Annual Meeting of the NCI Cohort Consortium (Abstract Submission)

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# Created User IP address First Name Middle Initial Last Name Degree(s) Position/Title/Career Status Organization Email List of Additional Authors Abstract Title Abstract Operations
5 Fri, 07/10/2026 - 12:21 Anonymous 10.208.24.52 Devendra Paudel Ph.D NIH T32 Post-doctoral scholar Johns Hopkins University dpaudel1@jh.edu
  • First Name: Devendra
    Last Name: Paudel
    Degrees: PhD
    Affiliation: Department of Environmental Health and Engineering, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
  • First Name: Haonan
    Last Name: Li
    Degrees: PhD
    Affiliation: Department of Environmental Health and Engineering, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
  • First Name: Daisy
    Last Name: Brumit
    Degrees: PhD
    Affiliation: Department of Environmental Health and Engineering, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
  • First Name: Catherine
    Last Name: Mullins
    Affiliation: Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA
  • First Name: Aryan
    Last Name: Patel
    Affiliation: Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA
  • First Name: Douglas
    Last Name: Walker
    Degrees: PhD
    Affiliation: Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA
  • First Name: Elizabeth
    Last Name: Platz
    Degrees: PhD
    Affiliation: Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
  • First Name: Cynthia
    Last Name: Sears
    Degrees: PhD
    Affiliation: Division of Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, MD, USA
  • First Name: Kala
    Last Name: Visvanathan
    Degrees: PhD
    Affiliation: Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
  • First Name: Marsha
    Last Name: Wills-Karp
    Degrees: PhD
    Affiliation: Department of Environmental Health and Engineering, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
  • First Name: Brian
    Last Name: Huang
    Degrees: PhD
    Affiliation: Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA
  • First Name: David
    Last Name: Conti
    Degrees: PhD
    Affiliation: Department of Biostatistics & Informatics, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA
  • First Name: Lida
    Last Name: Chatzi
    Degrees: PhD
    Affiliation: Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA
  • First Name: Tanya
    Last Name: Alderete
    Degrees: PhD
    Affiliation: Department of Environmental Health and Engineering, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
 Prediagnostic plasma per- and polyfluoroalkyl substances and colorectal cancer risk: a nested case-control study in the CLUE II cohort stratified by time to diagnosis Background
Epidemiologic evidence linking per- and polyfluoroalkyl substances (PFAS) to colorectal cancer (CRC) is inconsistent, despite IARC classification of PFOA as a human carcinogen and PFOS as a possible human carcinogen. Most prior studies measured PFAS at or near diagnosis, where subclinical disease may have altered circulating concentrations, limiting interpretation of observed associations.

Methods
Within the CLUE II prospective cohort (1989 baseline), we measured 38 plasma PFAS by LC-HRMS in 208 incident CRC cases (1989–2003) and 208 matched controls (age, sex, race, smoking, BMI). Fifteen PFAS with ≥70% detection were included in continuous analyses. The prespecified primary analysis tested whether the PFAS–CRC association varied with time from blood collection to diagnosis (PFAS × time interaction). Secondary analyses evaluated individual PFAS with Benjamini-Hochberg false discovery rate correction (q < 0.05) and tumor subsite. Biomarker reduction was assessed in an independent postdiagnostic cohort of early-onset (EAO; n = 75) and late-onset (LAO; n = 79) CRC cases.

Results
Sum total PFAS showed a significant PFAS × time interaction (p = 0.002): the model-estimated odds ratio (OR) per log₂ doubling increased from 0.49 (95% CI 0.30–0.79) at 2 years to 1.63 (95% CI 1.03–2.59) at 12 years before diagnosis, crossing the null at approximately 8 years. Fourteen of 15 individual PFAS had OR > 1 at 12 years (binomial p = 0.0005); five reached FDR significance (PFOA, PFHpS, PFECHS, PFHxS, PFOS; q < 0.05). Associations were directionally consistent across tumor subsites. In the postdiagnostic EAO/LAO cohort, PFAS concentrations were lower than contemporaneous NHANES reference values (2017–2020), consistent with disease-related biomarker reduction.

