Evidence map›Paper›PMID 30194485›Full record

ArticleJournal of cancer research and clinical oncology2018

POLE gene hotspot mutations in advanced pancreatic cancer.

Michael Guenther, Vivien Veninga, Joerg Kumbrink, Michael Haas, C Benedikt Westphalen, Stephan Kruger, Volker Heinemann, Thomas Kirchner, Stefan Boeck, Andreas Jung and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.6field-weighted citation impact, top 39% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

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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

11 authors at 3 institutions in 1 country.

Michael GuentherInstitute of Pathology, Medical Faculty, Ludwig-Maximilians-University, Thalkirchner Str. 36, 80337, Munich, Germany.
Vivien VeningaInstitute of Pathology, Medical Faculty, Ludwig-Maximilians-University, Thalkirchner Str. 36, 80337, Munich, Germany.
Joerg KumbrinkInstitute of Pathology, Medical Faculty, Ludwig-Maximilians-University, Thalkirchner Str. 36, 80337, Munich, Germany.
Michael HaasDepartment of Medicine III, University Hospital, LMU Munich, Munich, Germany.
C Benedikt WestphalenDepartment of Medicine III, University Hospital, LMU Munich, Munich, Germany.
Stephan KrugerDepartment of Medicine III, University Hospital, LMU Munich, Munich, Germany.
Volker HeinemannDepartment of Medicine III, University Hospital, LMU Munich, Munich, Germany.
Thomas KirchnerInstitute of Pathology, Medical Faculty, Ludwig-Maximilians-University, Thalkirchner Str. 36, 80337, Munich, Germany.
Stefan BoeckDepartment of Medicine III, University Hospital, LMU Munich, Munich, Germany.
Andreas JungInstitute of Pathology, Medical Faculty, Ludwig-Maximilians-University, Thalkirchner Str. 36, 80337, Munich, Germany.
Steffen OrmannsInstitute of Pathology, Medical Faculty, Ludwig-Maximilians-University, Thalkirchner Str. 36, 80337, Munich, Germany. steffen.ormanns@med.uni-muenchen.de.ORCID http://orcid.org/0000-0002-0754-9034
German Cancer Research Center · DELudwig-Maximilians-Universität München · DELMU Klinikum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposePancreatic ductal adenocarcinoma (PDAC) is a devastating disease, lacking relevant prognostic and predictive biomarkers. DNA polymerase epsilon (POLE) has important functions in the maintenance of genetic stability during DNA replication and has previously been associated with favorable prognosis in endometrial and colorectal cancer. However, its relevance in advanced pancreatic cancer (aPDAC) has not been examined to date.

methodsUsing pyrosequencing on tumoral DNA extracted from 60 samples from the AIO-PK0104 study as well as 55 samples from completed translational trials, we examined POLE hotspot mutations in exon 9 (P286R) and exon 13 (V411R/L/M) in the POLE gene exonuclease domain. DNA extracted from 37 endometrial carcinomas were tested as positive controls. Publically available sequencing databases were searched for POLE mutations in PDAC samples.

resultsFifty-three patients (pts) were men, 62 pts were women, median age was 61.2 years. Median overall survival (OS) was 7.4 months and median progression free survival (PFS) was 4.0 months. In four of the 37 endometrial carcinomas POLE mutations were detected in exon 9 (10.8%) and none in exon 13. In none of the overall 115 aPDAC tumors POLE gene hotspot mutations could be detected.

conclusionMutations in the hotspot regions of exon 9 and 13 of the POLE gene are very rare events in advanced pancreatic cancer. Thus, it is unlikely that POLE gene mutations contribute to genetic instability in the vast majority of aPDAC. POLE mutation does not serve as a relevant biomarker and should not be tested on a regular basis in PDAC.

Indexed as

Mutation, MissenseAdultAgedAged, 80 and overCarcinoma, Pancreatic DuctalDNA Polymerase IIExonsFemaleHumansKaplan-Meier EstimateMaleMiddle AgedPancreatic NeoplasmsSequence Analysis, DNADNA Polymerase IICheckpoint inhibitorsPancreatic cancerPolymerase epsilonTumor mutational burden

Identifiers

PMID30194485
PMCPMC11813388
OpenAlexW2890682625

What OpenQuestion holds

Textmetadata
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.