Evidence map›Paper›PMID 33030277›Full record

ArticleGenetic epidemiology2021

Variation in cancer risk among families with genetic susceptibility.

Theodore Huang, Danielle Braun, Henry T Lynch, Giovanni Parmigiani

Open access · greenAbstract read
In one paragraph

Article in Genetic epidemiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. 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

4 authors at 2 institutions in 1 country.

Theodore HuangDepartment of Data Sciences, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.ORCID 0000-0002-4651-6999
Danielle BraunDepartment of Data Sciences, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.ORCID 0000-0002-5177-8598
Henry T LynchHereditary Cancer Center, Creighton University School of Medicine, Omaha, Nebraska, USA.
Giovanni ParmigianiDepartment of Data Sciences, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.ORCID 0000-0002-8783-5961
Harvard University · USCreighton University · US

Funding

VectorP30CA006516 · NCI · DANA-FARBER CANCER INSTITUTE · PI A. Heather Eliassen · 1985 to 2026
$330.6M
Training Program in Cancer EpidemiologyT32CA009001 · NCI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI A. Heather Eliassen, Meir Stampfer · 1985 to 2026
$17.3M
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
NCI NIH HHS P30 CA006516NCI NIH HHS T32 CA009001NCI NIH HHS T32 CA009337
6 · The paper itself

Abstract

Germline mutations in many genes have been shown to increase the risk of developing cancer. This risk can vary across families who carry mutations in the same gene due to differences in the specific variants, gene-gene interactions, other susceptibility mutations, environmental factors, and behavioral factors. We develop an analytic tool to explore this heterogeneity using family history data. We propose to evaluate the ratio between the number of observed cancer cases in a family and the number of expected cases under a model where risk is assumed to be the same across families. We perform this analysis for both carriers and noncarriers in each family, using carrier probabilities when carrier statuses are unknown, and visualize the results. We first illustrate the approach in simulated data and then apply it to data on colorectal cancer risk in families carrying mutations in Lynch syndrome genes from Creighton University's Hereditary Cancer Center. We show that colorectal cancer risk in carriers can vary widely across families, and that this variation is not matched by a corresponding variation in the noncarriers from the same families. This suggests that the sources of variation in these families are to be found predominantly in variants harbored in the mutated MMR genes considered, or in variants interacting with them.

Indexed as

Colorectal Neoplasms, Hereditary NonpolyposisGenetic Predisposition to DiseaseHumansModels, GeneticMutationfrailty modelhereditary cancerrisk heterogeneity

Identifiers

PMID33030277
PMCPMC7902332
OpenAlexW3092034389

What OpenQuestion 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 OpenQuestion graph.