Conclusions
Prediagnostic plasma PFAS concentrations were positively associated with CRC risk at long prediagnostic intervals and inversely associated at short intervals, consistent with biomarker reduction near diagnosis. These findings highlight the importance of measurement timing and warrant confirmation in larger prospective cohorts.
4 Fri, 07/10/2026 - 11:44 Anonymous 10.208.24.52 Hannah E. Guard M.S. Research Assistant IV Department of Epidemiology, Harvard T.H. Chan School of Public Health hguard@hsph.harvard.edu
  • First Name: Lia
    Last Name: De Paula Oliveria
    Degrees: M.D.
    Affiliation: Department of Pathology, Johns Hopkins University School of Medicine
  • First Name: Aidan
    Last Name: Daluiski
    Affiliation: Department of Epidemiology, Harvard T.H. Chan School of Public Health
  • First Name: Adrianna
    Last Name: Amaral de Aragao
    Degrees: M.D.
    Affiliation: Department of Pathology, Johns Hopkins University School of Medicine
  • First Name: Jane B.
    Last Name: Vaselkiv
    Degrees: M.P.H.
    Affiliation: Department of Epidemiology, Harvard T.H. Chan School of Public Health
  • First Name: Sinead
    Last Name: Flanagan
    Degrees: M.B. B.Ch B.A.O., M.P.H.
    Affiliation: Department of Histopathology and Morbid Anatomy, Trinity Translational Medicine Institute, Trinity College Dublin
  • First Name: Colleen
    Last Name: McGrath
    Degrees: M.S.
    Affiliation: Department of Epidemiology, Harvard T.H. Chan School of Public Health
  • First Name: Magdalena
    Last Name: Brinker
    Degrees: M.S.
    Affiliation: Department of Epidemiological Methods and Etiological Research, Leibniz Institute for Prevention Research and Epidemiology – BIPS and Faculty of Human and Health Sciences, University of Bremen
  • First Name: Michelangelo
    Last Name: Fiorentino
    Degrees: M.D., Ph.D.
    Affiliation: Pathology Unit, Maggiore Hospital-AUSL Bologna and Department of Experimental, Diagnostic and Specialty Medicine (DIMES), University of Bologna
  • First Name: Massimo
    Last Name: Loda
    Degrees: M.D.
    Affiliation: Department of Pathology and Laboratory Medicine, New York Presbyterian Hospital, Weill Cornell Medicine
  • First Name: Corinne
    Last Name: Joshu
    Degrees: Ph.D., M.P.H., M.A.
    Affiliation: Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health; Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins
  • First Name: Lorelei
    Last Name: Mucci
    Degrees: Sc.D., M.P.H.
    Affiliation: Department of Epidemiology, Harvard T.H. Chan School of Public Health
  • First Name: Konrad
    Last Name: Stopsack
    Degrees: M.D., M.P.H.
    Affiliation: Department of Epidemiological Methods and Etiological Research, Leibniz Institute for Prevention Research and Epidemiology – BIPS and Faculty of Human and Health Sciences, University of Bremen
  • First Name: Tamara
    Last Name: Lotan
    Degrees: M.D.
    Affiliation: Department of Pathology, Johns Hopkins University School of Medicine
 Tumor expression of ERG, PTEN, and p53 and lethal prostate cancer in two prospective cohort studies Background: Tumor biomarkers, including PTEN loss and TP53 mutations, can identify prognostic subtypes of prostate cancer. We evaluated p53 and PTEN loss with or without ERG tumor protein expression and lethal prostate cancer in two prospective cohort studies.

Methods: 1,085 participants of the Health Professionals Follow-up Study and Physicians’ Health Study diagnosed with prostate cancer (1986-2017) and treated surgically were followed for lethality (metastasis or prostate cancer death) through 2022. PTEN loss, ERG, and p53-mutations in prostate tumors were assessed using validated immunohistochemistry assays on tissue microarrays. We estimated hazard ratios (HR) and 95% confidence intervals (CI) for associations between each biomarker and lethality using Cox proportional hazards models adjusted for Gleason score, pathologic TNM stage, and the other biomarkers. We also assessed the joint association of PTEN loss and ERG with lethality. We evaluated prognostic discrimination of the biomarkers in addition to clinical factors across time using time-varying area-under-the-curve (tAUC).

