Evidence map›Paper›PMID 31483856›Full record

ArticleInternational journal of cancer2020

Establishing a valid approach for estimating familial risk of cancer explained by common genetic variants.

Korbinian Weigl, Jenny Chang-Claude, Li Hsu, Michael Hoffmeister, Hermann Brenner

Abstract read
In one paragraph

Article in International journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Emerging trends in the global burden of colorectal cancer.Nature reviews. Clinical oncology · 2026
    Review
  2. Article
  3. Validation of Genetic Markers Associated with Survival in Colorectal Cancer Patients Treated with Oxaliplatin-Based Chemotherapy.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2022
    Observational
  4. Article
  5. Review
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

5 authors.

Korbinian WeiglDivision of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID 0000-0003-4453-2036
Jenny Chang-ClaudeUnit of Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Li HsuPublic Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA.
Michael HoffmeisterDivision of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID 0000-0002-8307-3197
Hermann BrennerDivision of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Funding

Statistical Methods in Genetic EpidemiologyR01AG014358 · NIA · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HSU, LI · 2002 to 2013
$2.4M
Colorectal Tumor Risk Prediction in the PLCO TrialU01CA185094 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI PETERS, ULRIKE · 2014 to 2016
$2.0M
NCI NIH HHS U01 CA185094NCI NIH HHS U01-CA185094NIA NIH HHS R01 AG014358
6 · The paper itself

Abstract

We critically examined existing approaches for the estimation of the excess familial risk of cancer that can be attributed to identified common genetic risk variants and propose an alternative, more straightforward approach for calculating this proportion using well-established epidemiological methodology. We applied the underlying equations of the traditional approaches and the new epidemiological approach for colorectal cancer (CRC) in a large population-based case-control study in Germany with 4,447 cases and 3,480 controls, who were recruited from 2003 to 2016 and for whom interview, medical and genomic data were available. Having a family history of CRC (FH) was associated with a 1.77-fold risk increase in our study population (95% CI 1.52-2.07). Traditional approaches yielded estimates of the FH-associated risk explained by 97 common genetics variants from 9.6% to 23.1%, depending on various assumptions. Our alternative approach resulted in smaller and more consistent estimates of this proportion, ranging from 5.4% to 14.3%. Commonly employed methods may lead to strongly divergent and possibly exaggerated estimates of excess familial risk of cancer explained by associated known common genetic variants. Our results suggest that familial risk and risk associated with known common genetic variants might reflect two complementary major sources of risk.

Indexed as

FamilyGenetic Predisposition to DiseaseAgedAged, 80 and overFemaleHumansMaleMiddle AgedNeoplasmsPolymorphism, Single NucleotideReproducibility of ResultsRisk Factorscommon genetic variantsexcess riskfamilial riskgenetic epidemiologyrisk proportion

Identifiers

PMID31483856
PMCPMC7121903

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.