVs exhibited protein profiles in the 130-25 kDa range and 93-123 nm sizes. They carried cytokines including TNF-α, IL-1β, IL-4, IFN-γ, and IL-10. Exposure of cardiomyocytes to sEVs (0.025 μg/mL to 2.5 μg/mL) from both Doxo-treated and untreated cells significantly reduced cardiomyocyte viability, shortened cell length by up to 20%, increased ROS production, and disrupted calcium homeostasis and mitochondrial membrane potential, indicating severe cellular stress and cardiotoxicity. These findings suggest that Doxo enhances sEVs production from breast cancer cells, which plays a key role in cardiotoxicity through their cytokine cargo. The study highlights the potential of these sEVs as biomarkers for early cardiotoxicity detection and as therapeutic targets to mitigate cardiovascular risks in chemotherapy patients. Future research should focus on understanding the mechanisms by which Doxorubicin-induced sEVs contribute to cardiotoxicity and exploring their diagnostic and therapeutic potential to improve patient safety and outcomes in cancer therapy.

Breast cancer (BC) survivors are at increased risk for cardiovascular disease (CVD) and require their primary care physicians to manage their long-term general medical care, including cardiovascular (CV) health. Yet, evidence exists that some primary care physicians possess insufficient knowledge about survivorship care. With the goal of bridging these knowledge gaps, a PubMed review was conducted from July 7, 2020, through October 2, 2020, with an updated PubMed review from January 3, 2024, through April 28, 2024, focusing on CV health considerations in the primary care of BC survivors. Search terms included variations of "breast cancer survivors" and "cardiovascular." In total, 152 publications were included. Breasts cancer survivors may have increased CVD risk because some anticancer therapies are cardiotoxic and risk factors for BC often also increase the risk for CVD. Multiple risk factors overlap for BC and CVD such as older age, Western diet, early menarche, physical inactivity, high body mass index, and smoking. In this review, results are summarized from studies that report the presence of CV risk factors and CVD in BC survivors. Also described are the CV effects of BC therapies (chemotherapy, hormonal agents, targeted therapies, and radiotherapy) and the type of CV evaluation (cardiac imaging and measurement of biomarkers) that these patients may need. Primary care physicians have an important role in managing the CV health of BC survivors from preventing, assessing, and managing CV risk factors to referring patients to appropriate specialists when needed.

In addition to the well-recognised cardiotoxicity of cancer treatment, possible aetiological links between cancer diagnosis and cardiovascular disease (CVD) have gained growing research interests. We aimed to estimate the CVD burden among cancer survivors and illustrate population-level associations between these two conditions.

We first conducted a prospective cohort study in the UK Biobank and a meta-analysis of previous population-based cohorts. HRs were estimated in the cohort study to evaluate the effect of cancer diagnosis on the subsequent risk of CVD compared with that of non-cancer individuals. We then systematically searched Pubmed, Embase and Cochrane Library to retrieve previous cohorts. Random-effect meta-analysis was performed to pool relative risk estimates. A combination of multiple statistical metrics was employed to appraise the evidence.

A total of 39 755 811 participants (5 898 597 cancer survivors vs 33 857 214 cancer-free controls) were identified in our study. In the cohort study, a 51% higher hazard of CVD risk was found among cancer survivors (95% CI 1.48 to 1.55, p<0.001). The hazard decreased to 29% after adjusting competing risk. The meta-analysis identified 104 published cohorts. We found a 1.34-fold increased CVD risk among patients with cancer (95% CI 1.22 to 1.47, p<0.001). The association remains significant among multiple cancer sites and multiple CVD subtypes. This association was consistent, irrespective of chemo or radiotherapy use. Evidence appraisal identified one convincing association between hematologic/lymphatic malignancies and ischaemic heart disease, along with 29 highly suggestive associations.

Our study provided comprehensive estimates of CVD incidence in cancer survivors and identified a significantly elevated CVD risk among patients with cancer, regardless of chemotherapy or radiotherapy. These findings underscore the need for routine assessment of CVD risk factors at cancer diagnosis to enhance the well-being and survival of patients with cancer.PROSPERO registration numberCRD42022307056.

The small molecule radiotracer 124I-PU-H71 is an imaging biomarker of epichaperome formation. The tracer has been established to localize in tissues under chronic stress, specifically in cancer cells and neurodegenerative brain cells. A first-in-human imaging trial using positron emission tomography (PET) in cancer patients revealed unexpected tracer accumulation in the myocardium.

To describe human 124I-PU-H71 myocardial biodistribution and pharmacokinetics in a series of cancer patients with no history of cardiovascular disease.

25 cancer patients (age 22-75 years, M:F - 7:18) with no history of cardiovascular disease received intravenous injections with microdose 124I-PU-H71 while at rest, followed by dynamic and gated/non-gated PET image data acquisitions. Region-of-interest (ROI) analysis of left ventricular myocardium (LVmyo) and background left atrium quantified tracer concentrations as standardized uptake value (SUV) and uptake ratios. Kinetic rate constants were evaluated by a two-tissue compartment model.

Myocardial accumulation of 124I-PU-H71 was prominent in all patients, with median LVmyo SUVmean (interquartile range, IQR) of 2.8 (IQR, 2.13-3.29), 2.5 (IQR, 1.94-2.98), 2.4 (IQR, 1.73-3.31) and 1.0 (IQR, 0.61-2.45), and median LVmyo/blood-pool ratios of 1.9 (IQR, 1.57-2.38), 2.0 (IQR, 1.53-2.32), 3.6 (IQR, 2.91-4.06) and 3.9 (IQR, 2.62-5.08) at 1-9 min, 14-23 min, 3-4 h and 21-25 h, respectively on non-gated PET images. Myocardium showed peak uptake within 2 min post-injection, with sustained myocardial tracer-concentration at 4 h post-injection. Pharmacokinetic modeling revealed median K1 = 0.45 ml/min/g (IQR, 0.38-0.62); k2 = 0.47 min- 1 (IQR, 0.27-0.71); k3 = 0.16 min- 1 (IQR, 0.09-0.26); and k4 = 0.0038 min- 1 (IQR, 0.0015-0.0057). Regional assessment demonstrated essentially uniform tracer uptake in LV and myocardial segments; with normal LVEF in all patients (mean 57.7 ± 3.5%); and no patients suffered cardiac events over subsequent 12-month period.

