The gas phase of tobacco smoke has been implicated as a major cause of cancer and chronic obstructive pulmonary disease. Furan, a component of the gas phase, is highly toxic and carcinogenic in rodents; however, its toxicity in humans has not been well investigated. Furan's toxicity results from cytochrome P450 2E1-catalyzed oxidation to cis-2-butene-1,4-dial (BDA). The structure of furan metabolites demonstrates that BDA reacts with glutathione (GSH) to form a reactive GSH conjugate, 2-(S-glutathionyl)succinaldehyde (GSH-BDA), which reacts with protein lysine groups as well as other cellular nucleophiles. In this report, GSH-BDA-glycerolphosphorylethanolamine (GSH-BDA-GPE), GSH-BDA-ethanolamine, and GSH-BDA-glutamic acid are identified as human hepatocellular metabolites of furan. To determine if the downstream mercapturic acid metabolites are present in human urine, stable isotopically labeled forms of the expected metabolites were used as internal standards in an established liquid chromatography-tandem mass spectrometry (LC-MS/MS) assay. This approach indicated that N-acetyl-S-(1-(2-hydroxyethyl)-1H-pyrrol-3-yl)cysteine sulfoxide (NAC-BDA-ethanolamine sulfoxide) was detected in human urine. A sensitive LC-MS/MS assay for this metabolite was developed and applied to urine samples from a variety of smoke-exposed individuals as well as nonsmokers. Its levels were 2.5-5 times higher in people who smoke than in nonsmokers. They were not elevated in exclusive e-cigarette or cannabis users. Two case-control studies were performed to determine whether NAC-BDA-lysine metabolites or NAC-BDA-ethanolamine sulfoxide were associated with smoking-related diseases. In the first study, there was no association between any of the furan metabolites and liver cancer. In the second study, there was a suggestive association between NAC-BDA-ethanolamine sulfoxide and the risk of smoking-related respiratory disease symptoms. However, the overall trend was not significant. Therefore, there was no clear link between this furan metabolite and the risk of smoking-related respiratory disease symptoms.

BACKGROUND:Observational studies have reported lower ovarian cancer risk among individuals taking aspirin frequently (i.e. daily/near daily). However, most studies relied on a single assessment of aspirin use, which may have led to misclassification and precluded the examination of patterns of use over time. We examined the association between aspirin use, assessed at multiple time points, and ovarian cancer risk. METHODS:Data were pooled from 10 prospective cohort studies from the Ovarian Cancer Cohort Consortium (n = 675 901 participants; 5528 cases; median follow-up = 13 years). Frequent aspirin use was self-reported via repeat questionnaires. We examined multiple time-updated, lagged aspirin-exposure metrics and risk of ovarian cancer by using pooled logistic regression adjusted for time-updated confounders. RESULTS:While ever frequent aspirin use was not associated with ovarian cancer [odds ratio (OR) 0.97; 95% confidence interval (CI): 0.91-1.03], individuals who reported long-term use experienced a 14% reduction in ovarian cancer risk (>6 years; OR 0.86; 95% CI: 0.77-0.97). This risk reduction was evident among individuals with at least three ovarian cancer risk factors (OR 0.65; 95% CI: 0.50-0.85) but not among individuals with fewer than three ovarian cancer risk factors (OR 0.94; 95% CI: 0.82-1.08), P-interaction = .02). Reduced ovarian cancer risks were also observed for low-dose aspirin use (OR 0.90; 95% CI: 0.80-1.01 for ever low-dose use; OR 0.75; 95% CI: 0.56-0.99 for long-term low-dose use) but not ever regular-dose use (OR 1.09; 95% CI: 0.94-1.27). CONCLUSION:Long-term use of aspirin, and particularly low-dose aspirin, is associated with lower ovarian cancer risk, especially among individuals with other established risk factors for ovarian cancer. Research should continue to explore the potential role of long-term, low-dose aspirin use for ovarian cancer primary prevention.

