Colorectal cancer (CRC) survivors often experience long-term symptoms after cancer treatments. But gastrointestinal (GI) symptom experiences are under-investigated in CRC survivors. We described ...persistent GI symptoms after cancer treatments in female CRC survivors and assessed GI symptoms' risk and life-impact factors.
A cross-sectional study utilized data from the Women's Health Initiative (WHI) Life and Longevity After Cancer (LILAC) study that recruited postmenopausal women. Correlation analyses and multivariable linear regression models were used.
CRC survivors after cancer treatments were included (N = 413, mean age 71.2 years old, mean time since diagnosis = 8.1 years). 81% of CRC survivors experienced persistent GI symptoms. Bloating/gas was the most prevalent (54.2%± 0.88) and severe GI symptom, followed by constipation (44.1%±1.06), diarrhea (33.4%±0.76), and abdominal/pelvic pain (28.6%±0.62). Significant risk factors for GI symptoms include time since cancer diagnosis (<5 years), advanced cancer stage, high psychological distress, poor dietary habits, and low physical activity. Fatigue and sleep disturbance were the most significant risk factors for long-term GI symptoms (β = 0.21, t = 3.557; β = 0.20, t = 3.336, respectively, Ps < .001). High severity of GI symptoms was positively associated with poor quality of life (QOL), increased daily life interferences (social and physical functions), and low body image satisfaction (Ps < .001).
Women CRC survivors experience a high GI symptom burden, highlighting the need to inform policy and improve the QOL of cancer survivors. Our findings will aid in identifying those more vulnerable to symptoms, and inform future survivorship care interventions (i.e., community-based cancer symptom management) by considering multiple risk factors (e.g., psychological distress).
Advances in cancer therapeutics have revolutionized survival outcomes in patients with cancer. However, cardiovascular toxicities associated with specific cancer therapeutics adversely affect the ...outcomes of patients with cancer. Recent studies have uncovered excess risks of these cardiotoxic events, especially in traditionally underrepresented populations. Despite advances in strategies to limit the risks of cardiovascular events among cancer survivors, relatively limited guidance is available to address the rapidly growing problem of disparate cardiotoxic risks among women and underrepresented patient populations. Previously decentralized and sporadic evaluations have led to a lack of consensus on the definitions, investigation, and potential optimal strategies to address disparate cardiotoxicity in contemporary cancer care (eg, with immunotherapy, biologic, or cytotoxic therapies) settings. This scientific statement aims to define the current state of evidence for disparate cardiotoxicity while proposing uniform and novel methodological approaches to inform the identification and mitigation of disparate cardio-oncology outcomes in future clinical trials, registries, and daily clinical care settings. We also propose an evidence-based integrated approach to identify and mitigate disparities in the routine clinical setting. This consensus scientific statement summarizes and clarifies available evidence while providing guidance on addressing inequities in the era of emerging anticancer therapies.
Advances in breast cancer (BC) treatment have contributed to improved survival, but BC survivors experience significant short-term and long-term cardiovascular mortality and morbidity, including an ...elevated risk of heart failure with preserved ejection fraction (HFpEF). Most research has focused on HF with reduced ejection fraction (HFrEF) after BC; however, recent studies suggest HFpEF is the more prevalent subtype after BC and is associated with substantial health burden. The increased HFpEF risk observed in BC survivors may be explained by treatment-related toxicity and by shared risk factors that heighten risk for both BC and HFpEF. Beyond risk factors with physiological impacts that drive HFpEF risk, such as hypertension and obesity, social determinants of health (SDOH) likely contribute to HFpEF risk after BC, impacting diagnosis, management and prognosis.Increasing clinical awareness of HFpEF after BC and screening for cardiovascular (CV) risk factors, in particular hypertension, may be beneficial in this high-risk population. When BC survivors develop HFpEF, treatment focuses on initiating guideline-directed medical therapy and addressing underlying comorbidities with pharmacotherapy or behavioural intervention. HFpEF in BC survivors is understudied. Future directions should focus on improving HFpEF prevention and treatment by building a deeper understanding of HFpEF aetiology and elucidating contributing risk factors and their pathogenesis in HFpEF in BC survivors, in particular the association with different BC treatment modalities, including radiation therapy, chemotherapy, biological therapy and endocrine therapy, for example, aromatase inhibitors. In addition, characterising how SDOH intersect with these therapies is of paramount importance to develop future prevention and management strategies.
Advances in cancer therapeutics have led to dramatic improvements in survival, now inclusive of nearly 20 million patients and rising. However, cardiovascular toxicities associated with specific ...cancer therapeutics adversely affect the outcomes of patients with cancer. Advances in cardiovascular imaging have solidified the critical role for robust methods for detecting, monitoring, and prognosticating cardiac risk among patients with cancer. However, decentralized evaluations have led to a lack of consensus on the optimal uses of imaging in contemporary cancer treatment (eg, immunotherapy, targeted, or biological therapy) settings. Similarly, available isolated preclinical and clinical studies have provided incomplete insights into the effectiveness of multiple modalities for cardiovascular imaging in cancer care. The aims of this scientific statement are to define the current state of evidence for cardiovascular imaging in the cancer treatment and survivorship settings and to propose novel methodological approaches to inform the optimal application of cardiovascular imaging in future clinical trials and registries. We also propose an evidence-based integrated approach to the use of cardiovascular imaging in routine clinical settings. This scientific statement summarizes and clarifies available evidence while providing guidance on the optimal uses of multimodality cardiovascular imaging in the era of emerging anticancer therapies.
