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OBJECTIVES: To examine if racial differences in cardiovascular health (CVH) are associated with cardiovascular disease (CVD) disparities among women with breast and gynecologic cancers. SAMPLE & SETTING: The sample consisted of 252 Black women and 93 White women without a self-reported history of cancer or CVD who developed a breast or gynecologic malignancy. Women who developed CVD before their cancer diagnosis were excluded. METHODS & VARIABLES: CVH was classified using metrics of the American Heart Association's Life's Simple 7 framework. Metrics were summed to create a total CVH score (0-7). Associations among race, ideal CVH (score of 5-7), and CVD incidence following cancer diagnosis were estimated with Cox proportional hazards models. RESULTS: Ideal CVH was similar between Black women (33%) and White women (37%). Race and CVH were not associated with CVD incidence. IMPLICATIONS FOR NURSING: In a small sample of women diagnosed with breast and gynecologic cancers, racial disparities in CVH and CVD incidence were not observed. Additional investigation of potential confounders relating to social determinants of health tied to the construct of race is warranted. [ABSTRACT FROM AUTHOR]

Background Although unopposed estrogen exposure is considered a major driver of endometrial carcinogenesis, chronic inflammation and insulin resistance and hyperinsulinemia are also major endometrial cancer risk factors. However, it is unclear whether diets with inflammatory or insulinemic potential are associated with risk of endometrial cancer. Methods We followed 48 330 women from the Nurses' Health Study (1984-2016) and 85 426 women from the Nurses' Health Study II (1989-2017). Using food frequency questionnaires, we calculated repeated measures of empirical dietary inflammatory pattern (EDIP) and empirical dietary index for hyperinsulinemia (EDIH) scores, which characterize the potential of the whole diet to modulate circulating biomarkers of inflammation or C-peptide, respectively. We used multivariable-adjusted Cox regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for type I endometrial cancer risk. Results We documented 1462 type I endometrial cancer cases over 2 823 221 person-years of follow-up. In the pooled multivariable-adjusted analyses, women in the highest compared with lowest quintiles were at higher risk of type I endometrial cancer (EDIP HRQ5vsQ1 = 1.46, 95% CI = 1.24 to 1.73; P trend <.001; EDIH HRQ5vsQ1 = 1.58, 95% CI = 1.34 to 1.87; P trend <.001). Additional adjustment for body mass index attenuated the associations (EDIP HR = 1.03, 95% CI = 0.87 to 1.22; EDIH HR = 1.01, 95% CI = 0.85 to 1.21), and mediation analyses showed that body mass index may explain 60.4% (95% CI = 37.4% to 79.6%; P <.001) and 71.8% (95% CI = 41.0% to 90.4%; P <.001) of the association of endometrial cancer with EDIP and EDIH, respectively. Conclusions In this large cohort study, higher dietary inflammatory and insulinemic potential were each associated with increased endometrial cancer incidence, and this association may be almost entirely mediated by adiposity. [ABSTRACT FROM AUTHOR]

Background: Oncology provider discussions of treatment options, outcomes of treatment, and end of life planning are essential to care for patients with advanced malignancies. Studies have shown that despite this, many patients do not have adequate care planning, including end of life planning. It is thought that the accessibility of information outside of clinical encounters and individual factors and/or beliefs may influence the patient's perception of disease. Aims: The objective of this study was to evaluate if patient understanding of treatment goals matched the provider and if there were areas of discrepancy. If a discrepancy was found, the survey inquired further into more specific aspects. Methods: A questionnaire-based survey was performed at a cancer hospital outpatient clinic. 100 consecutive and consenting patients who had stage IV non-curable lung, gastrointestinal (GI), or other cancer were included in the study. Patients must have had at least 2 visits with their oncologist. Results: 40 patients reported their disease might be curable and 60 reported their disease was not curable. Patients who reported their disease was not curable were more likely to be 65 years or older (P-value: 0.055). They were more likely to report that their doctor discussed the possibility of their cancer getting worse (78.3% VS 55%; P-value 0.024), that their doctor discussed end of life plans (58.3% VS 30%; P- value: 0.01), and that they had appointed a health care decision-maker (86.7% VS 62.5%; P-value: 0.01). 65% of patients who thought their disease might be curable reported that their doctor said it might be curable, compared with only 6.7% of patients who thought their disease was not curable (p < 0.001). Or, equivalently, 35% of patients who thought their disease might be curable reported that their doctor's opinion was that it was not curable, compared with 93% of patients who thought their disease was not curable (p < 0.001). Patients who had lung cancer were more likely to believe their cancer was not curable than patients with gastrointestinal or other cancer, though the difference was not statistically significant (p = 0.165). Patients who said their disease might be curable selected as possible reasons that a miracle (50%) or alternative medicine (66.7%) would get rid of the cancer, or said their family wanted them to believe the cancer would go away (16.7%) or that another doctor said it would (4.2%). Patients who said their disease might be curable said they did so due to alternative medications, another doctor, or their family. Restricting to the 70 patients who reported their doctors telling them their disease was not curable, 20% of them still said that they personally felt their disease might be curable. Patients below 65 years of age were more likely to disagree with the doctor in this case (P-value: 0.047). Conclusion: This survey of patients diagnosed with stage IV cancer shows that a significant number of patients had misunderstandings of the treatment and curability of their disease. Findings suggest that a notable proportion kept these beliefs even after being told by treating physicians that their disease is not curable. [ABSTRACT FROM AUTHOR]