BACKGROUND:Stomach cancer presents complex etiologic heterogeneity. Ethanol in alcoholic beverages and its metabolite acetaldehyde are carcinogens causally linked to several cancers, but their role in gastric carcinogenesis has not been established. We analyzed harmonized, individual-level prospective data to examine associations between alcohol intake and risk of stomach cancer and its subtypes. METHODS:2,009,951 participants in 20 cohorts (mean follow-up=9-29 years) within the Pooling Project of Prospective Studies of Diet and Cancer (n = 8,357 incident invasive gastric adenocarcinomas) were included. We used Cox regression to assess associations between alcohol intake and risk of stomach cancer overall and by anatomical and histological subtype and population subgroup, adjusting for confounders. RESULTS:Evidence for an association between alcohol intake and overall stomach cancer risk was weak (hazard ratio, HR, for ≥30 v 0.1-<5 g/day: 1.06 [95% confidence interval, CI, 0.96 to 1.16], P between-studies heterogeneity=0.43). Positive associations with stomach cancer risk were observed in never smokers (HR, for ≥30 v 0.1-<5 g/day: 1.20 [95% CI, 1.02 to 1.42]; P interaction=0.02) and for Asian studies (HR, 1.21 [95% CI, 1.02 to 1.42]; P interaction=0.01). Modest increased risks were observed for non-cardia cancers such as those of the fundus, body and greater curvature, but not distally located non-cardia cancers. HRs did not differ materially between diffuse- and intestinal-type cancers (P heterogeneity>0.05). CONCLUSION:There was little evidence of an overall association between alcohol intake and stomach cancer risk, although modest positive associations were observed among never smokers and in Asian cohorts.

Abstract Metabolic Dysregulation and Obesity Cancer Risk Consortium (MeDOC) is an NCI-sponsored program using team science and transdisciplinary approach to elucidate mechanisms linking obesity, metabolic dysregulation, and cancer risk. Both obesity and metabolic dysregulation contribute to a cascade of derangements in adipocyte function, growth factors, inflammation, gut microbiome, immune function, sex hormones, lipid and glucose metabolism which, in turn, can disrupt several downstream signaling pathways related to cancer initiation and progression. Given this complexity, integrating multi-omic, mouse models and epidemiologic data is critical. The MeDOC-Knowledge Base (MeDOC-KB) is a comprehensive atlas cataloging associations to link obesity, metabolic dysregulation, and cancer risk from consortium studies and external literature. A large language model-based agent harmonized biomarkers derived from metabolomics, proteomics, and lipidomics platforms such as Nightingale, Olink, and Metabolon, standardizing nomenclature and resolving cross-platform synonyms into a unified vocabulary. MeDOC-KB uses a Neo4j graph database architecture to enable efficient traversal of complex relationships among the biomarkers, publications, cohorts, and cancer sites. Literature data are extracted into four core tables (Citation, Cohort, Methods, and Association) and transformed into a graph structure where nodes represent publication, cohorts, biomarkers, and cancer sites while edges denote their relationships. MeDOC-KB is accessible through an interactive R Shiny web application. The current version contains 42,838 nodes and 189,709 relationships with 21,945 being biomarker-cancer associations spanning 1,645 biomarkers and 15 cancer outcomes, including 11 of the 13 known obesity related cancers. For example, MeDOC-KB reveals that insulin-like growth factor binding protein-1 (IGFBP-1) shows inverse associations with endometrial, colorectal, and pancreatic cancers across multiple cohorts, suggesting shared metabolic mechanisms. The platform enables researchers to identify biomarker patterns associated with obesity-induced metabolic dysregulation across cancer types, compare findings across cohorts, and discover understudied biomarker-cancer relationships. MeDOC-KB provides a critical resource for hypothesis generation regarding mechanistic pathways, biomarker validation across populations, and identification of promising targets for cancer prevention strategies in high-risk metabolic populations. The knowledge base is publicly accessible and will be continuously updated with consortium findings and literature. Citation Format: Madhan Subramanian, Sam Rosin, Stephanie Hall, Nisha Grover-Fairchild, Kim Robien, Loretta DiPietro, Marinella Temprosa. MeDOC-KB: Knowledge base for unraveling the metabolic links between obesity-related cancers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 5521.

