Meira Epplein

Overview:

Meira Epplein is a cancer epidemiologist interested in modifiable risk factors in under-served populations, with a focus on the association of infection and cancer.  She became Co-Leader of Cancer Control and Population Sciences at Duke Cancer Institute and Associate Professor of Population Health Sciences in the Duke University Medical Center in May of 2017.  Previously, she was a tenured faculty member at Vanderbilt University Medical Center, after two years as a post-doctoral fellow with the Multiethnic Cohort Study at the University of Hawaii.  Prior to earning her PhD in epidemiology from the University of Washington, she completed an MA in international studies, and spent five years as a program officer for the Asian research think tank, the National Bureau of Asian Research.

Dr. Epplein’s research program has centered around the bacteria Helicobacter pylori, a spiral, gram-negative bacterium that infects approximately 50% of the world’s population, and is the leading carcinogenic infectious agent according to the International Agency for Research on Cancer.  Her research seeks to understand the heterogeneity of H. pylori, to determine the most toxigenic forms of the bacteria so to identify the highest risk populations which can then be targeted for antibiotic therapy, which has been shown to be effective for risk reduction. At the same time, she is committed to furthering our understanding of the co-factors involved in both H. pylori-associated disease risk and benefit, as the bacteria has inhabited the stomachs of humans for over 100,000 years, and so very likely also confers certain biological advantages to its hosts.

As Principal Investigator, she has obtained three large NIH-funded grants to further explore the epidemiology of H. pylori heterogeneity: a 5-year career development award (K07) from NCI that focuses on infection, inflammation, and cancer; a 5-year R01 from NCI to develop an H. pylori blood biomarker for gastric cancer risk in East Asia; and a 4-year R01, again funded by NCI, to further investigate, in a large consortium of prospective cohorts across the United States, the novel preliminary finding of H. pylori protein-specific antibodies and the risk of colorectal cancer. She also serves as a Co-Investigator and lead gastric cancer and H. pylori researcher for the Southern Community Cohort Study (SCCS). In addition to serving as a standing member of the study section NCI Subcommittee J (Career Development Awards), she is an editorial board member of the journal Cancer Epidemiology, Biomarkers & Prevention, and is co-chair of the 2017 American Society of Preventive Oncology Annual Meeting Program Committee. 

Area of expertise: Epidemiology

Positions:

Associate Professor in Population Health Sciences

Population Health Sciences
School of Medicine

Associate Professor in Medicine

Medicine, Medical Oncology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

M.A. 1997

University of Washington

M.S. 2005

University of Washington

Ph.D. 2007

University of Washington

Grants:

Helicobacter pylori protein-specific antibodies and colorectal cancer risk

Administered By
Duke Cancer Institute
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

Publications:

An Approach to the Primary and Secondary Prevention of Gastric Cancer in the United States.

BACKGROUND & AIMS: Gastric cancer (GC) remains a leading cause of mortality among certain racial, ethnic, and immigrant groups in the United States (US). The majority of GCs are diagnosed at advanced stages, and overall survival remains poor. There exist no structured national strategies for GC prevention in the US. METHODS: On March 5-6, 2020 a summit of researchers, policy makers, public funders, and advocacy leaders was convened at Stanford University to address this critical healthcare disparity. After this summit, a writing group was formed to critically evaluate the effectiveness, potential benefits, and potential harms of methods of primary and secondary prevention through structured literature review. This article represents a consensus statement prepared by the writing group. RESULTS: The burden of GC is highly inequitably distributed in the US and disproportionately falls on Asian, African American, Hispanic, and American Indian/Alaskan Native populations. In randomized controlled trials, strategies of Helicobacter pylori testing and treatment have been demonstrated to reduce GC-specific mortality. In well-conducted observational and ecologic studies, strategies of endoscopic screening have been associated with reduced GC-specific mortality. Notably however, all randomized controlled trial data (for primary prevention) and the majority of observational data (for secondary prevention) are derived from non-US sources. CONCLUSIONS: There exist substantial, high-quality data supporting GC prevention derived from international studies. There is an urgent need for cancer prevention trials focused on high-risk immigrant and minority populations in the US. The authors offer recommendations on how strategies of primary and secondary prevention can be applied to the heterogeneous US population.
Authors
Huang, RJ; Epplein, M; Hamashima, C; Choi, IJ; Lee, E; Deapen, D; Woo, Y; Tran, T; Shah, SC; Inadomi, JM; Greenwald, DA; Hwang, JH
MLA Citation
Huang, Robert J., et al. “An Approach to the Primary and Secondary Prevention of Gastric Cancer in the United States.Clin Gastroenterol Hepatol, Oct. 2021. Pubmed, doi:10.1016/j.cgh.2021.09.039.
URI
https://scholars.duke.edu/individual/pub1498553
PMID
34624563
Source
pubmed
Published In
Clinical Gastroenterology and Hepatology : the Official Clinical Practice Journal of the American Gastroenterological Association
Published Date
DOI
10.1016/j.cgh.2021.09.039

Risk factors for gastric cancers in the United States: Variation by anatomic site and race/ethnicity.