Results: Over median 19 years follow-up, 113 lethal events occurred. The prevalence of each subtype was: 53% ERG-positive, 4% p53-positive, 14% complete PTEN loss (overall), 9% PTEN loss/ERG-positive, 5% PTEN loss/ERG-negative. PTEN loss (HR: 2.3, 95% CI: 1.5, 3.6) and p53 (HR: 2.9, 95% CI: 1.7, 5.1) were associated with lethal prostate cancer. PTEN loss/ERG-negative tumors had 4.3-fold higher risk of lethality (95% CI: 2.4, 7.8) compared to PTEN intact/ERG-negative tumors. The risk was not elevated in PTEN loss/ERG-positive tumors (HR: 1.3, 95% CI: 0.7, 2.3). tAUCs for p53 (0.55-0.57) and PTEN (0.59-0.65) were low. tAUCs for clinical factors ranged from 0.80 to 0.86 over time. The addition of the biomarkers did not add information for prognosis.

Conclusion/Discussion: Complete PTEN loss in ERG-negative tumors and p53 were associated with higher risk of lethal prostate cancer, but they did not meaningfully improve prediction of lethality beyond Gleason grade and stage.
3 Thu, 07/09/2026 - 14:22 Anonymous 10.208.24.52 Jessica Madrigal PhD, MS Associate Professor University of Illinois jmadri1@uis.edu
  • First Name: Caroline
    Last Name: Pruitt
    Degrees: MPH
    Affiliation: Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health
  • First Name: Jared
    Last Name: Fisher
    Degrees: Phd
    Affiliation: Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health
  • First Name: Julie
    Last Name: Palmer
    Degrees: PhD
    Affiliation: Slone Epidemiology Center, Boston University
  • First Name: Kimberly
    Last Name: Bertrand
    Degrees: PhD
    Affiliation: Slone Epidemiology Center, Boston University
  • First Name: Rena
    Last Name: Jones
    Degrees: PhD, MS
    Affiliation: Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health
 Chemical and metal emissions from industrial sources and breast cancer risk in the Black Women’s Health Study Background: Industrial facilities emit known mammary carcinogens and endocrine disrupting chemicals to air, including chemicals associated with breast cancer in epidemiological studies of post-menopausal and non-Hispanic White women. We investigated these relationships in a prospective cohort of Black women.

Methods: We used the US Environmental Protection Agency’s Toxics Release Inventory to estimate historical airborne emissions (1987-1995) of 19 chemicals and metals with prior evidence of mammary carcinogenicity and/or estrogenicity among 49,256 premenopausal and postmenopausal women enrolled (1995) in the Black Women’s Health Study. A total of 3,585 breast cancers were diagnosed through 2021. We constructed inverse distance- and wind-weighted average emissions metrics for each chemical within 2, 5 and 10km of the enrollment address. We estimated multivariable adjusted (age, region, smoking, parity, body mass index) HRs and 95% CIs for exposure tertiles (T) or quartiles (Q) in association with breast cancer risk.

Results: For cobalt exposure within 2km of the home, the HR for the highest tertile of exposure vs. non-exposed was 1.38, CI=0.97-1.98; p-trend=0.06. The association was attenuated for exposure within 5km (HRT3 vs. non-exposed=1.13, CI=0.96-1.32; p-trend=0.13) and 10km (HRT3 vs. non-exposed=1.06, CI=0.95-1.18; p-trend=0.34). For lead exposure within 2km of the home, the HR for the highest quartile versus non-exposed was 1.21, CI=0.81-1.78; p-trend=0.32; the HRs were similarly weakened at 5km and 10km. Associations with other chemicals and metals were null or lacked clear patterns.