Our study finds human myocardial epichaperome expression, as quantified by 124I-PU-H71 PET. Our data indicates PU-H71 PET merits further study as a myocardial epichaperome biomarker, with potential application in drug development, possibly as a biomarker in subclinical cardiac dysfunction.

This research aimed to develop and validate a clinical nomogram for predicting the probability of cardiovascular death (CVD) in patients with gastrointestinal stromal tumors (GIST). Information regarding patients diagnosed with GIST was extracted from the surveillance, epidemiology, and end results database. The multivariable competing risk model and multivariable Cox regression model were utilized to determine the independent predictive factors. A comparison was made between the results obtained from the 2 models. A nomogram was built to visualize the competing risk model. The nomogram's performance was assessed utilizing concordance index, calibrate curve, decision curve analysis, and risk stratification. A total of 9028 cases were enrolled for final analysis, with CVD accounting for 12.8% of all deaths since GIST diagnosis. The multivariate analysis of competing risks revealed that age, chemotherapy and marital status were identified as independent risk factors for CVD in GIST individuals. The nomogram model exhibited good calibration and strong discriminative ability, indicating its effectiveness in predicting outcomes, with a concordance index of 0.788 (95% confidence interval: 0.753-0.823) in the training set, and 0.744 (95% confidence interval: 0.673-0.815) in the validation set. Decision curve analysis indicated that the prediction model had good clinical practicability. Additionally, risk stratification analysis efficiently divided GIST individuals into high- and low-risk populations for CVD. This was the first research to construct and validate a predictive nomogram using a competing risk model to estimate the individual probabilities of CVD in GIST patients. The nomogram can assist clinicians in making personalized treatment and monitoring plans.

Certain anticancer therapies inevitably increase the risk of cardiovascular events, now the second leading cause of death among cancer patients. This underscores the critical need for developing effective drugs or regimens for cardiovascular protection. Statins possess properties such as antioxidative stress, anti-inflammatory effects, antifibrotic activity, endothelial protection, and immune modulation. These pathological processes are central to the cardiotoxicity associated with anticancer treatment. There is prospective clinical evidence confirming the protective role of statins in chemotherapy-induced cardiotoxicity. Numerous preclinical studies have demonstrated that statins can ameliorate heart and endothelial damage caused by radiotherapy, although clinical studies are scarce. In the animal models of trastuzumab-induced cardiomyopathy, statins provide protection through anti-inflammatory, antioxidant, and antifibrotic mechanisms. In animal and cell models, statins can mitigate inflammation, endothelial damage, and cardiac injury induced by immune checkpoint inhibitors. Chimeric antigen receptor (CAR)-T cell therapy-induced cardiotoxicity and immune effector cell-associated neurotoxicity syndrome are associated with uncontrolled inflammation and immune activation. Due to their anti-inflammatory and immunomodulatory effects, statins have been used to manage CAR-T cell therapy-induced immune effector cell-associated neurotoxicity syndrome in a clinical trial. However, direct evidence proving that statins can mitigate CAR-T cell therapy-induced cardiotoxicity is still lacking. This review summarizes the possible mechanisms of anticancer therapy-induced cardiotoxicity and the potential mechanisms by which statins may reduce related cardiac damage. We also discuss the current status of research on the protective effect of statins in anticancer treatment-related cardiovascular disease and provide directions for future research. Additionally, we propose further studies on using statins for the prevention of cardiovascular disease in anticancer treatment.

Despite clear evidence-based supporting a benefit to exercise on physical and psychological metrics in patients with cancer, recruitment to exercise trials amongst cancer survivors is suboptimal. We explore current recruitment rates, strategies, and common barriers to participation in exercise oncology trials in cancer survivorship.

A systematic review was conducted using a pre-defined search strategy in EMBASE, CINAHL, Medline, Cochrane Library, and Web of Science. The search was performed up to 28/02/2022. Screening of titles and abstracts, full-text review, and data extraction was completed in duplicate.

Of the 3204 identified studies, 87 papers corresponding to 86 trials were included. Recruitment rates were highly variable with a median rate of 38% (range 0.52-100%). Trials recruiting prostate cancer patients only had the highest median recruitment rate (45.9%) vs trials recruiting colorectal cancer patients only which had the lowest (31.25%). Active recruitment strategies such as direct recruitment via a healthcare professional were associated with higher recruitment rates (rho = 0.201, p = 0.064). Common reasons for non-participation included lack of interest (46.51%, n (number of studies) = 40); distance and transport (45.3%, n = 39); and failure to contact (44.2%, n = 38).

Recruitment of cancer survivors to exercise interventions is suboptimal with barriers being predominantly patient-oriented. This paper provides the benchmark for current recruitment rates to exercise oncology trials, providing data for trialists planning future trial design and implementation, optimise future recruitment strategies, and evaluate their own recruitment success against current practice.

Enhanced recruitment to cancer survivorship exercise trials is necessary in facilitating the publication of definitive exercise guidelines, generalisable to varying cancer cohorts.

CRD42020185968.

Sarcopenia is prevalent among 11-25% of adult cancer survivors, depending on the cancer type, although the available data on post-treatment survivors in Japan are limited. If cancer patients develop cachexia, they may experience sustained weight loss as a result, ultimately leading to sarcopenia. Conversely, some patients experience post-treatment weight gain, resulting in sarcopenic obesity. Both sarcopenia and obesity elevate the risk of cardiovascular diseases and mortality; therefore, the importance of sarcopenia prevention and management is undeniable. The Guidelines for Exercise for Cancer Survivors recommend continued physical activity. Recent studies have reported the effectiveness of multimodal interventions, combining pharmacological, nutritional, and exercise approaches, necessitating multidisciplinary care for post-treatment sarcopenia. Innovative health interventions using mobile devices have also gained attention. However, studies on sarcopenia in post-treatment cancer survivors, especially those regarding exercise interventions, remain scarce in Japan, primarily due to limited insurance coverage for such post-treatment interventions and workforce challenges. It is clear that some cancer survivors have sarcopenia, which can lead to worse survival and secondary illness. While the benefits of exercise are clear, a comprehensive approach to sarcopenia is a further challenge for the future.

