Graham A. Colditz

Association between diabetic control and progression of monoclonal gammopathy of undetermined significance to multiple myeloma

Spatial mapping of fibroblast subtypes in primary colorectal cancer.

Standardized mean differences of primary outcomes found in randomized controlled trials of wellness interventions among medical trainees: A systematic review and meta-analysis.

Generalizability of an AI-based mammogram risk score (MRS) for breast cancer among diverse populations of women

Transcriptome predictors of second breast events in ductal carcinoma in situ: a case‒control study including Black and White women

Colditz

A Framework for Aligning 5-Year and Lifetime Breast Cancer Risk in Women Without High-Penetrance Mutations.

Spatial Mapping of the Precancer-to-Cancer Transition in Breast and Prostate

Identification of cycling regulatory T cell precursors as conductors of immune escape during breast carcinoma progression

Immune escape during the ductal carcinoma in situ (DCIS)-to-invasive breast cancer (IBC) transition shapes tumor evolution. Through transcriptomic mapping of the immune landscapes of normal breast, DCIS, and IBC from large patient cohorts, we identified T and myeloid cells as the primary distinguishing features between DCIS and IBC. We discovered cycling regulatory T cells (cycTreg) as an orchestrator of immunosuppression in IBC. cycTreg frequency predicts cytotoxic CD8 + , TCR diversity, disease-specific survival in IBC, and recurrence in DCIS. In a rat model of breast cancer, we demonstrated that cycTreg act as precursors to mature Treg and are inducible by tumor-localized type 2 dendritic cells. Profiling of tumors subjected to αOX40 and αPD-L1 therapies revealed an IL-33-mediated fibroblast-cycTreg signaling loop, the disruption of which enhances intratumoral antigen-experienced CD8 + effectors and systemic immunosurveillance. Our study defines cycTreg as critical inducers of immune escape and promising immuno-oncology targets in breast cancer.

Reliability of Stromal Markers Immunofluorescent Staining in Breast Tissue Assessment

Refined breast cancer risk model achieves a 0.68 C-index in women with benign breast disease.

Accelerating discovery of cancer causes for prevention in the era of rising early-onset cancers

Cancer in younger adults is rising globally, with notable birth-cohort effects. This epidemiological shift underscores the urgent need to accelerate the identification of novel causes and underlying biological networks, with the aim of translating these insights into prevention and interception strategies. In this perspective, we revisit the major milestones in the discovery of cancer causes and outline challenges that hinder progress. To address these challenges, we advocate closer integration of epidemiologic and mechanistic studies and propose three interconnected frameworks that extend current epidemiologic approaches: a tissue ecosystem-anchored framework for cancer cause discovery, a biological state-based framework for precision cancer risk assessment, and a dynamic framework to characterize cancer preventability. This roadmap aims to stimulate conceptual, resource, and methodological advances to accelerate cancer etiology research and prevention in the era of rising early-onset cancers.

Quantifying the contribution of modifiable risk factors for progression of MGUS to multiple myeloma in a Veteran population

Personalizing cancer risk: a systematic review of risk communication strategies

Efficacy of Interventions for Newly Diagnosed Multiple Myeloma: An Umbrella Review.

Each 1 percentage point increase in body fat percentage was associated with a 4% higher odds of prevalent MGUS (aOR 1.04; 95% CI 1.01-1.07).

Subsequent breast cancer risk after benign biopsy in racially diverse women: Siteman Cancer Center

Differential life expectancies and life years lost associated with multiple myeloma in the United States: a simulation modelling study

Overestimation of multiple myeloma survival from cancer registry data

Adherence to healthy dietary patterns and risk of premature aging in adult survivors of childhood cancer in the St. Jude Lifetime Cohort Study

Background Adult survivors of childhood cancer are at higher risk of premature aging compared to their cancer‐free peers due to the cancer and its treatments. However, little is known about the effect of adherence to healthy dietary patterns on aging in childhood cancer survivors. Methods A cross‐sectional analysis was conducted of 3322 participants (mean age, 30.5 years; standard deviation [SD], 8.4) from the St. Jude Lifetime Cohort Study. Diet was measured by a food frequency questionnaire and used to assess the Healthy Eating Index (HEI)‐2015 and alternate Mediterranean diet (aMED) scores. Premature aging was assessed by the deficit accumulation index and categorized into low, medium, and high risk. Multinomial logistic regressions adjusting for confounders were used to estimate odds ratios (ORs) with 95% confidence intervlas (CIs). Results The mean (SD) HEI‐2015 score was 60.0 (10.9) of 100, and the aMED score was 4.2 (2.0) of 9. Twenty percent and 8% of survivors were in the medium and high deficit accumulation index categories, respectively. Higher adherence to HEI‐2015 (OR high vs. low = 0.80; 95% CI, 0.69–0.93 per 10‐point increment) and aMED (OR high vs. low = 0.91; 95% CI, 0.84–0.98 per 1‐point increment) were associated with a lower risk of premature aging. The associations remained consistent among survivors who received radiation or chemotherapy. Conclusion Adherence to a healthy diet may contribute to reducing the premature aging risk in adult survivors of childhood cancer. Interventions that support healthy eating in this population could potentially have benefits for long‐term health outcomes.

Investigating the relationship between breast cancer risk factors and an AI-generated mammographic texture feature in the Nurses’ Health Study II

The mammogram risk score (MRS), an AI-driven mammographic texture feature, strongly predicts breast cancer risk independently of breast density, though underlying mechanisms remain unclear. Using data from the Nurses' Health Study II (292 cases, 561 controls), we validated MRS's association with breast cancer and evaluated its relationships with established breast cancer risk factors through observational analyses, polygenic score analyses, and Mendelian randomization. MRS was significantly associated with breast cancer risk before (OR=1.92 per SD increase; 95% CI:1.57 to 2.35; 10-year AUC=0.69) and after adjustment for predicted BI-RADS density (OR=1.85; 95% CI:1.49 to 2.30). Early life body size and adult body mass index (BMI) were inversely associated with MRS, while benign breast disease history and predicted BI-RADS density showed positive associations; after adjusting for density, associations between MRS and the other three risk factors were attenuated. Polygenic score analyses and Mendelian randomization consistently demonstrated significant positive associations between genetic predictors of breast density measures (dense area, percent density, predicted BI-RADS density) and MRS. After adjusting for predicted BI-RADS density and BMI, genetic predictors of higher waist-to-hip ratio were significantly associated with increased MRS. Our findings reveal robust associations between breast density measures and MRS and suggest a potential impact of central obesity on MRS. Future larger-scale validation studies are needed.