Conclusion: Suggestive findings of increased breast cancer risk in association with relatively high air emissions of cobalt and lead from industrial sources near the home warrant further study.
2 Tue, 07/07/2026 - 17:30 Anonymous 10.208.28.70 Yilda G. Macias M.P.H. PhD Candidate Department of Epidemiology, University of Washington School of Public Health; Public Health Sciences Division, Fred Hutchinson Cancer Center ymacia29@uw.edu
  • First Name: Katie
    Last Name: O'Brien
    Degrees: Ph.D, MSPH
    Affiliation: Epidemiology Branch, National Institute of Environmental Health Sciences
  • First Name: Amanda
    Last Name: Phipps
    Degrees: Ph.D., M.P.H.
    Affiliation: Department of Epidemiology, University of Washington School of Public Health; Public Health Sciences Division, Fred Hutchinson Cancer Center
  • First Name: Caroline
    Last Name: Um
    Degrees: Ph.D., M.P.H., RD
    Affiliation: Population Science, American Cancer Society
  • First Name: Nathalie
    Last Name: Kliemann
    Degrees: Ph.D.
    Affiliation: Division of Genetics and Epidemiology, The Institute of Cancer Research
  • First Name: Dale
    Last Name: Sandler
    Degrees: Ph.D., M.P.H.
    Affiliation: Epidemiology Branch, National Institute of Environmental Health Sciences
  • First Name: Martin
    Last Name: Lajous
    Degrees: M.D., ScD
    Affiliation: Center for Research on Population Health, National Institute of Public Health, Mexico; Department of Global Health and Population, Harvard T.H. Chan School of Public Health
  • First Name: Montserrat
    Last Name: Garcia-Closas
    Degrees: M.D., M.P.H., DrPH
    Affiliation: Division of Genetics and Epidemiology, The Institute of Cancer Research
  • First Name: Amy
    Last Name: Berrington de Gonzalez
    Degrees: Ph.D.
    Affiliation: Division of Genetics and Epidemiology, The Institute of Cancer Research
  • First Name: Holly
    Last Name: Harris
    Degrees: ScD, M.P.H.
    Affiliation: Department of Epidemiology, University of Washington School of Public Health; Public Health Sciences Division, Fred Hutchinson Cancer Center
 Polyendocrine metabolic ovarian syndrome and pancreatic cancer risk: A pooled analysis across four prospective cohorts Background: Despite sharing several risk factors, the association between pancreatic cancer and polyendocrine metabolic ovarian syndrome (PMOS), a common endocrinopathy affecting 8-13% of reproductive-aged individuals, remains understudied. Insulin resistance, reported in 35-80% of individuals with PMOS and compounded by obesity and type 2 diabetes, represents one plausible shared mechanism. Three retrospective studies reported a positive association between PMOS and pancreatic cancer, but findings were limited by small sample sizes, single-timepoint covariate assessment, and inconsistent exposure classification.

Methods: We will utilize participant data from over 400,000 women across four prospective cohorts: the Sister Study (SIS), the Cancer Prevention Study-3 (CPS-3), the Mexican Teachers Cohort (MTC), and the Generations Study (GS). Incident pancreatic cancers were identified via self-reports, registry linkage, and mortality records. To capture a broader range of PMOS presentations, we will consider four exposure definitions: self-reported PMOS, menstrual cycle irregularity (MCI), either condition, or both conditions. Pooled logistic regression with one-year intervals will be used to estimate odds ratios and 95% confidence intervals, adjusting for time-varying covariates selected a priori based on established PMOS and pancreatic cancer associations. Cohort-specific estimates will be meta-analyzed to assess heterogeneity prior to pooling.

Results: Cohort-specific analyses have been completed for SIS and CPS-3. In SIS, all four exposures showed suggestively positive associations with pancreatic cancer risk (OR range = 1.33 – 1.43). In CPS-3, PMOS and the combined exposure could not be evaluated due to low numbers of PMOS-exposed pancreatic cancer cases; associations were null to weakly positive across MCI and either condition (OR range = 1.07 – 1.12).

Discussion: To our knowledge, this will provide the first prospective evaluation of PMOS and pancreatic cancer risk. Findings may inform risk stratification efforts for individuals with PMOS, a population disproportionately burdened by metabolic comorbidities and underrepresented in epidemiologic research.
1 Tue, 06/09/2026 - 12:45 Anonymous 10.208.24.28 Carissa Grose n/a Interim Co-director of the Protein Expression Laboratory Frederick National Laboratory for Cancer Research carissa.grose@nih.gov
  • First Name: William
    Last Name: Burgan
    Degrees: MS, PMP
    Affiliation: Frederick National Laboratory for Cancer Research
 Protein Expression Laboratory Services at Frederick National Laboratory for Cancer Research The Protein Expression Laboratory Services at Frederick National Laboratory for Cancer Research generates DNA, cell line, and protein reagents for biomedical research from basic science to drug discovery. The team uses cutting-edge protein production technologies to generate proteins using bacteria, insect cells, or mammalian cells at scales from micrograms to grams.