Pancreatic cancer incidence is rising, yet few modifiable risk factors have been identified. The Mediterranean diet, which lowers inflammation and improves healthy weight maintenance and insulin control, may lower pancreatic cancer risk, yet the evidence for this association is inconsistent. To investigate the association, we conducted a pooled analysis of 2,315,406 individuals from 23 prospective cohorts in the Pooling Project of Prospective Studies of Diet and Cancer (DCPP), of whom 10,748 developed incident pancreatic cancer over a mean follow-up duration ranging from 8.1 to 23.3 years across studies. Adherence to the Mediterranean diet was assessed using the alternative Mediterranean diet score (aMED) and a modified score excluding alcohol (maMED). Study- and sex-specific hazard ratios (HRs) and 95

The gas phase of tobacco smoke has been implicated as a major cause of cancer and chronic obstructive pulmonary disease. Furan, a component of the gas phase, is highly toxic and carcinogenic in rodents; however, its toxicity in humans has not been well investigated. Furan's toxicity results from cytochrome P450 2E1-catalyzed oxidation to cis-2-butene-1,4-dial (BDA). The structure of furan metabolites demonstrates that BDA reacts with glutathione (GSH) to form a reactive GSH conjugate, 2-(S-glutathionyl)succinaldehyde (GSH-BDA), which reacts with protein lysine groups as well as other cellular nucleophiles. In this report, GSH-BDA-glycerolphosphorylethanolamine (GSH-BDA-GPE), GSH-BDA-ethanolamine, and GSH-BDA-glutamic acid are identified as human hepatocellular metabolites of furan. To determine if the downstream mercapturic acid metabolites are present in human urine, stable isotopically labeled forms of the expected metabolites were used as internal standards in an established liquid chromatography-tandem mass spectrometry (LC-MS/MS) assay. This approach indicated that N-acetyl-S-(1-(2-hydroxyethyl)-1H-pyrrol-3-yl)cysteine sulfoxide (NAC-BDA-ethanolamine sulfoxide) was detected in human urine. A sensitive LC-MS/MS assay for this metabolite was developed and applied to urine samples from a variety of smoke-exposed individuals as well as nonsmokers. Its levels were 2.5-5 times higher in people who smoke than in nonsmokers. They were not elevated in exclusive e-cigarette or cannabis users. Two case-control studies were performed to determine whether NAC-BDA-lysine metabolites or NAC-BDA-ethanolamine sulfoxide were associated with smoking-related diseases. In the first study, there was no association between any of the furan metabolites and liver cancer. In the second study, there was a suggestive association between NAC-BDA-ethanolamine sulfoxide and the risk of smoking-related respiratory disease symptoms. However, the overall trend was not significant. Therefore, there was no clear link between this furan metabolite and the risk of smoking-related respiratory disease symptoms.

Background Malnutrition is common in adults with hematologic malignancies and can negatively impact treatment outcomes. Objective This systematic review evaluated the association between nutrition support interventions compared to alternative or usual care, and primary outcomes (nutritional status, anthropometric measures, length of stay, readmissions, quality of life) and secondary outcomes (survival, mucositis, graft-vs-host disease, delayed engraftment, inflammation, cost, and calorie or protein intake), in adults with hematologic malignancies. Methods MEDLINE, CINAHL, Cochrane CENTRAL, Food Science Source, and SPORTDiscus databases were searched for controlled trials and observational studies published in English in peer-reviewed journals from January 2000 – July 2024. Risk of bias (RoB) was assessed using Cochrane’s RoB 2 tool for randomized controlled trials (RCTs), RoB in Non-randomized Studies of Interventions (ROBINS-I) for non-RCTs, RoB in Non-randomized Studies of Exposures (ROBINS-E) for observational studies. Meta-analyses used a maximum likelihood random-effects model, and heterogeneity was quantified using I2. Certainty of evidence for primary outcomes was evaluated using the Grading of Recommendations, Assessment, and Evaluation (GRADE) method. Results Twenty-one articles (11 RCTs, 9 cohorts, 1 non-RCT) representing 2,122 participants were included. RoB was low (2 studies), some concerns/moderate (11 studies), and high (8 studies). Meta-analysis indicated a decrease in length of stay for enteral nutrition over parenteral nutrition, and no effect on length of stay for glutamine-enriched nutrition support; however, evidence was very low certainty. Individualized nutrition support interventions including calculation of estimated needs demonstrated benefit in decreasing weight loss. Overall, the association between nutrition support interventions and nutritional status, weight, readmissions, quality of life, and secondary outcomes was uncertain (very low certainty). Conclusion No single nutrition support intervention emerged as superior for all outcomes of interest, though current best practices were supported. Certainty of evidence was very low for primary outcomes, and heterogeneity limited conclusions for secondary outcomes. Further high-quality research is needed.

