Evidence map›Paper›PMID 24185513›Full record

ArticleNature genetics2013

Exome sequencing identifies distinct mutational patterns in liver fluke-related and non-infection-related bile duct cancers.

Waraporn Chan-On, Maarja-Liisa Nairismägi, Choon Kiat Ong, Weng Khong Lim, Simona Dima, Chawalit Pairojkul, Kiat Hon Lim, John R McPherson, Ioana Cutcutache, Hong Lee Heng and 29 more

Abstract read
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In one paragraph

Article in Nature genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 274 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
274citing papers in PubMed, 2 pooled it
37.2field-weighted citation impact, top 1% 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

274 citing papers in PubMed, 2 syntheses or guidelines pooled it, 488 citations in OpenAlex.

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214 more citing papers are in PubMed but not listed here.

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

39 authors at 7 institutions in 4 countries.

Waraporn Chan-On1] Laboratory of Cancer Epigenome, Division of Medical Sciences, National Cancer Centre Singapore, Singapore. [2] Division of Cancer and Stem Cell Biology, Duke-National University of Singapore Graduate Medical School, Singapore. [3] Liver Fluke and Cholangiocarcinoma Research Center, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand. [4].
Maarja-Liisa Nairismägi
Choon Kiat Ong
Weng Khong Lim
Simona Dima
Chawalit Pairojkul
Kiat Hon Lim
John R McPherson
Ioana Cutcutache
Hong Lee Heng
London Ooi
Alexander Chung
Pierce Chow
Peng Chung Cheow
Ser Yee Lee
Su Pin Choo
Iain Bee Huat Tan
Dan Duda
Anca Nastase
Swe Swe Myint
Bernice Huimin Wong
Anna Gan
Vikneswari Rajasegaran
Cedric Chuan Young Ng
Sanjanaa Nagarajan
Apinya Jusakul
Shenli Zhang
Priya Vohra
Willie Yu
DaChuan Huang
Paiboon Sithithaworn
Puangrat Yongvanit
Sopit Wongkham
Narong Khuntikeo
Vajaraphongsa Bhudhisawasdi
Irinel Popescu
Steven G Rozen
Patrick Tan
Bin Tean Teh
National University of Singapore · SGNational Cancer Centre Singapore · SGKhon Kaen University · THSingapore General Hospital · SGInstitutul Clinic Fundeni · RONational University Cancer Institute, Singapore · SGHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The impact of different carcinogenic exposures on the specific patterns of somatic mutation in human tumors remains unclear. To address this issue, we profiled 209 cholangiocarcinomas (CCAs) from Asia and Europe, including 108 cases caused by infection with the liver fluke Opisthorchis viverrini and 101 cases caused by non-O. viverrini-related etiologies. Whole-exome sequencing (n = 15) and prevalence screening (n = 194) identified recurrent somatic mutations in BAP1 and ARID1A, neither of which, to our knowledge, has previously been reported to be mutated in CCA. Comparisons between intrahepatic O. viverrini-related and non-O. viverrini-related CCAs demonstrated statistically significant differences in mutation patterns: BAP1, IDH1 and IDH2 were more frequently mutated in non-O. viverrini CCAs, whereas TP53 mutations showed the reciprocal pattern. Functional studies demonstrated tumor suppressive functions for BAP1 and ARID1A, establishing the role of chromatin modulators in CCA pathogenesis. These findings indicate that different causative etiologies may induce distinct somatic alterations, even within the same tumor type.

Indexed as

Bile Ducts, IntrahepaticFasciola hepaticaAnimalsBile Duct NeoplasmsCholangiocarcinomaExomeFascioliasisFemaleGene FrequencyGenetic Predisposition to DiseaseHumansIsocitrate DehydrogenaseMaleMutationSequence Analysis, DNATumor Cells, CulturedBAP1 protein, humanIDH1 protein, humanIDH2 protein, humanIsocitrate DehydrogenaseTumor Suppressor ProteinsUbiquitin Thiolesterase

Identifiers

PMID24185513
OpenAlexW2033522521

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.