Evidence map›Paper›PMID 38971221›Full record

ArticleJournal of the Academy of Nutrition and Dietetics2025

Coffee, Phosphoinositide 3-Kinase Signaling Pathway, and Prostate Cancer: A Prospective Study in the Health Professionals Follow-Up Study.

Rui Song, Konrad H Stopsack, Junkun Ren, Lorelei A Mucci, Steven K Clinton, Massimo Loda, Molin Wang, Edward L Giovannucci, Kathryn M Wilson, Stephanie A Smith-Warner

Abstract read
In one paragraph

Article in Journal of the Academy of Nutrition and Dietetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

10 authors.

Rui SongDepartment of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Analysis Group, Boston, Massachusetts.
Konrad H StopsackClinical and Translational Epidemiology Unit, Massachusetts General, Hospital and Harvard Medical School, Boston, Massachusetts; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
Junkun RenDepartment of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Department of Earth, Atmospheric, and Planetary Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts; Biology Department, Woods Hole Oceanographic Institution, Falmouth, Massachusetts.
Lorelei A MucciAnalysis Group, Boston, Massachusetts.
Steven K ClintonDivision of Medical Oncology, Department of Internal Medicine, The Ohio State University College of Medicine, Columbus, Ohio; Genitourinary Oncology, The Arthur G. James Cancer Hospital, The Ohio State University, Columbus, Ohio; Molecular Carcinogenesis and Chemoprevention, The Ohio State University Comprehensive Cancer Center, Columbus, Ohio.
Massimo LodaDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, New York; Department of Pathology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts.
Molin WangClinical and Translational Epidemiology Unit, Massachusetts General, Hospital and Harvard Medical School, Boston, Massachusetts; Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Edward L GiovannucciDepartment of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
Kathryn M WilsonDepartment of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Navitas Data Sciences, Pottstown, Pennsylvania.
Stephanie A Smith-WarnerDepartment of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts. Electronic address: swarner@hsph.harvard.edu.

Funding

Cancer Epidemiology Cohort in Male Health ProfessionalsU01CA167552 · NCI · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI Lorelei Mucci, Walter C. Willett · 2017 to 2026
$17.0M
Project 3: Analysis of intrinsic and extrinsic factors that promote prostate neuroendocrine differentiationP01CA265768 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MICHAEL M. SHEN · 2022 to 2026
$13.4M
Weill Cornell Medicine (WCM) SPORE in Prostate CancerP50CA211024 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI RICKMAN, DAVID S. · 2017 to 2021
$10.9M
NCI NIH HHS P01 CA265768NCI NIH HHS P50 CA211024NCI NIH HHS U01 CA167552
6 · The paper itself

Abstract

backgroundHigher coffee intake has been associated with reduced risk of prostate cancer, particularly aggressive forms. The activation of the phosphoinositide 3-kinase (PI3K) signaling pathway plays an important role in prostate carcinogenesis.

objectiveTo evaluate associations between prediagnostic coffee intake and a PI3K activation score, the expression/presence of PI3K regulators, and downstream effectors in tumor tissue from men with prostate cancer in the Health Professionals Follow-Up Study, a prospective cohort study conducted in the United States.

designA case-only study design was applied. Coffee intake was assessed using validated food frequency questionnaires completed in 1986 and every 4 years thereafter until prostate cancer diagnosis. PARTICIPANTS

settingStudy participants comprised 1242 men diagnosed with prostate cancer from 1986 to 2009 and with tumor markers assessed from tissue microarrays constructed from tumor specimens.

main outcome measuresThe outcomes include the PI3K activation score; expression of insulin receptor and insulin-like growth factor 1 receptor; angiogenesis markers; and presence of the tumor suppressor phosphatase and tensin homolog, chronic and acute inflammation, simple atrophy, and post-atrophic hyperplasia. STATISTICAL ANALYSES PERFORMED: Multivariable linear or logistic regression was conducted to estimate associations between coffee intake and tumor marker expression/presence.

resultsAmong coffee drinkers (86.6% of the population), median (25th, 75th percentile) coffee intake was 2 c/day (1, 3 c/day). The associations between coffee consumption and the tumor markers of interest were generally weak with modest precision. When comparing men who drank >3 c/day coffee with nondrinkers, the absolute percent difference in the PI3K activation score and angiogenesis markers ranged from 0.6% to 3.6%. The odds ratios for phosphatase and tensin homolog loss, insulin-like growth factor 1 receptor and insulin receptor expression, and presence of chronic and acute inflammation, simple atrophy, and postatrophic hyperplasia also were not statistically significant, were imprecise, and ranged from 0.82 to 1.58.

conclusionsCoffee intake was not observed to be associated with PI3K activation, related regulators, and several effectors in prostate tumor tissue. Studies exploring alternative pathways or earlier steps in carcinogenesis are needed to investigate the underlying mechanisms of the coffee and prostate cancer association.

Indexed as

CoffeeProstatic NeoplasmsSignal TransductionAdultAgedBiomarkers, TumorFollow-Up StudiesHumansMaleMiddle AgedPhosphatidylinositol 3-KinasesProspective StudiesPTEN PhosphohydrolaseSurveys and QuestionnairesUnited StatesBiomarkers, TumorCoffeePhosphatidylinositol 3-KinasesPTEN PhosphohydrolaseCoffeeCohort studiesNutritionProstate cancerTumor markers

Identifiers

PMID38971221
PMCPMC12912192

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.