Black women in the United States have higher breast cancer mortality rates compared to women of other races/ethnicities. Heterogeneity in body composition between Black and non-Black women may contribute to differences in relative drug dosing and chemotherapy toxicities, leading to treatment delays and lower treatment completion rates. This study evaluated the extent to which drug dose/kilogram (kg) fat free mass (FFM) differs by race, and whether measures of FFM or adipose tissue (AT) are independently and/or jointly associated with hematologic toxicity, treatment delays, treatment discontinuation, and relative dose intensity (RDI). Women who were treated with neo/adjuvant anthracycline- and/or taxane-containing regimens for breast cancer between 2012–2019 and had an abdominal CT scan within 12 weeks of chemotherapy initiation were included in this retrospective study. Visceral and subcutaneous AT area and FFM were measured using CT scan slices at the L3 vertebra level. Results: A total of 230 women met the inclusion criteria. On average, Black women were older and had higher weight, FFM and AT compared to non-Black women; however, Black women had lower percent FFM. No statistically significant differences in initial or cumulative drug dose/kg FFM were observed between Black vs non-Black women for any individual drug. Similarly, neither FFM or AT were independently or jointly associated with incidence of hematologic toxicity, treatment delays or discontinuation for any individual chemotherapy drug. Current BSA-based chemotherapy dosing regimens do not appear to contribute to disparities in treatment-associated toxicity or chemotherapy completion.

BACKGROUND:Malnutrition is common in adults with hematologic malignancies and can negatively influence treatment outcomes. OBJECTIVE:This systematic review evaluated the association between nutrition support interventions compared with alternative or usual care, and primary outcomes (nutritional status, anthropometric measures, length of stay, readmissions, and quality of life) and secondary outcomes (survival, mucositis, graft-vs-host disease, delayed engraftment, inflammation, cost, and calorie or protein intake), in adults with hematologic malignancies. METHODS:MEDLINE, CINAHL, Cochrane CENTRAL, Food Science Source, and SPORTDiscus databases were searched for controlled trials and observational studies published in English in peer-reviewed journals from January 2000 to July 2024. Risk of bias (RoB) was assessed using the Cochrane RoB 2 tool for randomized controlled trials (RCTs), RoB in Non-randomized Studies of Interventions for non-RCTs, and RoB in Nonrandomized Studies of Exposures for observational studies. Meta-analyses used a maximum likelihood random-effects model, and heterogeneity was quantified using I2. Certainty of evidence for primary outcomes was evaluated using the Grading of Recommendations, Assessment, Development, and Evaluation method. RESULTS:Twenty-one articles (11 RCTs, 9 cohorts, 1 non-RCT) representing 2122 participants were included. RoB was low (2 studies), some concerns/moderate (11 studies), and high (8 studies). Meta-analysis indicated a decrease in length of stay for enteral nutrition over parenteral nutrition, and no effect on length of stay for glutamine-enriched nutrition support; however, evidence was of very low certainty. Individualized nutrition support interventions, including the calculation of estimated needs, demonstrated benefit in decreasing weight loss. Overall, the association between nutrition support interventions and nutritional status, weight, readmissions, quality of life, and secondary outcomes was uncertain (very low certainty). CONCLUSIONS:No single nutrition support intervention emerged as superior for all outcomes of interest, although current best practices were supported. Certainty of evidence was very low for primary outcomes, and heterogeneity limited conclusions for secondary outcomes. Further high-quality research is needed.