Introduction: Racial and ethnic disparities in gynecologic cancer care have been documented. Treatment at academic facilities is associated with improved survival, yet no study has examined independent associations between race and ethnicity with facility type among gynecologic cancer patients., Materials & Methods: We used the National Cancer Database and identified 484,455 gynecologic cancer (cervix, ovarian, uterine) patients diagnosed between 2004 and 2020. Facility type was dichotomized as academic vs. non-academic, and we used logistic regression to estimate multivariable-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) between race and ethnicity and facility type. Secondarily, we examined joint effects of race and ethnicity and facility type on overall survival using Cox proportional hazards regression., Results: We observed higher odds of treatment at academic (vs. non-academic) facilities among American Indian/Alaska Native (OR = 1.42, 95% CI = 1.28-1.57), Asian (OR = 1.64, 95% CI = 1.59-1.70), Black (OR = 1.69, 95% CI = 1.65-1.72), Hispanic (OR = 1.70, 95% CI = 1.66-1.75), Native Hawaiian/Pacific Islander (OR = 1.74, 95% CI = 1.57-1.93), and other race (OR = 1.29, 95% CI = 1.20-1.40) patients compared with White patients. In the joint effects survival analysis with White, academic facility-treated patients as the reference group, Asian, Hispanic, and other race patients treated at academic or non-academic facilities had improved overall survival. Conversely, Black patients treated at academic facilities [Hazard Ratio (HR) = 1.10, 95% CI = 1.07-1.12] or non-academic facilities (HR = 1.19, 95% CI = 1.16-1.21) had worse survival., Discussion: Minoritized gynecologic cancer patients were more likely than White patients to receive treatment at academic facilities. Importantly, survival outcomes among patients receiving care at academic institutions differed by race, requiring research to investigate intra-facility survival disparities., Competing Interests: Declaration of competing interest Dr. Plascak reports honoraria payments from National Comprehensive Cancer Network and North American Association of Central Cancer Registries. Dr. Backes reports personal fees from Agenus, CEC Oncology, Clovis, Eisai, Merck, AstraZeneca, GSK, ImmunoGen, BioNTech, Daiichi Sankyo, EMD Serono, and Myriad and research funding from Clovis, Eisai, Immunogen, Merck, Beigene, Tempus, and Natera. All other authors have no conflicts of interest to disclose., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Although unopposed estrogen exposure is considered a major driver of endometrial carcinogenesis, chronic inflammation and insulin resistance and hyperinsulinemia are also major endometrial cancer risk factors. However, it is unclear whether diets with inflammatory or insulinemic potential are associated with risk of endometrial cancer., Methods: We followed 48 330 women from the Nurses' Health Study (1984-2016) and 85 426 women from the Nurses' Health Study II (1989-2017). Using food frequency questionnaires, we calculated repeated measures of empirical dietary inflammatory pattern (EDIP) and empirical dietary index for hyperinsulinemia (EDIH) scores, which characterize the potential of the whole diet to modulate circulating biomarkers of inflammation or C-peptide, respectively. We used multivariable-adjusted Cox regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for type I endometrial cancer risk., Results: We documented 1462 type I endometrial cancer cases over 2 823 221 person-years of follow-up. In the pooled multivariable-adjusted analyses, women in the highest compared with lowest quintiles were at higher risk of type I endometrial cancer (EDIP HRQ5vsQ1 = 1.46, 95% CI = 1.24 to 1.73; Ptrend < .001; EDIH HRQ5vsQ1 = 1.58, 95% CI = 1.34 to 1.87; Ptrend < .001). Additional adjustment for body mass index attenuated the associations (EDIP HR = 1.03, 95% CI = 0.87 to 1.22; EDIH HR = 1.01, 95% CI = 0.85 to 1.21), and mediation analyses showed that body mass index may explain 60.4% (95% CI = 37.4% to 79.6%; P < .001) and 71.8% (95% CI = 41.0% to 90.4%; P < .001) of the association of endometrial cancer with EDIP and EDIH, respectively., Conclusions: In this large cohort study, higher dietary inflammatory and insulinemic potential were each associated with increased endometrial cancer incidence, and this association may be almost entirely mediated by adiposity., (© The Author(s) 2022. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.)