Although the risk of CVD is increased in cancer survivors, few studies have investigated the CVD risk in survivors of gastrointestinal (GI) cancer. Therefore, we evaluated the CVD risk using the 10-year atherosclerotic cardiovascular disease (ASCVD) risk score for GI cancer survivors and associated physical activity factors.

Using the 2014-2019 Korean National Health and Nutrition Examination Surveys, data were collected for 262 GI cancer survivors and 1,310 cancer-free controls matched at a 1:5 ratio based on age and sex. The International Physical Activity Questionnaire Short-Form was used to assess physical activity, and the Euro QoL Questionnaire 5-Dimensional Classification (EQ-5D) was used to assess the health-related quality of life.

A multiple logistic regression analysis demonstrated a lower risk of ASCVD in GI cancer survivors than in controls (adjusted odds ratio [aOR] = 0.73, 95% confidence interval [CI] = 0.55-0.97). Moreover, the risk of having a high ASCVD score was significantly lower in individuals who performed sufficient aerobic physical activity (aOR = 0.59, 95% CI = 0.47-0.75) and those with an EQ-5D score 1 or 2 (aOR = 0.36, 95% CI = 0.20-0.65 and aOR = 0.31, 95% CI = 0.16-0.58, respectively).

This population-based study demonstrated that engaging in sufficient physical activity can reduce the ASCVD risk among GI cancer survivors.

Cancer survival is improving, making optimal management of long-term treatment-related adverse effects increasingly important. Exercise and a healthy diet are beneficial and regularly recommended in cancer survivorship guidelines; however, few cancer survivors meet these recommendations so there is a need to explore why. This study aimed to understand experiences receiving exercise and diet support among Australian breast and prostate cancer survivors during and following treatment, and to explore what support they would like to receive.

Adults who completed active treatment for breast or prostate cancer were recruited via a private cancer care centre. Using a qualitative descriptive study design, participants attended in-person focus groups that were recorded, transcribed, then analysed using reflexive thematic analysis.

In total, 26 cancer survivors (15 breast, 11 prostate) participated in one of seven focus groups (4 breast, 3 prostate). Two themes were developed: 1) It was just brushed over, and 2) Wanting more. Theme 1 reports that exercise, and especially diet, were rarely discussed. If they were, it was often limited to general recommendations. Theme 2 shows that participants wanted more specific and personalised support, and information about how exercise and/or diet could benefit their cancer treatment.

Despite strong interest in receiving personalised exercise and diet support, neither are routinely provided to Western Australian breast and prostate cancer survivors. If support was provided, there was inconsistency in the level and type of support provided. These findings identify important gaps in exercise and diet support provision to cancer survivors and will inform future strategies aiming to improve cancer survivorship care.

People living with and beyond cancer (LWBC) are advised to achieve a body mass index (BMI) within the healthy range (≥ 18.5 and < 25). Not perceiving a need for weight change may be a barrier to achieving a healthy weight. This study aimed to explore factors associated with perceived need for weight change among people LWBC.

Adults diagnosed with breast, prostate, or colorectal cancer were recruited through National Health Service sites in Essex and London. Participants (N = 5835) completed the 'Health and Lifestyle After Cancer' survey, which included a question on perceived need to change weight. Associations between perceived need for weight change and BMI, and perceived need for weight change and health and demographic variables, were analyzed using chi-square tests and logistic regression, respectively.

The proportion of participants perceiving a need to lose weight differed according to BMI category: healthy weight (23%), overweight (64%), obese (85%) (P < 0.001). Having overweight or obesity but not perceiving a need to lose weight was associated with being older, male, non-white, not married or cohabiting, and having cancer that had spread, no formal qualifications, no comorbidities, and having received chemotherapy.

Perceived need to lose weight is prevalent among people LWBC with obesity and overweight. This group may be interested in weight management support. Demographic and health factors were associated with having obesity or overweight but not perceiving a need to lose weight.

Weight loss interventions for people LWBC are needed. A subset of people LWBC with overweight and obesity may need additional information or motivators to engage with weight management.

Despite the rapidly emerging evidence on the contributions of physical activity to improving cancer-related health outcomes, adherence to physical activity among young adults with lymphoma remains suboptimal. Guided by self-determination theory (SDT), the Lymfit intervention (a 12-week individualized exercise program with bi-weekly kinesiologist support and an activity tracker) aimed to foster autonomous motivation toward physical activity. This pilot randomized controlled trial aimed to evaluate the feasibility, acceptability, and preliminary effects of Lymfit. Young adults (N = 26; mean age of 32.1 years) with lymphoma who were newly diagnosed and those up to six months after completing treatment were recruited and randomly assigned one-to-one to either the intervention group (n = 13) or a wait-list control group (n = 13). All a priori feasibility benchmarks were met, confirming the feasibility of the study in terms of recruitment uptake, retention, questionnaire completion, intervention fidelity, missing data, Fitbit wear adherence, and control group design. The intervention acceptability assessment showed high ratings, with eight out of ten items receiving >80% high ratings. At post-intervention, an analysis of covariance models showed a clinically significant increase in self-reported physical activity levels, psychological need satisfaction, and exercise motivation in the intervention group compared to controls. Lymfit also led to meaningful changes in six quality-of-life domains in the intervention group, including anxiety, depression, fatigue, sleep disturbance, social roles and activities, and pain interference. The findings support Lymfit as a promising means to meet psychological needs and increase the autonomous motivation for physical activity in this group. A fully powered efficacy trial is warranted to assess the validity of these findings.

Nutrition plays an important role in cancer survivorship. This systematic review and meta-analysis aim to critically assess and quantify the effectiveness of nutrition care interventions provided by dietitians to survivors who have completed treatment for cancer.

A systematic review of randomized controlled trials (RCTs) published from January 2004 to November 2023 reporting the effectiveness of primary care dietetic interventions with adult cancer survivors was conducted. PubMed, Scopus, CINAHL, Embase, ProQuest and PsycINFO databases were searched for key terms. Meta-analyses were conducted where there were sufficient studies of the same cancer type and outcomes.