BACKGROUND:This study aimed to investigate the association between alcohol consumption and squamous cell cancers of the upper aerodigestive tract (UADT), using data from 28 cohorts within the Pooling Project of Prospective Studies of Diet and Cancer (DCPP). METHODS:Individual-level data from 2 365 437 participants were pooled. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox models to quantify the association between alcohol consumption (g/day) and UADT cancer risk, adjusting for potential confounders. Analyses were conducted by sex, smoking status, geographic region, and alcoholic beverages. RESULTS:Over a median follow-up of 15.5 years, 6903 UADT cancer cases were identified. Alcohol consumption was positively associated with UADT cancer risk overall. Even at intakes as low as 5-<15 g/day, the HR estimate was 1.12 (95% CI = 1.03 to 1.21) compared with the reference group (0.1-<5 g/day). The HR10 g/day (95% CI) was 1.16 (1.14 to 1.18) for women and 1.12 (1.11 to 1.13) for men (Pheterogeneity < .0001). HR10 g/day estimates were 1.14 (1.13 to 1.15) in current, 1.10 (1.09 to 1.12) in former, and 1.15 (1.12 to 1.18) in never smokers. Consistent UADT HR10 g/day estimates were observed across all beverage types. HR10 g/day estimates varied across geographic regions, with HR10 g/day (95% CI) equal to 1.15 (1.14 to 1.17) in Europe-Australia, 1.13 (1.11 to 1.15) in Asia, and 1.11 (1.09 to 1.12) in North America (Pheterogeneity < .0001). CONCLUSION:Alcohol consumption was associated with UADT cancer risk, irrespective of smoking status or beverage type. However, due to differential baseline risks, alcohol is expected to impact the UADT cancer burden more in smokers than never smokers. These findings support public health strategies to reduce alcohol consumption.

Recent efforts by numerous organizations and societies have found limited scientific evidence to support oncology nutrition guideline development. This project was undertaken to describe oncology nutrition studies that are underway or recently completed and to evaluate factors related to the completion and publication of study findings. Searches of ClinicalTrials.gov and the Australian New Zealand Clinical Trials Registry were performed in January 2025 using combinations of the terms: cancer, nutrition, diet, and oncology. Search results were merged and duplicates were removed using R/RStudio, and then, each entry was manually reviewed for eligibility in REDCap. Eligibility criteria were as follows: a study start date between January 2015 and December 2024, participants who were actively receiving cancer treatment, and a measure of diet/nutritional status and/or a nutrition intervention. Descriptive statistics, including stratified analyses, were conducted in R/RStudio. The database searches identified 1866 unique study listings. After exclusion criteria were applied, 444 studies met the inclusion criteria. Most studies (n = 352, 79.3

BACKGROUND:Alcohol is a known carcinogen, yet the evidence for an association with pancreatic cancer risk is considered as limited or inconclusive by international expert panels. We examined the association between alcohol intake and pancreatic cancer risk in a large consortium of prospective studies. METHODS AND FINDINGS:Population-based individual-level data was pooled from 30 cohorts across four continents, including Asia, Australia, Europe, and North America. A total of 2,494,432 participants without cancer at baseline (62% women, 84% European ancestries, 70% alcohol drinkers [alcohol intake ≥ 0.1 g/day], 47% never smokers) were recruited between 1980 and 2013 at the median age of 57 years and 10,067 incident pancreatic cancer cases were recorded. In age- and sex-stratified Cox proportional hazards models adjusted for smoking history, diabetes status, body mass index, height, education, race and ethnicity, and physical activity, pancreatic cancer hazard ratios (HR) and 95% confidence intervals (CI) were estimated for categories of alcohol intake and in continuous for a 10 g/day increase. Potential heterogeneity by sex, smoking status, geographic regions, and type of alcoholic beverage was investigated. Alcohol intake was positively associated with pancreatic cancer risk, with HR30-to-<60 g/day and HR≥60 g/day equal to 1.12 (95% CI [1.03,1.21]) and 1.32 (95% CI [1.18,1.47]), respectively, compared to intake of 0.1 to <5 g/day. A 10 g/day increment of alcohol intake was associated with a 3% increased pancreatic cancer risk overall (HR: 1.03; 95% CI [1.02,1.04]; pvalue < 0.001) and among never smokers (HR: 1.03; 95% CI [1.01,1.06]; pvalue = 0.006), with no evidence of heterogeneity by sex (pheterogeneity = 0.274) or smoking status (pheterogeneity = 0.624). Associations were consistent in Europe-Australia (HR10 g/day = 1.03, 95% CI [1.00,1.05]; pvalue = 0.042) and North America (HR10 g/day = 1.03, 95% CI [1.02,1.05]; pvalue < 0.001), while no association was observed in cohorts from Asia (HR10 g/day = 1.00, 95% CI [0.96,1.03]; pvalue = 0.800; pheterogeneity = 0.003). Positive associations with pancreatic cancer risk were found for alcohol intake from beer (HR10 g/day = 1.02, 95% CI [1.00,1.04]; pvalue = 0.015) and spirits/liquor (HR10 g/day = 1.04, 95% CI [1.03,1.06]; pvalue < 0.001), but not wine (HR10 g/day = 1.00, 95% CI [0.98,1.03]; pvalue = 0.827). The differential associations across geographic regions and types of alcoholic beverages might reflect differences in drinking habits and deserve more investigations. CONCLUSIONS:Findings from this large-scale pooled analysis support a modest positive association between alcohol intake and pancreatic cancer risk, irrespective of sex and smoking status. Associations were particularly evident for baseline alcohol intake of at least 15 g/day in women and 30 g/day in men.