<jats:p> 189 </jats:p><jats:p> Background: Gastric cancer (GC) is a high mortality cancer in the US. Differences in risk factors by anatomic location and race/ethnicity have been suggested but remain understudied in the US population. Methods: The Multiethnic Cohort (MEC) is a prospective cohort study that collected data on 5 racial/ethnic groups [Whites (W), Blacks (B), Latino (L), Japanese-American (JA), and Hawaiian (HA)] from Hawaii and Los Angeles in 1993-1996. Participants completed a detailed baseline survey and were followed for development of incident cancer. Cox regression models were used to calculate hazard ratios (HR) and 95% confidence intervals (CI) to identify GC risk factors by anatomic location (cardia, non-cardia) and by race/ethnicity. Results: Data from 192,626 participants was available. The cohort was 25% W, 17% B, 23% L, 28% JA, and 7% HA. During a median follow up of 20.3 years, 1,109 non-cardia and 201 cardia incident GCs were diagnosed. Older age (per year, non-cardia HR 1.08, 95% CI 1.07-1.92; cardia HR 1.06, 95% CI 1.05-1.09), male sex (non-cardia HR 1.6, 95% CI 1.4-1.8; cardia HR 3.0, 95% CI 2.1-4.4), and current (non-cardia HR 1.7, 95% CI 1.5-2.2, cardia HR 3.4, 95% CI 2.2-5.3) or former (non-cardia HR 1.3, 95% CI 1.1-1.5; cardia HR 2.0, 95% CI 1.3-2.9) smoking were associated with both cancer types. Notably, race/ethnicity (ref W: B HR 3.0, 95% CI 2.2-4.0; L HR 2.5, 95% CI 1.8-3.3; JA HR 3.9, 95% CI 3.0-5.1; HA HR 3.9, 95% CI 2.8-5.5), foreign-born (ref: self &amp; parents US born: HR 1.3 95% CI 1.1-1.7), and family history of GC (OR 1.9, 95% CI 1.5-2.3) were associated with non-cardia GC. BMI ≥30 (HR 1.6, 95% CI 1.1-2.3), having ≥1 drink/week (HR 1.6, 95% CI 1.1-2.3), and being JA (ref W: HR 1.9, 95% CI 1.2-2.9) were associated with cardia GC. Risk factors other than age differed by race/ethnicity for non-cardia GC. Male sex was a risk factor for B, L and JA only. Having less than a high school education was a risk factor for B and JA only, smoking a risk factor for L and JA only, and having diabetes a risk factor for B only. Being in the highest sodium intake quartile was a risk factor among W and HA. A family history of GC was a risk factor for W, L, and JA. Having foreign-born parents was a risk factor for W and being foreign-born was a risk factor for JA. Conclusions: GC risk factors differ between subtypes and, for non-cardia, between race/ethnic groups. These differences provide an insight into the etiology of GC and the disproportionate incidence rates in high-risk groups, potentially aiding in the design of targeted intervention strategies. </jats:p>
Authors
In, H; Friedmann, P; Sarkar, S; Rapkin, B; Castle, PE; Epplein, M
MLA Citation
In, Haejin, et al. “Risk factors for gastric cancers in the United States: Variation by anatomic site and race/ethnicity.Journal of Clinical Oncology, vol. 39, no. 3_suppl, American Society of Clinical Oncology (ASCO), 2021, pp. 189–189. Crossref, doi:10.1200/jco.2021.39.3_suppl.189.
URI
https://scholars.duke.edu/individual/pub1480814
Source
crossref
Published In
Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology
Volume
39
Published Date
Start Page
189
End Page
189
DOI
10.1200/jco.2021.39.3_suppl.189

Association of Combined Sero-Positivity to Helicobacter pylori and Streptococcus gallolyticus with Risk of Colorectal Cancer.