Twelve RCTs representing 1138 cancer survivors (519 breast cancer; 75 prostate cancer; 544 colorectal cancer) were included. Primary outcome measures included weight loss (n = 6), quality of life (n = 2), reducing lymphedema-related arm volume (n = 2), nutritional status (n = 1) and increasing fruit and vegetable intake (n = 1). Weight loss was observed in studies where this was the primary outcome. Results for quality of life varied. Meta-analyses of RCTs with breast cancer survivors showed that dietitian intervention achieved a mean of 3.7 kg greater intentional weight loss and 2.3% greater body fat decrease than control (p < 0.0001).

This study provides evidence for the effectiveness of primary care dietetic interventions by dietitians with cancer survivors, particularly with respect to intentional weight and fat loss in breast cancer survivors.

Dietitians can play a key role in managing weight and improving long term health outcomes and prognosis for cancer survivors beyond the acute care setting.

Over the years, strides in colon cancer detection and treatment have boosted survival rates; yet, post-colon cancer survival entails cardiovascular disease (CVD) risks. Research on CVD risks and acute cardiovascular events in colorectal cancer survivors has been limited.

To compare the CVD risk and adverse cardiovascular outcomes in current colon cancer survivors compared to a decade ago.

We analyzed 2007 and 2017 hospitalization data from the National Inpatient Sample, studying two colon cancer survivor groups for CVD risk factors, mortality rates, and major adverse events like pulmonary embolism, arrhythmia, cardiac arrest, and stroke, adjusting for confounders via multivariable regression analysis.

Of total colon cancer survivors hospitalized in 2007 (n = 177542) and 2017 (n = 178325), the 2017 cohort often consisted of younger (76 vs 77 years), male, African-American, and Hispanic patients admitted non-electively vs the 2007 cohort. Furthermore, the 2017 cohort had higher rates of smoking, alcohol abuse, drug abuse, coagulopathy, liver disease, weight loss, and renal failure. Patients in the 2017 cohort also had higher rates of cardiovascular comorbidities, including hypertension, hyperlipidemia, diabetes, obesity, peripheral vascular disease, congestive heart failure, and at least one traditional CVD (P < 0.001) vs the 2007 cohort. On adjusted multivariable analysis, the 2017 cohort had a significantly higher risk of pulmonary embolism (PE) (OR: 1.47, 95%CI: 1.37-1.48), arrhythmia (OR: 1.41, 95%CI: 1.38-1.43), atrial fibrillation/flutter (OR: 1.61, 95%CI: 1.58-1.64), cardiac arrest including ventricular tachyarrhythmia (OR: 1.63, 95%CI: 1.46-1.82), and stroke (OR: 1.28, 95%CI: 1.22-1.34) with comparable all-cause mortality and fewer routine discharges (48.4% vs 55.0%) (P < 0.001) vs the 2007 cohort.

Colon cancer survivors hospitalized 10 years apart in the United States showed an increased CVD risk with an increased risk of acute cardiovascular events (stroke 28%, PE 47%, arrhythmia 41%, and cardiac arrest 63%). It is vital to regularly screen colon cancer survivors with concomitant CVD risk factors to curtail long-term cardiovascular complications.

The testicular niche, which includes the germ cells, somatic cells, and extracellular matrix, plays a crucial role in maintaining the proper functions of the testis. Gonadotoxic treatments, such as chemotherapy and radiation therapy, have significantly improved the survival rates of cancer patients but have also been shown to have adverse effects on the testicular microenvironment. Therefore, repairing the testicular niche after gonadotoxic treatments is essential to restore its function. In recent years, several approaches, such as stem cell transplantation, gene therapy, growth factor therapy, and pharmacological interventions have been proposed as potential therapeutic strategies to repair the testicular niche. This comprehensive review aims to provide an overview of the current understanding of testis damage and repair mechanisms. We will cover a range of topics, including the mechanism of gonadotoxic action, repair mechanisms, and treatment approaches. Overall, this review highlights the importance of repairing the testicular niche after gonadotoxic treatments and identifies potential avenues for future research to improve the outcomes for cancer survivors.

Multiple myeloma (MM) is a prevalent hematological tumor, and recent clinical data have highlighted the significance of atrial fibrillation (AF) as a crucial complication affecting the prognosis of MM. This review aims to consolidate findings from published clinical studies, focusing on the epidemiological characteristics of AF in MM patients and the associated risks arising from MM treatments such as autologous hematopoietic stem cell transplantation, proteasome inhibitors, and immunomodulatory agents.

While existing data partially demonstrate a strong correlation between MM and AF, further clinical studies are necessary to comprehensively investigate their association. These studies should encompass various aspects, including the risk of AF resulting from MM treatment, the impact of AF-induced embolic events and heart failure on MM prognosis, as well as the influence of AF management methods like catheter ablation or left atrial appendage closure on MM prognosis.

The supplementation of future data will provide more precise guidance for managing MM patients. By incorporating information regarding AF risk associated with MM treatment and examining the effects of AF management strategies on MM prognosis, healthcare professionals can enhance their decision-making process when caring for individuals with MM.

Chemotherapy-induced cardiotoxicity is a significant problem, ranking as the second most frequent cause of mortality in cancer patients. This adverse outcome encompasses many cardiovascular problems, such as heart failure. Sacubitril/valsartan has shown potential in the management of heart failure, however, its effectiveness in treating chemotherapy-induced heart failure has not been extensively explored. We performed a case series to investigate the safety and effectiveness of sacubitril/valsartan in treating chemotherapy-induced cardiomyopathy in Saudi Arabia.

The case series was conducted at a single medical center in Makkah, Saudi Arabia. The data gathered included patient demographics, clinical features, laboratory results, echocardiographic findings, and medication information. The data underwent analysis using descriptive statistics.

Out of the total of eight patients who were part of the investigation, a notable majority of six individuals exhibited substantial enhancements in their ejection fraction (EF) after receiving sacubitril/valsartan medication.

Our case series provides significant insights by revealing improvements in ejection fraction (EF) in six out of eight patients who had chemotherapy-induced cardiomyopathy after receiving sacubitril/valsartan treatment.