Evidence to support the development of practice guidelines on nutrition interventions during active cancer treatment is limited despite the established role of nutrition in cancer prevention and long-term survivorship. To address this gap, the National Cancer Institute funded the Exercise and Nutrition Interventions to Improve Cancer Treatment-Related Outcomes (ENICTO) research consortium. This manuscript focuses on the nutrition-specific work within the ENICTO Consortium. We present a conceptual framework describing how nutritional interventions may enhance cancer treatment tolerance and timely completion of chemotherapy. We also describe how each ENICTO research project selected specific nutrition-related data items and collection methods to test hypotheses outlined in the conceptual framework. Research and consortium-wide projects are described in relation to advancing the scientific rigor of research in the field, including the standardization of nutrition assessment tools and measures. We conclude with a call to action for further research to support the development of evidence-based oncology nutrition practice guidelines relevant to the treatment period within the cancer continuum.

Chemotherapy treatment-related side effects are common and increase the risk of suboptimal outcomes. Exercise interventions during cancer treatment improve self-reported physical functioning, fatigue, anxiety, and depression, but it is unclear whether these interventions improve important clinical outcomes, such as chemotherapy relative dose intensity. The National Cancer Institute funded the Exercise and Nutrition to Improve Cancer Treatment-Related Outcomes (ENICTO) Consortium to address this knowledge gap. This article describes the mechanisms hypothesized to underpin intervention effects on clinically relevant treatment outcomes, briefly outlines each project's distinct research aims, summarizes the scope and organizational structure of ENICTO, and provides an overview of the integrated common data elements used to pursue research questions collectively. In addition, the article includes a description of consortium-wide activities and broader research community opportunities for collaborative research. Findings from the ENICTO Consortium have the potential to accelerate a paradigm shift in oncology care such that patients with cancer could receive exercise and nutrition programming as the standard of care in tandem with chemotherapy to improve relative dose intensity for a curative outcome.

BackgroundA substantial percentage of the US population is not up to date on guideline-recommended cancer screenings. Identifying interventions that effectively improve screening rates would enhance the delivery of such screening. Interventions involving health IT (HIT) show promise, but much remains unknown about how HIT is optimized to support cancer screening in primary care. ObjectiveThis scoping review aims to identify (1) HIT-based interventions that effectively support guideline concordance in breast, cervical, and colorectal cancer screening provision and follow-up in the primary care setting and (2) barriers or facilitators to the implementation of effective HIT in this setting. MethodsFollowing scoping review guidelines, we searched MEDLINE, CINAHL Plus, Web of Science, and IEEE Xplore databases for US-based studies from 2015 to 2021 that featured HIT targeting breast, colorectal, and cervical cancer screening in primary care. Studies were dual screened using a review criteria checklist. Data extraction was guided by the following implementation science frameworks: the Reach, Effectiveness, Adoption, Implementation, and Maintenance framework; the Expert Recommendations for Implementing Change taxonomy; and implementation strategy reporting domains. It was also guided by the Integrated Technology Implementation Model that incorporates theories of both implementation science and technology adoption. Reporting was guided by PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews). ResultsA total of 101 studies met the inclusion criteria. Most studies (85/101, 84.2%) involved electronic health record–based HIT interventions. The most common HIT function was clinical decision support, primarily used for panel management or at the point of care. Most studies related to HIT targeting colorectal cancer screening (83/101, 82.2%), followed by studies related to breast cancer screening (28/101, 27.7%), and cervical cancer screening (19/101, 18.8%). Improvements in cancer screening were associated with HIT-based interventions in most studies (36/54, 67% of colorectal cancer–relevant studies; 9/14, 64% of breast cancer–relevant studies; and 7/10, 70% of cervical cancer–relevant studies). Most studies (79/101, 78.2%) reported on the reach of certain interventions, while 17.8% (18/101) of the included studies reported on the adoption or maintenance. Reported barriers and facilitators to HIT adoption primarily related to inner context factors of primary care settings (eg, staffing and organizational policies that support or hinder HIT adoption). Implementation strategies for HIT adoption were reported in 23.8% (24/101) of the included studies. ConclusionsThere are substantial evidence gaps regarding the effectiveness of HIT-based interventions, especially those targeting guideline-concordant breast and colorectal cancer screening in primary care. Even less is known about how to enhance the adoption of technologies that have been proven effective in supporting breast, colorectal, or cervical cancer screening. Research is needed to ensure that the potential benefits of effective HIT-based interventions equitably reach diverse primary care populations.