Some but not all past studies reported associations between components of air pollution and breast cancer, namely fine particulate matter ≤2.5 μm (PM2.5) and nitrogen dioxide (NO2). It is yet unclear ...whether risks differ according to estrogen receptor (ER) and progesterone receptor (PR) status.
This analysis includes 47,591 women from the Sister Study cohort enrolled from August 2003 to July 2009, in whom 1,749 invasive breast cancer cases arose from enrollment to January 2013. Using Cox proportional hazards and polytomous logistic regression, we estimated breast cancer risk associated with residential exposure to NO2, PM2.5, and PM10.
Although breast cancer risk overall was not associated with PM2.5 HR = 1.03; 95% confidence intervals (CI), 0.96-1.11, PM10 (HR = 0.99; 95% CI, 0.98-1.00), or NO2 (HR = 1.02; 95% CI, 0.97-1.07), the association with NO2 differed according to ER/PR subtype (P = 0.04). For an interquartile range (IQR) difference of 5.8 parts per billion (ppb) in NO2, the relative risk (RR) of ER(+)/PR(+) breast cancer was 1.10 (95% CI, 1.02-1.19), while there was no evidence of association with ER(-)/PR(-) (RR = 0.92; 95% CI, 0.77-1.09; Pinteraction = 0.04).
Within the Sister Study cohort, we found no significant associations between air pollution and breast cancer risk overall. But we observed an increased risk of ER(+)/PR(+) breast cancer associated with NO2.
Though these results suggest there is no substantial increased risk for breast cancer overall in relation to air pollution, NO2, a marker of traffic-related air pollution, may differentially affect ER(+)/PR(+) breast cancer.
Aims
There is conflicting evidence whether heart failure (HF) is a risk factor for incident cancer. Despite population‐based cohorts demonstrating this association, an analysis of the Physician's ...Health Study found no association in a cohort of mostly healthy males. We investigated the association of HF with incident cancer among a large cohort of post‐menopausal women.
Methods and results
A prospective cohort study of 146 817 post‐menopausal women age 50 to 79 years enrolled in the Women's Health Initiative from 1993–1998, and followed through 2015. The primary exposure was adjudicated incident HF diagnosis, including preserved and reduced ejection fraction in a sub‐cohort. The primary outcome was adjudicated incident total and site‐specific cancers. Hazard ratios were calculated using multivariable‐adjusted Cox proportional hazard regression models. Over a median follow‐up of 8.4 years, 3272 and 17 474 women developed HF and cancer, respectively. HF developed in 235 women prior to cancer. HF was associated with subsequent incident cancer hazard ratio (HR) 1.28, 95% confidence interval (CI) 1.11–1.48. Associations were observed for obesity‐related cancers (HR 1.24, 95% CI 1.02–1.51), as well as lung and colorectal cancers (HR 1.58, 95% CI 1.09–2.30 and HR 1.52, 95% CI 1.02–2.27, respectively). HF with preserved ejection fraction (HR 1.34, 95% CI 1.06–1.67), but not HF reduced ejection fraction (HR 0.99, 95% CI 0.74–1.34), was associated with total cancer.
Conclusion
Heart failure was associated with an increase in cancer diagnoses in post‐menopausal women. This association was strongest for lung cancer. Further research is needed to appreciate the underlying mechanisms responsible for this association.
Heart failure (HF) is significantly associated with an increased risk of developing cancer among post‐menopausal women. HFpEF, heart failure with preserved ejection fraction.
A major goal in cell signaling research is the quantification of phosphorylation pharmacodynamics following perturbations. Traditional methods of studying cellular phospho-signaling measure one ...analyte at a time with poor standardization, rendering them inadequate for interrogating network biology and contributing to the irreproducibility of preclinical research. In this study, we test the feasibility of circumventing these issues by coupling immobilized metal affinity chromatography (IMAC)-based enrichment of phosphopeptides with targeted, multiple reaction monitoring (MRM) mass spectrometry to achieve precise, specific, standardized, multiplex quantification of phospho-signaling responses. A multiplex immobilized metal affinity chromatography- multiple reaction monitoring assay targeting phospho-analytes responsive to DNA damage was configured, analytically characterized, and deployed to generate phospho-pharmacodynamic curves from primary and immortalized human cells experiencing genotoxic stress. The multiplexed assays demonstrated linear ranges of ≥3 orders of magnitude, median lower limit of quantification of 0.64 fmol on column, median intra-assay variability of 9.3%, median inter-assay variability of 12.7%, and median total CV of 16.0%. The multiplex immobilized metal affinity chromatography- multiple reaction monitoring assay enabled robust quantification of 107 DNA damage-responsive phosphosites from human cells following DNA damage. The assays have been made publicly available as a resource to the community. The approach is generally applicable, enabling wide interrogation of signaling networks.
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