Treatments of lymphoma can lead to reduced physical functioning, cancer-related fatigue, depression, anxiety, and insomnia. These side effects can negatively impact the cancer survivor's quality of life. Mounting evidence indicates that physical activities are highly therapeutic in mitigating the short- and long-term side effects of cancer treatments. Yet, lymphoma survivors' participation in physical activities remains suboptimal, which has been further exacerbated by the deleterious effects of isolation during the COVID-19 pandemic. The Lymfit intervention aims to offer motivational support, expert guidance, and a personalized exercise prescription to optimize physical activities among lymphoma survivors. This proof-of-concept study explores implementation feasibility (retention, technical and safety), and the preliminary effects of Lymfit on various health outcomes.

This was a single-armed trial with a pre-and post-test design. Twenty lymphoma survivors were recruited to participate in the 12-week Lymfit intervention. Wearable activity trackers (Fitbit) were given to participants as a motivational tool and for data collection purposes. Participants received a personalized exercise prescription designed by a kinesiologist. Physiologic metrics were collected by the Fitbit monitors and were stored in the Lymfit database. Self-reported questionnaires measuring health outcomes were collected at baseline and post-intervention.

The retention rate of this trial was 70%. Minimal technical issues and no adverse effects were reported. Lymfit led to significant improvements in sleep disturbances and the ability to participate in social activities and decreased fear of cancer recurrence. It also increased daily steps and decreased sedentary time in participants who did not meet the recommended physical activity guidelines.

With access to resources and fitness centers being limited during the pandemic, the Lymfit intervention filled an immediate need to provide physical activity guidance to lymphoma survivors. Findings provide preliminary support that implementing the Lymfit intervention is feasible and demonstrated promising results.

Life expectancy (LE) is an indicator of societal progress among rapidly aging populations. In recent decades, the displacement of deaths from cardiovascular disease (CVD) and cancer have been key drivers in further extending LE on the continent, though improvements vary markedly by country, sex, and over time. This study provides a comparative overview of the age-specific contributions of CVD and cancer to increasing LE in the 27 European Union member states, plus the U.K.

Cause-by-age decompositions of national changes in LE were conducted for the years 1995-1999 and 2015-2019 based on the standard approach of multiple decrement life tables to quantify the relative impact over time. The contributions of CVD and cancer mortality changes to differences in LE were computed by sex and age for each of the 28 countries. We examine the difference between the member states before 2004 ("founding countries") and those which accessed the EU after 2004 ("A10 countries").

Among men, declines in CVD mortality in the founding countries of the EU were larger contributors to increasing LE over the last decades than malignant neoplasms: 2.26 years were gained by CVD declines versus 1.07 years for cancer, with 2.23 and 0.84 years gained in A10 countries, respectively. Among women in founding countries, 1.81 and 0.54 additional life years were attributable to CVD and cancer mortality declines, respectively, while in A10 countries, the corresponding values were 2.33 and 0.37 years. Lung and stomach cancer in men, and breast cancer in women were key drivers of gains in LE due to cancer overall, though rising mortality rates from lung cancer diminished the potential impact of increasing female LE in both EU founding (e.g., France, Spain, and Sweden) and A10 countries (e.g., Croatia, Hungary, and Slovenia), notably among cohorts aged 55-70 years. Over the 25 years, the LE gap between the two sets of countries narrowed from 6.22 to 5.59 years in men, and from 4.03 to 3.12 years for women, with diminishing female mortality from CVD as a determinative contributor.

This study underscores the continued existence of an East-West divide in life expectancy across the EU27 + 1, evident on benchmarking the founding vs. A10 countries. In EU founding countries, continuous economic growth alongside improved health care, health promotion and protection policies have contributed to steady declines in mortality from chronic diseases, leading to increases in life expectancy. In contrast, less favourable mortality trends in the EU A10 countries indicate greater economic and health care challenges, and a failure to implement effective health policies.

Atrial fibrillation (AF) is a prevalent cardiac dysrhythmia, particularly affecting older adults, with its prevalence rising due to the aging population. AF is linked to several adverse outcomes, including embolic stroke, heart failure, and cancer. The association between AF and cancer is intricate and not yet fully understood. Studies suggest that the rise in cancer survivorship, along with cancer treatments, may contribute to an increased incidence of AF among cancer patients. This literature review was conducted using various databases to explore the relationship between AF and cancer. Studies from 2002 to 2022 were included, focusing on the adult population. Independent authors evaluated and validated the studies, ensuring rigorous methodology. The connection between AF and cancer appears multifaceted. There is evidence of increased cancer incidence within the first few months following an AF diagnosis, with potential shared risk factors like age, obesity, and smoking. Medications used to treat AF, notably amiodarone, were associated with increased cancer risk. Colon cancer risk might be linked to anticoagulation-induced gastrointestinal bleeding. It remains uncertain whether AF diagnosis leads to early cancer detection or if cancer itself contributes to AF development. The complex interplay between AF and cancer involves shared risk factors, potential medication-related influences, and unclear causal directions. The intricacies of this relationship warrant further research to clarify the underlying mechanisms and potential interactions. A comprehensive meta-analysis could provide more insights into this intriguing association and guide future clinical interventions.

Introduction Cancer is a condition where abnormal cells proliferate uncontrollably, leading to metastasis, which can be related to death. Breast cancer is the most prevalent type among women worldwide. Early detection with screening mammography has contributed to the decline in breast cancer incidence and mortality. Breast cancer patients are more likely to develop cardiovascular disease, with elderly patients dying from complications. Understanding the patients' cardiovascular status prior to treatment is essential. The study's objective was to evaluate the cardiovascular characteristics of women with breast cancer at diagnosis within the designated time frame of one year. Methodology This was a retrospective study that focused on patients in Taif City, Saudi Arabia, who were initially diagnosed with primary breast cancer over a span of one year. The inclusion criteria encompassed eligible patients, while those not meeting the criteria were excluded. Data extraction from patients' records was conducted, and the analysis was executed using IBM SPSS Statistics for Windows, Version 26.0 (Released 2019; IBM Corp., Armonk, New York, United States). Results This study analyzed the cardiovascular attributes of breast cancer patients, focusing on 136 female cases. The study found significant patterns concerning cardiovascular risk factors in breast cancer patients, categorized by menopausal status. Premenopausal female cases had a mean age of 43.09 ± 8.31 years, while postmenopausal patients had an average age of 58.07 ± 11.70 years. Postmenopausal patients had a higher prevalence of overweight/obesity, irregular menstrual cycles, type II diabetes, hypertension, and hyperlipidemia compared to their premenopausal counterparts. No significant differences were found between the two groups regarding low-density lipoprotein (LDL) cholesterol levels, axillary lymph node metastasis, or distant metastasis. This study emphasized the importance of regular check-ups for menopausal women to detect potential health complications early. Conclusion In summary, breast cancer is a global health concern, and understanding its impact on the cardiovascular system is crucial for comprehensive patient care. A study in Saudi Arabia found associations between cardiovascular risk factors and menopausal status in breast cancer patients. Postmenopausal patients had more prevalent risk factors, emphasizing the need for proactive assessment and management. Age-appropriate screenings and interventions are essential. Integrated healthcare approaches should consider the interplay between breast cancer and cardiovascular health, with medical professionals vigilant in evaluating and addressing risk factors to mitigate complications and optimize long-term outcomes.

