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Anne Eaton

Anne Eaton

· Assistant ProfessorVerified

University of Minnesota · Biostatistics & Health Data Science

Active 1962–2026

h-index36
Citations3.5k
Papers20688 last 5y
Funding
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About

Anne Eaton, PhD, MS, is an Assistant Professor in the Division of Biostatistics & Health Data Science at the School of Public Health, University of Minnesota. She develops statistical methods to understand processes happening over time that cannot be observed completely due to complex observation and/or censoring processes. Her work is driven by common issues arising in cancer research, including multiple related time-to-event endpoints and data collection schedules that differ across patients. In her methodological and collaborative work, she strives to translate data into information that is meaningful to researchers, doctors, and patients. Her expertise includes survival analysis, multistate models, non-parametric methods, and clinical trial design. Dr. Eaton is a member of the Masonic Cancer Center and has been recognized with the Delta Omega Honorary Society in Public Health in 2020. She holds a PhD and MS in Biostatistics from the University of Minnesota and a BA in Mathematics from Grinnell College. She teaches in the Biostatistics (MPH, MS, PhD) program at the School of Public Health.

Research topics

  • Internal medicine
  • Medicine
  • Machine Learning
  • Oncology
  • Computer Science
  • Statistics
  • Immunology
  • Mathematics

Selected publications

  • Body mass index and waist-hip ratio – Risk factors for aortic valve disease: The atherosclerosis risk in communities (ARIC) study

    American Journal of Preventive Cardiology · 2026-04-01

    articleOpen access

    Elevated body mass index (BMI) has been associated with increased risk of aortic valve stenosis (AS) in observational and Mendelian randomization studies; however, its association, and that of waist-hip ratio (WHR), with aortic valve insufficiency (AI) remains unclear. We investigated the association of BMI and WHR with incident aortic valve disease (AVD) in the ARIC Study. We analyzed ARIC participants with echocardiograms at Visits 5 (2011-13) and 7 (2018-19). BMI and WHR were assessed at Visit 5. Incident AVD between Visits 5 and 7 was categorized as aortic valve sclerosis, AI without stenosis, and AS. Multinomial regression models were employed. Among 1,931 participants (mean age of 73.5 ± 4.2 years, 59.7% female, and 23.2% Black), 572 (29.6%) developed AVD (345 aortic valve sclerosis, 159 AI, and 68 AS). Higher BMI was associated with a greater incidence of aortic valve sclerosis (OR: 1.29 per 1-SD (5.08 kg/m2), 95% CI: 1.13-1.48) and AS (OR: 1.28, 95% CI: 1.00-1.63), but not AI (OR: 0.93, 95% CI: 0.75-1.14). Higher WHR was associated with an increased risk of incident aortic valve sclerosis (OR: 1.17 per 1-SD (0.079), 95% CI: 1.00-1.35), AS (OR: 1.44, 95% CI: 1.11-1.85), and also AI (OR: 1.24, 95% CI: 1.01-1.53). Higher BMI is a risk factor for incident aortic valve sclerosis and AS, but not AI. Greater WHR is a risk factor not only for incident aortic valve sclerosis and AS, but also for incident AI. Avoiding abdominal obesity may prevent non-rheumatic AVD in older adults.

  • 08-1: MOST PATIENTS RETAIN ISLET FUNCTION >5 YEARS POST-TPIAT: DATA FROM THE LONG-TERM ISLET FUNCTION AND IMPACT AFTER TPIAT (LIFT) STUDY

    Transplantation · 2025-06-01

    article

    Introduction: In the LIFT study, we are rigorously assessing islet function and glycemic physiology in patients 5-20 years out from TPIAT. Methods: Patients who had TPIAT 5-20 years prior underwent islet function testing with a 4-hour frequently sampled mixed meal tolerance test (MMTT, BoostHP). Other measures included HbA1c, continuous glucose monitoring (CGM), and insulin dose. We compared area under the curve (AUC) glucose and AUC C-peptide from MMTT, HbA1c, insulin dose, and CGM data in patients categorized by (1) insulin independent, (2) partial islet graft function (defined by C-peptide ≥0.6 ng/mL but on insulin); and (3) islet graft failure (C-peptide <0.6 ng/mL and on insulin). Results: To date, we have enrolled a representative sample of 122 patients post-TPIAT. Participants were 49 (IQR 33, 54) years old at time of study, 75% female, with a duration of 9.5 (6.9, 12.0) years post-TPIAT, transplanted IEQ/kg of 4,022 (2,849, 5,475). At the time of study, 39 (32%) were insulin independent, 73 (60%) had partial islet function, and only 10 (8%) had islet graft failure. Transplanted islet mass was highest in the insulin independent and lowest in islet failure (p=0.004). HbA1c was <7% in 92%, 47%, and 20% of insulin independent, partial islet function, and islet failure respectively (p<0.001). Time in range (TIR, 70-180 mg/dL) on CGM was 95% (89, 97%) for insulin independent, 67% (52, 82%) for partial function, vs 45% (38, 63%) for those with graft failure (p<0.001) (Table). AUC C-peptide was lowest for islet graft failure, with increasing C-peptide levels in partial function and insulin independent; AUC glucose was lowest in insulin independent. (Figure)Conclusions: >90% of representative TPIAT patients had islet function ~10 years after TPIAT, supporting long-term benefit of IAT. CGM data, HbA1c, and MMTT support better glycemic control with islet function (insulin independent or partial function) vs failed islets.

