Evidence map›Paper›PMID 35406583›Full record

ArticleCancers2022

Utility of Continuous Disease Subtyping Systems for Improved Evaluation of Etiologic Heterogeneity.

Ruitong Li, Tomotaka Ugai, Lantian Xu, David Zucker, Shuji Ogino, Molin Wang

Abstract read
In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. The Cancer Spectrum Theory.Cancer discovery · 2024
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Ruitong LiBroad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Tomotaka UgaiDepartment of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Lantian XuDepartment of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
David ZuckerDepartment of Statistics and Data Science, Hebrew University, Jerusalem 91905, Israel.ORCID 0000-0002-2104-4913
Shuji OginoBroad Institute of MIT and Harvard, Cambridge, MA 02142, USA.ORCID 0000-0002-3909-2323
Molin WangDepartment of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.

Funding

Statistical MethodsP01CA087969 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI ELIASSEN, A. HEATHER, TAMIMI, RULLA M · 2000 to 2019
$77.8M
Spatial Immunopathological Epidemiology of Colorectal Adenoma-Carcinoma SpectrumR01CA248857 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Jonathan Andrew Nowak, Shuji Ogino · 2020 to 2026
$6.6M
Accelerating Transdisciplinary Epidemiology of Colorectal CancerR35CA197735 · NCI · DANA-FARBER CANCER INST · PI OGINO, SHUJI · 2015 to 2021
$6.0M
Cancer Research UK 27140Cancer Research UK UK C10674/A27140NCI NIH HHS P01 CA087969NCI NIH HHS R01 CA248857NIH HHS R35 CA197735, R01 CA151993, R01 CA248857, U01 CA167552, UM1 CA167552, P01 CA055075, UM1 CA186107, P01 CA087969
6 · The paper itself

Abstract

Molecular pathologic diagnosis is important in clinical (oncology) practice. Integration of molecular pathology into epidemiological methods (i.e., molecular pathological epidemiology) allows for investigating the distinct etiology of disease subtypes based on biomarker analyses, thereby contributing to precision medicine and prevention. However, existing approaches for investigating etiological heterogeneity deal with categorical subtypes. We aimed to fully leverage continuous measures available in most biomarker readouts (gene/protein expression levels, signaling pathway activation, immune cell counts, microbiome/microbial abundance in tumor microenvironment, etc.). We present a cause-specific Cox proportional hazards regression model for evaluating how the exposure-disease subtype association changes across continuous subtyping biomarker levels. Utilizing two longitudinal observational prospective cohort studies, we investigated how the association of alcohol intake (a risk factor) with colorectal cancer incidence differed across the continuous values of tumor epigenetic DNA methylation at long interspersed nucleotide element-1 (LINE-1). The heterogeneous alcohol effect was modeled using different functions of the LINE-1 marker to demonstrate the method's flexibility. This real-world proof-of-principle computational application demonstrates how the new method enables visualizing the trend of the exposure effect over continuous marker levels. The utilization of continuous biomarker data without categorization for investigating etiological heterogeneity can advance our understanding of biological and pathogenic mechanisms.

Indexed as

bioinformaticsenvironmentepigenomicsimmune responseimmunologyinterdisciplinary researchmicrobiologymolecular epidemiologytargeted interventiontime-to-event data

Identifiers

PMID35406583
PMCPMC8997600

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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 OpenQuestion graph.