Acute lymphoblastic/lymphocytic leukemia (ALL) occurring post-cancer diagnosis (secondary ALL - sALL) is increasingly recognized as a discrete entity, constituting up to as much as 5-10% of all new ALL diagnoses, and carrying its own biologic, prognostic and therapeutic significance. In this review, we will outline the history and current state of research into sALL. We will explore the evidence for differences underlining its existence as a distinct subgroup, as well as examining what might be driving such differences etiologically, including prior chemotherapy. We will examine these distinctions on population-, chromosomal-, and molecular-levels, and we will consider whether they translate to differences in clinical outcome, and whether they do - or should - warrant differences in treatment selection.

Improvements in early detection and treatment of gynecologic malignancies have led to an increasing number of survivors who are at risk of long-term cardiac complications from cancer treatment. Multimodality therapies for gynecologic malignancies, including conventional chemotherapy, targeted therapeutics, and hormonal agents, place patients at risk of cancer therapy-related cardiovascular toxicity during and following treatment. Although the cardiotoxicity associated with some female predominant cancers (eg, breast cancer) have been well recognized, there has been less recognition of the potential adverse cardiovascular effects of anticancer therapies used to treat gynecologic malignancies. In this review, the authors provide a comprehensive overview of the cancer therapeutic agents used in gynecologic malignancies, associated cardiovascular toxicities, risk factors for cardiotoxicity, cardiac imaging, and prevention strategies.

As phospholipid extracellular vesicles (EVs) secreted by various cells, exosomes contain non-coding RNA (ncRNA), mRNA, DNA fragments, lipids, and proteins, which are essential for intercellular communication. Several types of cells can secrete exosomes that contribute to cancer initiation and progression. Cancer cells and the immune microenvironment interact and restrict each other. Tumor-derived exosomes (TDEs) have become essential players in this balance because they carry information from the original cancer cells and express complexes of MHC class I/II epitopes and costimulatory molecules. In the present study, we aimed to identify potential targets for exosome therapy by examining the specific expression and mechanism of exosomes derived from cancer cells. We introduced TDEs and explored their role in different tumor immune microenvironment (TIME), with a particular emphasis on gastrointestinal cancers, before briefly describing the therapeutic strategies of exosomes in cancer immune-related therapy.

Antiblastic drugs-induced cardiomyopathy remains a relevant cause of morbidity and mortality, during and after chemotherapy, despite the progression in protective therapy against cardiovascular diseases and myocardial function. In the last few decades, many groups of researchers have focused their attention on studying the metabolic profile, first in animals, and, subsequently, in humans, looking for profiles which could be able to predict drug-induced cardiotoxicity and cardiovascular damage. In clinical practice, patients identified as being at risk of developing cardiotoxicity undergo a close follow-up and more tailored therapies. Injury to the heart can be a consequence of both new targeted therapies, such as tyrosine kinase inhibitors, and conventional chemotherapeutic agents, such as anthracyclines. This review aims to describe all of the studies carried on this topic of growing interest.

Cardiotoxicity is a serious complication of cancer therapy. It is the second leading cause of morbidity and mortality in cancer survivors and is associated with a variety of factors, including oxidative stress, inflammation, apoptosis, autophagy, endoplasmic reticulum stress, and abnormal myocardial energy metabolism. A number of studies have shown that traditional Chinese medicine (TCM) can mitigate chemoradiotherapy-associated cardiotoxicity via these pathways. Therefore, this study reviews the effects and molecular mechanisms of TCM on chemoradiotherapy-related cardiotoxicity. In this study, we searched PubMed for basic studies on the anti-cardiotoxicity of TCM in the past 5 years and summarized their results. Angelica Sinensis, Astragalus membranaceus Bunge, Danshinone IIA sulfonate sodium (STS), Astragaloside (AS), Resveratrol, Ginsenoside, Quercetin, Danggui Buxue Decoction (DBD), Shengxian decoction (SXT), Compound Danshen Dripping Pill (CDDP), Qishen Huanwu Capsule (QSHWC), Angelica Sinensis and Astragalus membranaceus Bunge Ultrafiltration Extract (AS-AM),Shenmai injection (SMI), Xinmailong (XML), and nearly 60 other herbs, herbal monomers, herbal soups and herbal compound preparations were found to be effective as complementary or alternative treatments. These preparations reduced chemoradiotherapy-induced cardiotoxicity through various pathways such as anti-oxidative stress, anti-inflammation, alleviating endoplasmic reticulum stress, regulation of apoptosis and autophagy, and improvement of myocardial energy metabolism. However, few clinical trials have been conducted on these therapies, and these trials can provide stronger evidence-based support for TCM.

Sedentary behaviors (SB) after cancer diagnosis are associated with poor prognosis for certain cancers, and cancer patients and survivors report high levels of SB. Reducing SB may be a feasible and effective intervention strategy to improve outcomes. This systematic review aims to identify and evaluate the literature on interventions to reduce SB in cancer patients and survivors.