  • Supplementary Figure S2 from Human Effectors of Acute and Chronic GVHD Overexpress CD83 and Predict Mortality

    2025-11-25

    articleOpen access

    &lt;p&gt;Clinical outcomes based on grade II-IV acute GVHD or frequency of circulating CD83, CD4 T cells&lt;/p&gt;

  • Predictors of Diabetes Outcomes at 1 year after Islet Autotransplantation: Data from a Multicenter Cohort Study

    2025-07-09

    preprintOpen access

    &lt;p dir="ltr"&gt;Objective Total pancreatectomy with islet autotransplantion (TPIAT) may relieve pain for patients with intractable recurrent acute or chronic pancreatitis. In this first multicenter cohort study of TPIAT, we aimed to identify predictors of favorable diabetes outcomes following TPIAT to aid in surgical counseling and decision making.&lt;/p&gt;&lt;p dir="ltr"&gt;Research Design and Methods We included 384 patients (mean age 29.6 (SD 17.1) years; 61.7% female) who underwent TPIAT and were enrolled in the NIH-sponsored multicenter Prospective Observational Study of TPIAT (POST). Outcomes are reported for insulin use, HbA1c, and islet graft function. Univariable and multivariable modelling was performed to evaluate predictors of diabetes outcomes after TPIAT. &lt;/p&gt;&lt;p dir="ltr"&gt; Results At one year post-TPIAT, 83% of patients retained islet function (c-peptide &gt;0.3ng/ml), 20% were off insulin, and 60% had HbA1c &lt;7%. Outcomes were most favorable in those with normoglycemia pre-TPIAT and in children. In multivariable analysis, insulin independence at one year was associated with pediatric age (OR 2.3, 95% CI: 1.3–4.3 vs adults) and pre-transplant HbA1c (OR 4.0 (95% CI: 1.7-9.1) per 1% decrease HbA1c). The odds of achieving a goal HbA1c &lt;7% was associated with white race (OR 4.3 (1.7-11)) and pre-TPIAT HbA1c (OR 2.2 (1.1- 4.3) per 1% decrease). Islet graft function was associated with pre-TPIAT fasting C-peptide (OR 2.18 (1.42, 3.35) per 1 ng/mL increase) and baseline HbA1c (OR 1.89 (1.18-3) per 1% decrease). &lt;/p&gt;&lt;p dir="ltr"&gt;Conclusions Normoglycemic patients and children more often were off insulin. In multivariable models, pre-TPIAT HbA1c was strongly predictive of insulin independence, islet function, and HbA1c&lt;7% at 1 year.&lt;/p&gt;

  • Supplementary Figure S6 from Human Effectors of Acute and Chronic GVHD Overexpress CD83 and Predict Mortality

    2025-11-25

    articleOpen access

    &lt;p&gt;Targeting CD83 in human AML&lt;/p&gt;

  • Association of Left Atrial Function With Mitral Regurgitation: The Atherosclerosis Risk in Communities Study

    Journal of the American Heart Association · 2025-08-12

    articleOpen access

    BACKGROUND: Lower left atrial (LA) function may precede LA enlargement and contribute to mitral regurgitation (MR). We examined the association of LA reservoir strain (a measure of LA function) with MR in the ARIC (Atherosclerosis Risk in Communities) study. METHODS: We analyzed ARIC participants with echocardiograms at Visits 5 (2011-2013) and 7 (2018-2019). LA reservoir strain was measured at Visit 5. MR was diagnosed by echocardiography. The cross-sectional association was assessed at Visit 5, and the prospective association was examined through Visit 7 using multivariable logistic regression. RESULTS: In the cross-sectional analysis (n=4689, mean age 75.2±5.0 years, 60.2% female, 19.9% Black), 1927 participants (41.1%) had prevalent MR. Each 1-SD (7.53%) lower LA reservoir strain was associated with higher odds of prevalent MR (odds ratio [OR], 1.12 [95% CI, 1.04-1.20]). In the prospective analysis (n=1480, mean age 73.5±4.2 years, 54.9% female, 22.6% Black), 409 participants developed MR. A 1-SD (6.71%) lower LA reservoir strain was associated with higher odds of incident MR (OR, 1.18 [95% CI, 1.04-1.34]); the association was partially attenuated after adjusting for post-Visit 5 heart failure and atrial fibrillation (OR, 1.14 [95% CI, 1.00-1.30]) and further attenuated after adjusting for LA volume index from Visit 5 (OR, 1.11 [95% CI, 0.98-1.27]). CONCLUSIONS: LA reservoir strain is associated with prevalent and incident MR in older adults. The association between lower LA reservoir strain and incident MR may be partially explained by LA enlargement, apart from atrial fibrillation and heart failure.