Abstract Research suggests that medical comorbidity is associated with reduced relative dose intensity (RDI) in patients receiving chemotherapy for treatment of breast cancer. We aimed to determine factors associated with RDI of specific chemotherapy drugs in anthracycline- and/or taxane-based regimens. Women with a diagnosis of lymph node positive, invasive breast cancer who received neoadjuvant or adjuvant chemotherapy with either doxorubicin (DOX) + paclitaxel (PAC) or docetaxel (DOCE)-containing regimens at a single centerfrom2012 to2019 were included in this retrospective study. Age, race, comorbidities, height, weight, and chemotherapy regimen and dose were abstracted from the electronic health record. BMI was calculated using height and weight measured in clinic at the time initial chemotherapy orders were written and categorized according to US national guidelines (18.5 to < 25, 25 to < 30, and >30kg/m2). Presence of diabetes (DM) and hypertension (HTN) at time of diagnosis were determined by chart review. The oncologists’ initial chemotherapy orders (dose and duration) were used as the basis for RDI calculations. Cumulative actual dose received and duration of treatment were compared to planned dose and duration for individual chemotherapy drug and by regimen (DOX+PAC vs. DOCE). Associations between patient characteristics and RDI were evaluated in bivariate and multivariable analyses. A total of 230 women met the inclusion criteria, with 125 receiving a DOX+PAC regimen and 105 receiving a DOCE-based regimen. A higher percentage of women on DOX+PAC received >85% RDI compared to women receiving DOCE (80.8% vs 67.6%). Women aged 65+ years had lower median RDI [IQR] for DOCE than younger women (0.83 [0.67 - 0.98] vs 0.94 [0.84 - 1.00], p = 0.04), and a lower percentage in the older group received >85% RDI (35.3% vs 73.9%, p< 0.01). Median RDIs of PAC and DOX+PAC were lower for Black women than for White and Asian women (PAC: 0.91 [0.75 - 1.00] vs 1.00 [0.89 - 1.00], p = 0.02, DOX+PAC: 0.92[0.87-0.99] vs. 0.97 [0.91-1.00], p = 0.03), and the percent of Black women receiving >85% RDI of PAC was also lower (55.3% vs 77.6%, p = 0.01). BMI category was associated with median RDI for PAC (p= 0.03) and DOX+PAC (p = 0.01), with women in the >30kg/m2 category having the lowest median RDIs and PAC RDI >85% (p < 0.01). Median RDI of DOX+PAC was lower for women with DM (0.89 [0.84-0.92] vs. 0.96 [0.88-1:00], p = 0.03), and a lower percentage of women with DM received DOX RDI >85% compared to women without DM (66.7% vs 91.6%, p < 0.01). Median RDI was lower among women with HTN compared to women without for PAC (0.85 [0.73 - 1.00] vs 0.98 [0.83 - 1.00], p = 0.01) and DOX+PAC (0.91 [0.84 - 0.97] vs 0.97 [0.90 - 1.00], p = 0.01), and a lower percentage of women with HTN received >85% RDI for PAC (50.0% vs 73.3%, p = 0.01). Multiple logistic regression models adjusted for age (continuous), race, BMI (continuous), DM, and HTN had modestly improved predictive value compared to null models (McFadden’s R2 = 0.10 to 0.19); each year of increased age was associated with lower odds of RDI > 85% for DOX (OR [95% confidence interval] 0.91 [0.84-0.97], p = < 0.01), DOX+PAC (0.95 [0.90-0.99], p = 0.02), and DOCE (0.93 [0.88-0.97], p < 0.01), and DM with lower odds for DOX (0.26 [0.07-0.95], p = 0.04). Our findings of associations between increasing age, Black race, BMI, DM, and HTN and reduced RDI are consistent with prior research and present new data regarding associations between medical comorbidities and individual components of chemotherapy regimens. Citation Format: Heather Wopat, Annette Aldous, Adam Ciarleglio, Kendall Anderson, Kim Robien. Associations of age, body mass index, diabetes and hypertension with relative dose intensity among women receiving anthracycline- and/or taxane-based chemotherapy for invasive breast cancer [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO5-16-09.