Studies were identified via database searches in December 2020. Two authors evaluated study eligibility. Data were extracted and checked, and risk of bias was assessed by the study team. Of 1401 records identified, nine studies involving 394 cancer patients or survivors were included in this review. Six were randomized trials, three were non-randomized intervention studies, and almost all (n = 8) focused on feasibility with small sample sizes. All studies were conducted within the previous 5 years in Canada, Australia, USA, and South Korea. Cancer types studied were breast (n = 3), prostate (n = 2), colorectal or peritoneal (n = 1), and mixed types (n = 3). Intervention duration of 12 weeks was most common (n = 7). Five studies had multiple intervention components, and six studies included wearable devices to measure and/or prompt behavior change. There was an overall trend where intervention groups reduced SB vs. control groups, often coupled with an increase in moderate-to-vigorous physical activity. This review suggests that there is some promise for intervention strategies to reduce SB in cancer patients and survivors. There is a need for more high-quality randomized controlled trials to understand how to best decrease SB in cancer patients and survivors.

Chemotherapy, radiotherapy, targeted therapy, and immunotherapy have brought hope to cancer patients. With the prolongation of survival of cancer patients and increased clinical experience, cancer-therapy-induced cardiovascular toxicity has attracted attention. The adverse effects of cancer therapy that can lead to life-threatening or induce long-term morbidity require rational approaches to prevention and treatment, which requires deeper understanding of the molecular biology underpinning the disease. In addition to the drugs used widely for cardio-protection, traditional Chinese medicine (TCM) formulations are also efficacious and can be expected to achieve "personalized treatment" from multiple perspectives. Moreover, the increased prevalence of cancer in patients with cardiovascular disease has spurred the development of "reverse cardio-oncology", which underscores the urgency of collaboration between cardiologists and oncologists. This review summarizes the mechanisms by which cancer therapy induces cardiovascular toxicity, the combination of antineoplastic and cardioprotective drugs, and recent advances in reverse cardio-oncology.

Most Americans take dietary supplements (DSs) and use is even higher among cancer survivors. This secondary analysis seeks to identify types, reasons, and costs of supplements used by 367 older cancer survivors enrolled in the Harvest for Health vegetable gardening trial and evaluate associations between supplement intake and medical/socio-demographic factors. Descriptive statistics were used to identify supplement type and reasons for use. Average market price was used to estimate cost. Fifty-nine percent of the sample reported supplement use. Female (OR 2.11, 95% CI 1.35-3.30), non-Hispanic White (OR 1.77, 95% CI 1.05-3.0), and breast and gynecological survivors (OR 1.57, 1.03-2.38) were significantly more likely to report DS use compared to males, minorities, and survivors of other cancers. Use of vitamins (39%), multivitamins (23%), and minerals (12%) were the most prevalent. Commonly reported reasons for supplement use were to improve general health (47%) or treat medical conditions (39%) and cancer-related symptoms (12%). DSs daily costs ranged from USD 0.02 to 19.81, with a mean of USD 1.28 ± 1.74, a median of USD 0.78, and a mode of USD 0.34. DS use is prevalent among older cancer survivors, with overall health reported as the leading reason for use. Out-of-pocket recurrent costs can be substantial and underscore the need to promote a nutrient-rich diet whenever possible in this vulnerable population.

Cancer-related mortality has significantly declined over the past several decades as a result of improved screening, diagnostics, and therapeutics. Although cancer patients and survivors are living longer, there is increased risk of both short-term and long-term cardiovascular complications, including arrhythmia. In this review, we highlight the current evidence detailing the connections between atrial fibrillation and cancer, provide insight into the mechanisms driving this relationship, and share practical considerations for the management of atrial fibrillation in cancer patients and cancer survivors.

Atrial fibrillation is an increasingly recognized condition among cancer patients, with epidemiological data showing increased incidence and worse outcomes in patients with cancer. Studies also describe a bidirectional relationship between cancer and atrial fibrillation, attributable in part to shared risk factors but also potentially due to shared biology. Cancer treatment-associated arrhythmia is an active area of investigation, with ongoing research to identify the mechanisms and pathophysiology behind this phenomenon. Furthermore, management of atrial fibrillation in patients with cancer presents unique challenges, particularly in management of anti-coagulation. Cancer patients have increased risk of developing atrial fibrillation due to the shared risk factors and biology of the two conditions. Moreover, various cancer therapeutics are known to be arrhythmogenic; however, mechanisms remain unclear. Further research is needed to better understand the pathophysiology of atrial fibrillation in cancer patient in order to establish prevention and treatment strategies specific to this population.

Cancer patients were found at a high risk of death from cardiovascular disease. This study aims to assess cardiovascular mortality risk and identify the potential risk factors associated with cardiovascular mortality among gastric cancer patients.

Gastric cancer patients were collected from the Surveillance Epidemiology and End Results database during 1975-2016. Standardized mortality ratios were calculated to compare cardiovascular mortality rates between gastric cancer patients and the general US population. Univariable Cox analysis and multivariable stepwise Cox analysis were adopted to identify the potential risk factors for cardiovascular disease death after gastric cancer diagnosis.

There were 10 886 cardiovascular disease deaths identified among 165 433 individuals with gastric cancer observed for 410207.20 person-years. Gastric cancer patients were at a higher cardiovascular disease mortality risk (standardized mortality ratio = 3.35, 95% confidence interval: 3.24-3.47, P < 0.05). The study showed that older age at diagnosis (>80 years vs. 0-69 years, hazard ratio = 7.05, 95% confidence interval: 6.66-7.46, P < 0.001; 70-80 years vs. 0-69 years, hazard ratio = 3.35, 95% confidence interval: 3.19-3.53, P < 0.001), male sex (vs. female, hazard ratio = 1.39, 95% confidence interval: 1.33-1.45, P < 0.001), black race (vs. white, hazard ratio = 1.31, 95% confidence interval: 1.24-1.38, P < 0.001), without a partner (divorced/separated vs. married/partnered, hazard ratio = 1.35, 95% confidence interval: 1.25-1.45, P < 0.001; single vs. married/partnered, hazard ratio = 1.20, 95% confidence interval: 1.12-1.29, P < 0.001; widowed vs. married/partnered, hazard ratio = 1.41, 95% confidence interval: 1.34-1.48, P < 0.001), living in the northern plains (vs. pacific coast, hazard ratio = 1.23, 95% confidence interval: 1.16-1.29, P < 0.001) and surgery not performed (vs. performed, hazard ratio = 1.70, 95% confidence interval: 1.61-1.79, P < 0.001) were significantly associated with increased risk of cardiovascular disease death. Compared with patients with localized stage, distant staged patients were less likely to die of cardiovascular disease (hazard ratio = 0.88, 95% confidence interval: 0.83-0.94, P < 0.001).