  • 805 Bone density and cystic fibrosis in the world of highly effective modulator therapy: increasing screening rates in our adult cystic fibrosis clinic

    Journal of Cystic Fibrosis · 2025-10-01

    articleOpen accessSenior author
  • CD83 CAR T overcome CD19 antigen loss in B cell malignancies after CD19-directed therapy

    Blood · 2025-11-03

    articleOpen access

    Abstract Chimeric antigen receptor T cells (CAR T) targeting CD19 can cure approximately a third of patients with aggressive B cell malignancies, but relapse due to CD19 antigen loss and serious infections resulting from B cell aplasia remain major causes of death following CD19 CAR T. Here, we demonstrate that CD83 is a clinically relevant target for CAR T therapy in patients with B cell malignancies and that CD83 CAR T can effectively kill tumors even in the context of CD19 antigen loss. CD83 was highly expressed on B cell acute lymphoblastic leukemia (ALL; n=40, 43% of lymphoblasts CD83+), mantle cell lymphoma (MCL; n=5, 69% of lymphoma cells CD83+), and diffuse large B cell lymphoma (DLBCL; n=2, 80% of lymphoma cells CD83+), yet low on healthy B cells (16% of B cells CD83+; n=9 healthy donors). In contrast, CD19 was expressed on B cell malignancies and circulating B cells alike (96-100% of leukemia/lymphoma or B cells CD19+). Focusing on ALL, CD83 antigen density was 10 times lower than CD19 (1051 vs 10882 MESF, ANOVA, P=0.0001), but similar to CD20 or CD22. Therefore, CD83 CAR T therapy for B cell leukemia or lymphoma carries a low risk for B cell aplasia and related infectious complications, otherwise observed with CD19 CAR T. In a cohort of B ALL patients treated with CD19-directed therapy (n=6, including brexucabtagene autoleucel or blinatumomab), CD19 antigen expression on lymphoblasts was significantly reduced upon relapse. Conversely, CD83 antigen was well expressed on B ALL lymphoblasts at diagnosis and relapse (99% to 24% of lymphoblasts CD19+, P=0.0012; 30% to 48% of lymphoblasts CD83+, P=0.3918, mixed-effects analysis). B ALL CD19 expression is susceptible to selective pressure when subjected to anti-CD19 therapy, like CAR T or bispecific engagers. The persistent expression of CD83 on B ALL lends itself toward a form of targeted rescue therapy. CD83 CAR T effectively killed Raji (94.1% of cells CD83+) and Nalm6 (99.4% of cells CD83+) cell lines, often outperforming CD19 CAR T, especially against CD19 knock-out Raji targets. When cocultured with Raji target cells, CD83 CAR T produced more IFNγ (2665 v 3319 pg/ml, P=0.0001) and less IL-6 (53 v 20 pg/ml, P=0.0001) than CD19 CAR T. Thus, the target cell-stimulated CD83 CAR T displayed a cytokine profile favoring potency over toxicity, compared to CD19 CAR T. The CD83 CAR T product consisted of a rich central memory population and expressed significantly less PD-1, suggesting a propensity toward durable persistence and resistance to exhaustion. In NSG mice bearing luciferase-transduced Raji tumors, CD19 or CD83 CAR T monotherapy significantly extended survival compared to untreated mice (n=7-8 mice per group, median survival 24 vs 51.5 [P=0.0003] or 40.5 [P=0.0035] days, respectively). To mimic the expected clinical scenario of using CD83 CAR T in an era of commercial cell products, we tested the sequential use of CD83 CAR T after the initial infusion of CD19 CAR T in the Raji model. The sequential CD19=&amp;gt;CD83 CAR T approach resulted in superior mouse survival compared to either cell product alone (median survival undefined at 60 days, with 75% of mice alive, P=0.03, Log-rank test). Sequential CD19=&amp;gt;CD83 CAR T cleared the tumor burden in treated mice by day +48. Our preclinical evidence justifies further translational investigation of CD83 CAR T in B cell leukemia and lymphoma, as a strategy to overcome the complications of B cell aplasia and CD19 antigen loss.

