Evidence map›Paper›PMID 28933000›Full record

ArticleFamilial cancer2018

Evaluation of current prediction models for Lynch syndrome: updating the PREMM5 model to identify PMS2 mutation carriers.

A Goverde, M C W Spaander, D Nieboer, A M W van den Ouweland, W N M Dinjens, H J Dubbink, C J Tops, S W Ten Broeke, M J Bruno, R M W Hofstra and 2 more

Abstract read
In one paragraph

Article in Familial cancer, 2018. 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.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

A GoverdeDepartment of Clinical Genetics, Erasmus MC, University Medical Center, Rotterdam, The Netherlands.ORCID 0000-0002-3238-4411
M C W SpaanderDepartment of Gastroenterology and Hepatology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands.
D NieboerDepartment of Public Health, Erasmus MC, University Medical Center, Rotterdam, The Netherlands.
A M W van den OuwelandDepartment of Clinical Genetics, Erasmus MC, University Medical Center, Rotterdam, The Netherlands.
W N M DinjensDepartment of Pathology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands.
H J DubbinkDepartment of Pathology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands.
C J TopsDepartment of Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands.
S W Ten BroekeDepartment of Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands.
M J BrunoDepartment of Gastroenterology and Hepatology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands.
R M W HofstraDepartment of Clinical Genetics, Erasmus MC, University Medical Center, Rotterdam, The Netherlands.
E W SteyerbergDepartment of Medical Statistics and Bioinformatics, Leiden University Medical Center, Leiden, The Netherlands.
A WagnerDepartment of Clinical Genetics, Erasmus MC, University Medical Center, Rotterdam, The Netherlands. a.wagner@erasmusmc.nl.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Until recently, no prediction models for Lynch syndrome (LS) had been validated for PMS2 mutation carriers. We aimed to evaluate MMRpredict and PREMM5 in a clinical cohort and for PMS2 mutation carriers specifically. In a retrospective, clinic-based cohort we calculated predictions for LS according to MMRpredict and PREMM5. The area under the operator receiving characteristic curve (AUC) was compared between MMRpredict and PREMM5 for LS patients in general and for different LS genes specifically. Of 734 index patients, 83 (11%) were diagnosed with LS; 23 MLH1, 17 MSH2, 31 MSH6 and 12 PMS2 mutation carriers. Both prediction models performed well for MLH1 and MSH2 (AUC 0.80 and 0.83 for PREMM5 and 0.79 for MMRpredict) and fair for MSH6 mutation carriers (0.69 for PREMM5 and 0.66 for MMRpredict). MMRpredict performed fair for PMS2 mutation carriers (AUC 0.72), while PREMM5 failed to discriminate PMS2 mutation carriers from non-mutation carriers (AUC 0.51). The only statistically significant difference between PMS2 mutation carriers and non-mutation carriers was proximal location of colorectal cancer (77 vs. 28%, p < 0.001). Adding location of colorectal cancer to PREMM5 considerably improved the models performance for PMS2 mutation carriers (AUC 0.77) and overall (AUC 0.81 vs. 0.72). We validated these results in an external cohort of 376 colorectal cancer patients, including 158 LS patients. MMRpredict and PREMM5 cannot adequately identify PMS2 mutation carriers. Adding location of colorectal cancer to PREMM5 may improve the performance of this model, which should be validated in larger cohorts.

Indexed as

HeterozygoteModels, StatisticalAdultArea Under CurveCohort StudiesColorectal Neoplasms, Hereditary NonpolyposisFemaleHumansMaleMiddle AgedMismatch Repair Endonuclease PMS2Retrospective StudiesROC CurveSensitivity and SpecificityMismatch Repair Endonuclease PMS2PMS2 protein, humanColorectal cancerHereditary cancerLynch syndromePrediction models

Identifiers

PMID28933000
PMCPMC5999171

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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 OpenQuestion graph.