Previously, we found that risk of colorectal cancer (CRC) is increased in individuals with serum antibody response to both Helicobacter pylori (HP) Vacuolating Cytotoxin (VacA) toxin or Streptococcus gallolyticus (SGG) pilus protein Gallo2178. In the present analysis, we tested the hypothesis that combined seropositivity to both antigens is a better indicator of CRC risk than seropositivity to single antigens. We used multiplex serologic assays to analyze pre-diagnostic serum for antibody responses from 4063 incident CRC cases and 4063 matched controls from 10 US cohorts. To examine whether combined SGG Gallo2178 and HP VacA sero-status was associated with CRC risk, we used conditional logistic regression models to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Compared to dual sero-negative individuals, there was no increased risk for individuals sero-positive to SGG Gallo2178 only (OR: 0.93; 95% CI: 0.66-1.31) or to HP VacA only (OR: 1.08; 95% CI: 0.98-1.19). However, dual sero-positive individuals had a >50% increased odds of developing CRC (OR: 1.54; 95% CI: 1.16-2.04), suggesting an interaction between antibody responses to these two pathogens and CRC risk (pinteraction = 0.06). In conclusion, this study suggests that dual sero-positivity to HP VacA and SGG Gallo2178 is an indicator of increased risk of CRC.
Authors
Epplein, M; Le Marchand, L; Cover, TL; Song, M; Blot, WJ; Peek, RM; Teras, LR; Visvanathan, K; Chen, Y; Sesso, HD; Zeleniuch-Jacquotte, A; Berndt, SI; Potter, JD; Ryser, MD; Haiman, CA; Wassertheil-Smoller, S; Tinker, LF; Waterboer, T; Butt, J
MLA Citation
Epplein, Meira, et al. “Association of Combined Sero-Positivity to Helicobacter pylori and Streptococcus gallolyticus with Risk of Colorectal Cancer.Microorganisms, vol. 8, no. 11, Oct. 2020. Pubmed, doi:10.3390/microorganisms8111698.
URI
https://scholars.duke.edu/individual/pub1463771
PMID
33143263
Source
pubmed
Published In
Microorganisms
Volume
8
Published Date
DOI
10.3390/microorganisms8111698

Racial Differences in Helicobacter pylori CagA Sero-prevalence in a Consortium of Adult Cohorts in the United States.

BACKGROUND: Prevalence of Helicobacter pylori (H. pylori) infection, the main risk factor for gastric cancer, has been decreasing in the United States; however, there remains a substantial racial disparity. Moreover, the time-trends for prevalence of CagA-positive H. pylori infection, the most virulent form, are unknown in the U.S. POPULATION: We sought to assess prevalence of CagA-positive H. pylori infection over time by race in the United States. METHODS: We utilized multiplex serology to quantify antibody responses to H. pylori antigens in 4,476 participants across five cohorts that sampled adults from 1985 to 2009. Using log-binomial regression models, we calculated prevalence ratios and 95% confidence intervals for the association between H. pylori-CagA sero-prevalence and birth year by race. RESULTS: African Americans were three times more likely to be H. pylori-CagA sero-positive than Whites. After adjustment, H. pylori-CagA sero-prevalence was lower with increasing birth year among Whites (P trend = 0.001), but remained stable for African Americans. When stratified by sex and education separately, the decline in H. pylori-CagA sero-positivity among Whites remained only for females (P trend < 0.001) and was independent of educational attainment. Among African Americans, there was no difference by sex; furthermore, sero-prevalence increased with increasing birth year among those with a high school education or less (P = 0.006). CONCLUSIONS: Among individuals in the United States born from the 1920s to 1960s, H. pylori-CagA sero-prevalence has declined among Whites, but not among African Americans. IMPACT: Our findings suggest a widening racial disparity in the prevalence of the most virulent form of H. pylori, the main cause of gastric cancer.
Authors
Varga, MG; Butt, J; Blot, WJ; Le Marchand, L; Haiman, CA; Chen, Y; Wassertheil-Smoller, S; Tinker, LF; Peek, RM; Potter, JD; Cover, TL; Hyslop, T; Zeleniuch-Jacquotte, A; Berndt, SI; Hildesheim, A; Waterboer, T; Pawlita, M; Epplein, M
MLA Citation
Varga, Matthew G., et al. “Racial Differences in Helicobacter pylori CagA Sero-prevalence in a Consortium of Adult Cohorts in the United States.Cancer Epidemiol Biomarkers Prev, vol. 29, no. 10, Oct. 2020, pp. 2084–92. Pubmed, doi:10.1158/1055-9965.EPI-20-0525.
URI
https://scholars.duke.edu/individual/pub1457268
PMID
32856604
Source
pubmed
Published In
Cancer Epidemiol Biomarkers Prev
Volume
29
Published Date
Start Page
2084
End Page
2092
DOI
10.1158/1055-9965.EPI-20-0525

A Summary of the 2020 Gastric Cancer Summit at Stanford University.

Authors
Huang, RJ; Koh, H; Hwang, JH; Summit Leaders,
MLA Citation
Huang, Robert J., et al. “A Summary of the 2020 Gastric Cancer Summit at Stanford University.Gastroenterology, vol. 159, no. 4, Oct. 2020, pp. 1221–26. Pubmed, doi:10.1053/j.gastro.2020.05.100.
URI
https://scholars.duke.edu/individual/pub1463574
PMID
32707045
Source
pubmed
Published In
Gastroenterology
Volume
159
Published Date
Start Page
1221
End Page
1226
DOI
10.1053/j.gastro.2020.05.100