  • Supplementary Figure S4 from Human Effectors of Acute and Chronic GVHD Overexpress CD83 and Predict Mortality

    2025-11-25

    articleOpen access

    &lt;p&gt;Human CD83 cell surface tissue microarray (TMA)&lt;/p&gt;

  • Integrated CTC- and EV-based detection of PSMA protein and efficacy of <sup>177</sup> Lu-PSMA-617 radioligand therapy.

    Journal of Clinical Oncology · 2025-05-28 · 1 citations

    article

    5083 Background: Blood-based predictive biomarkers of sensitivity to 177 Lu-PSMA-617 are lacking, and may facilitate clinical decisions. Here, we studied whether integrated PSMA protein detection in circulating tumor cells (CTCs) and extracellular vesicles (EVs) is associated with outcomes in patients receiving 177 Lu-PSMA therapy. Methods: We enrolled 100 metastatic castrate-resistant prostate cancer (mCRPC) pts who were candidates for 177 Lu-PSMA into a prospective biomarker trial. Blood samples were collected for CTC and EV analysis at baseline, at the time of response, and at progression. Baseline characteristics included serum PSA, alkaline phosphatase (ALP), hemoglobin, albumin, and radiographic tumor burden. PSMA+ CTCs were enumerated using an AI-empowered holographic imaging platform combined with in-flow protein marker analysis (Astrin Biosciences, St. Paul, MN); PSMA protein was quantified in plasma EVs using shotgun proteomics via mass spectrometry (Arafa et al., Cancers 2024; 16: 4261). We assessed the impact of PSMA+ CTCs and EV-derived PSMA protein on PSA 50 responses, PFS, and OS. Multivariable Cox regressions were used to adjust for baseline PSA, ALP, and hemoglobin. Exploratory analyses of other EV-derived proteins were also conducted. Results: Of 100 enrolled pts, 47% had Gleason sum 9-10, 62% had &gt;10 bone mets, 12% had visceral mets, 72% had received ≥3 prior systemic therapies, and median PSA was 57 (range 1.5–5,000) ng/mL. High PSMA+ CTC counts (&gt; median) were associated with shorter overall survival (OS) (HR 2.71, 95%CI 1.18–6.21, p=0.02). PSA 50 response rates were similar for those with high and low PSMA+ CTC counts (39% vs 42%, p=0.8). Shotgun proteomics from plasma EV samples identified &gt;11 000 unique proteins, of which 12% represented the cell surfaceome. EV-PSMA protein correlated with baseline PSA, ALP, and tumor burden (all p&lt;0.05). High EV-PSMA protein (&gt; median) was associated with worse OS (1.81, 95%CI 0.97–3.35, p=0.06). PSA 50 response rates were similar for those with high and low EV-PSMA protein (48% vs 42%, p=0.5). After multivariate adjustment, nonsignificant trends for shorter OS persisted for pts with high PSMA+ CTCs (HR 1.71, 95%CI 0.72–4.05) and high EV-PSMA levels (HR 1.49, 95%CI 0.78–2.84). Worse OS was also observed in pts with high EV levels of B7-H3 (HR 2.85, 95%CI 1.58–5.14, p=0.002), Trop-2 (HR 2.23, 95%CI 1.22–4.05, p=0.008), and STEAP1 (HR 1.69, 95%CI 0.93–3.06, p=0.08) proteins. Conclusions: In mCRPC pts receiving 177 Lu-PSMA, high PSMA+ CTC counts and high EV-derived PSMA levels portended poor survival. PSMA protein may be a novel blood-based biomarker of 177 Lu-PSMA sensitivity, facilitating treatment decisions, with relevance for other PSMA-targeting strategies. The robust detection and prognostic impact of additional cell-surface proteins ( e.g. B7-H3, Trop-2, STEAP1) may fuel the development of alternative novel therapeutics.

Frequent coauthors

  • Srinath Chinnakotla

    University of Minnesota Medical Center

    176 shared
  • Gregory J. Beilman

    176 shared
  • Timothy L. Pruett

    University of Minnesota

    176 shared
  • Guru Trikudanathan

    University of Minnesota

    176 shared
  • Sarah Jane Schwarzenberg

    University of Minnesota Children's Hospital

    176 shared
  • Martin L. Freeman

    176 shared
  • Jaimie D. Nathan

    176 shared
  • Timothy B. Gardner

    Dartmouth–Hitchcock Medical Center

    175 shared

Education

  • Ph.D., Public Health

    University of Minnesota

    2000
  • M.S., Public Health

    University of Minnesota

    1995

Awards & honors

  • Delta Omega, Honorary Society in Public Health, 2020
  • Member, Masonic Cancer Center (MCC)
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