Evidence map›Paper›PMID 35583099›Full record

ArticleGenetic epidemiology2022

Statistical methods for Mendelian models with multiple genes and cancers.

Jane W Liang, Gregory E Idos, Christine Hong, Stephen B Gruber, Giovanni Parmigiani, Danielle Braun

Open access · greenAbstract read
In one paragraph

Article in Genetic epidemiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 29% of its field
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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. A validation of models for prediction of pathogenic variants in mismatch repair genes.Genetics in medicine : official journal of the American College of Medical Genetics · 2022
    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 at 2 institutions in 1 country.

Jane W LiangDepartment of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.
Gregory E IdosCenter for Precision Medicine, City of Hope, Duarte, California, USA.
Christine HongCenter for Precision Medicine, City of Hope, Duarte, California, USA.
Stephen B GruberCenter for Precision Medicine, City of Hope, Duarte, California, USA.
Giovanni ParmigianiDepartment of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.
Danielle BraunDepartment of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.
City of Hope · USHarvard University · US

Funding

VectorP30CA006516 · NCI · DANA-FARBER CANCER INSTITUTE · PI JENNIFER W MACK · 1985 to 2026
$330.6M
Training Grant in Quantitative Sciences for Cancer ResearchT32CA009337 · NCI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI QUACKENBUSH, JOHN, TRIPPA, LORENZO · 1986 to 2025
$12.3M
Mentored Career DevelopmentKL2TR001854 · NCATS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Elizabeth Rhea Erwin Burner, Amy Elizabeth West · 2016 to 2026
$9.0M
NCATS NIH HHS KL2 TR001854NCI NIH HHS P30 CA006516NCI NIH HHS T32 CA009337
6 · The paper itself

Abstract

Risk evaluation to identify individuals who are at greater risk of cancer as a result of heritable pathogenic variants is a valuable component of individualized clinical management. Using principles of Mendelian genetics, Bayesian probability theory, and variant-specific knowledge, Mendelian models derive the probability of carrying a pathogenic variant and developing cancer in the future, based on family history. Existing Mendelian models are widely employed, but are generally limited to specific genes and syndromes. However, the upsurge of multigene panel germline testing has spurred the discovery of many new gene-cancer associations that are not presently accounted for in these models. We have developed PanelPRO, a flexible, efficient Mendelian risk prediction framework that can incorporate an arbitrary number of genes and cancers, overcoming the computational challenges that arise because of the increased model complexity. We implement an 11-gene, 11-cancer model, the largest Mendelian model created thus far, based on this framework. Using simulations and a clinical cohort with germline panel testing data, we evaluate model performance, validate the reverse-compatibility of our approach with existing Mendelian models, and illustrate its usage. Our implementation is freely available for research use in the PanelPRO R package.

Indexed as

Genetic Predisposition to DiseaseNeoplasmsBayes TheoremCohort StudiesHumansModels, Geneticgermline panel gene testingMendelian modelspathogenic variantsprecision preventionrisk prediction

Identifiers

PMID35583099
PMCPMC9452449
OpenAlexW4280528226

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

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 Socratic graph.