Objective: To explore Central American men's perceptions of healthy body weight, factors that influence weight gain and increase awareness of being overweight/obese, consequences of excess weight gain and gender similarities and differences in body weight. Design: In-depth, qualitative interviews were conducted with low-income, overweight or obese Central American men residing in the USA (n = 25). Setting: Semi-structured, individual interviews (via Zoom or phone call) were conducted in Washington, DC in 2020-2021. Methods: Participants discussed their thoughts on the meaning of healthy weight; the role that weight management plays in the likelihood of getting diseases such as diabetes, cancer or hypertension; and whether having a healthy weight is different for men and women. Audio-recorded interviews were transcribed and analysed to identify themes using NVivo v12. Results: Participants were first-generation immigrants (mean age 50.9 +/- 6.4) and had resided in the USA for 23.7 +/- 10.2 years. They defined healthy weight as having the energy to carry on daily activities, not carrying extra body fat, being in good physical health, and having a balance between height and weight. Participants discussed having an unbalanced diet, not engaging in physical activity and getting older influenced weight gain. Factors that raised awareness of their weight gain included doctors' advice and cognisance of their current body weight. Participants in the study discussed the connection between weight status and some chronic diseases (i.e. cardiovascular diseases, diabetes and SARS-CoV-2 virus infection); cancer was the least discussed. Participants discussed that both men and women should have a healthy weight and contributing factors to why men weigh more than women. Conclusion: Health promotion interventions for Central American immigrant men should consider framing weight management as a means to continue fulfilling important social and cultural roles and responsibilities. Future research should examine Central American men's perceptions of weight management as part of cancer prevention.

BACKGROUND:The incidence of differentiated thyroid cancer (DTC) is higher in women than in men but whether sex steroid hormones contribute to this difference remains unclear. Studies of reproductive and hormonal factors and thyroid cancer risk have provided inconsistent results. METHODS:Original data from 1 252 907 women in 16 cohorts in North America, Europe, Australia and Asia were combined to evaluate associations of DTC risk with reproductive and hormonal factors. Multivariable-adjusted Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% CIs. RESULTS:During follow-up, 2142 women were diagnosed with DTC. Factors associated with higher risk of DTC included younger age at menarche (<10 vs 10-11 years; HR, 1.28; 95% CI, 1.00-1.64), younger (<40; HR, 1.31; 95% CI, 1.05-1.62) and older (≥55; HR, 1.33; 95% CI, 1.05-1.68) ages at menopause (vs 40-44 years), ever use of menopausal hormone therapy (HR, 1.16; 95% CI, 1.02-1.33) and previous hysterectomy (HR, 1.25; 95% CI, 1.13-1.39) or bilateral oophorectomy (HR, 1.14; 95% CI, 1.00-1.29). Factors associated with lower risk included longer-term use (≥5 vs <5 years) of oral contraceptives (HR, 0.86; 95% CI, 0.76-0.96) among those who ever used oral contraception and baseline post-menopausal status (HR, 0.82; 95% CI, 0.70-0.96). No associations were observed for parity, duration of menopausal hormone therapy use or lifetime number of reproductive years or ovulatory cycles. CONCLUSIONS:Our study provides some evidence linking reproductive and hormonal factors with risk of DTC. Results should be interpreted cautiously considering the modest strength of the associations and potential for exposure misclassification and detection bias. Prospective studies of pre-diagnostic circulating sex steroid hormone measurements and DTC risk may provide additional insight.