Gastric cancer patients were at an increased risk of cardiovascular disease death. Older age at diagnosis, male sex, black race, without a partner, living in the northern plains and surgery not performed were significantly associated with cardiovascular disease death after gastric cancer diagnosis.

Doxorubicin (DOX) induces endothelial cell (EC) senescence, which contributes to endothelial dysfunction and cardiovascular complications. Senolytic drugs selectively eliminate senescent cells to ameliorate senescence-mediated pathologies. Previous studies have demonstrated differences between immortalized and primary EC models in some characteristics. However, the response of DOX-induced senescent ECs to senolytics has not been determined across these two models. In the present work, we first established a comparative characterization of DOX-induced senescence phenotypes in immortalized EA.hy926 endothelial-derived cells and primary human umbilical vein EC (HUVECs). Thereafter, we evaluated the senolytic activity of four senolytics across both ECs. Following the DOX treatment, both EA.hy926 and HUVECs shared similar senescence phenotypes characterized by upregulated senescence markers, increased SA-β-gal activity, cell cycle arrest, and elevated expression of the senescence-associated secretory phenotype (SASP). The potentially senolytic drugs dasatinib, quercetin, and fisetin demonstrated a lack of selectivity against DOX-induced senescent EA.hy926 cells and HUVECs. However, ABT-263 (Navitoclax) selectively induced the apoptosis of DOX-induced senescent HUVECs but not EA.hy926 cells. Mechanistically, DOX-treated EA.hy926 cells and HUVECs demonstrated differential expression levels of the BCL-2 family proteins. In conclusion, both EA.hy926 cells and HUVECs demonstrate similar DOX-induced senescence phenotypes but they respond differently to ABT-263, presumably due to the different expression levels of BCL-2 family proteins.

Cancer treatments are associated with cardiotoxic events that predispose to cardiac pathology and compromise the survival of patients, making necessary the identification of new molecular biomarkers to detect cardiotoxicity. This scoping review aims to identify the available evidence on novel molecular biomarkers associated with cardiotoxicity in the adult population undergoing cancer therapy.

The databases Medline, Web of Science, Scopus, and Embase were screened for the identification of published studies until 23 August 2020, searching for novel molecular biomarkers reported in cancer therapy-related cardiac dysfunction in adult patients. A total of 42 studies that met the eligibility criteria were included. Fourteen studies reported 44 new protein biomarkers, 18 studies reported 57 new single nucleotide polymorphism biomarkers, and 11 studies reported 171 new gene expression profiles associated with cardiotoxicity. Data were extracted for 272 novel molecular biomarkers reported and evaluated in 7084 cancer patients, of which only 13 were identified in more than one study (MPO, sST2, GDF-15, TGF-B1, rs1056892, rs1883112, rs4673, rs13058338, rs1695, miR-1, miR-25-3p, miR-34a-5p, and miR-423-5p), showing values for area under the curve > 0.73 (range 0.74-0.85), odds ratio 0.26-7.17, and hazard ratio 1.28-1.80.

Multiple studies presented a significant number of novel molecular biomarkers as promising predictors for risk assessment of cardiac dysfunction related to cancer therapy, but the characteristics of the studies carried out and the determinations applied do not allow suggesting the clinical use of these molecular biomarkers in the assessment of cancer therapy-induced cardiotoxicity.

Evidence regarding the relationship between colorectal cancer and the risk of cardiovascular disease (CVD) is limited. Thus, in this study, we aimed to determine the standardised incidence ratio (SIR) of CVDs in colorectal cancer patients in Taiwan.

A population-based cohort study enrolling the incident colorectal cancer population based on the Cancer Registry Database from 2007 to 2016 was conducted (n = 94,233, mean age: 62.4 years, 43.0% women). New cases of CVD, including coronary heart disease and ischemic stroke, through 31 December 2018 were obtained from the National Health Insurance Research Database and National Death Registry. Compared with the general population (n = 1,977,659, mean age: 44.3 years, 49.6% women), age- and sex-specific SIRs for CVDs were calculated by the time since diagnosis.

A total of 6852 cardiovascular events occurred in colorectal cancer patients during a median follow-up of 4.4 years. The SIR of CVD was highest in the first year after diagnosis (SIR: 1.45, 95% confidence interval: 1.39-1.50); however, this decreased to the same value as that of the general population in later years. Similar patterns were observed for the SIR of coronary heart disease. However, the SIR of ischemic stroke among colorectal cancer patients was low from the second year following cancer diagnosis.

Colorectal cancer patients are at an increased risk of developing CVD, especially coronary heart disease, during the first 3 years following colorectal cancer diagnosis.

The aim of this study is to establish the correlation between a CAC score derived from the CT component of PET/CT scan (CAC-PET) using in-house software as compared to the conventional technique (CAC-Standard). In addition, the incidence of high CAC scores in asymptomatic cancer patients with low-to-intermediate cardiovascular risk will be determined.

100 patients referred for oncologic PET/CT were prospectively recruited to have a conventional CAC score after their PET/CT. Patients with a history of cardiac disease were excluded. The nongated CT images from the PET/CT (CAC-PET) were analysed using validated in-house software with the results compared to those from gated CT analysed using the standard technique (CAC-Standard).

The correlation of CAC scores between the two scan types was moderate [slope, 0.95; R2 = 0.91; limits of agreement (LOA) = 0.29-5.65]. Using a conventional categorical analysis, there was complete agreement in 73% of patients with one category difference in the remainder. [interclass correlation (ICC) = 0.90; Cohen's kappa = 0.63]. In total 28% of these asymptomatic low-to-intermediate-risk cancer patients had CAC scores over 300.

Estimation of CAC from the CT component of PET/CT scans is a reliable method for the detection of significant CAC in cancer patients and correlates well with the standard method. This technique should permit the calculation of cardiovascular risk in cancer patients undergoing PET/CT without any additional radiation exposure. A significant number of asymptomatic low-to-intermediate-risk cancer patients were found to have a high risk of cardiovascular disease.