Evidence map›Paper›PMID 32895052›Full record

ArticleBMC biology2020

Malignant transformation and genetic alterations are uncoupled in early colorectal cancer progression.

Soulafa Mamlouk, Tincy Simon, Laura Tomás, David C Wedge, Alexander Arnold, Andrea Menne, David Horst, David Capper, Markus Morkel, David Posada and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

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  12. Breast cancer metastasis: Is it a matter of OMICS and proper ex-vivo models?Computational and structural biotechnology journal · 2022
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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

12 authors at 5 institutions in 3 countries.

Soulafa MamloukInstitute of Pathology, Charité Universitätsmedizin Berlin, Berlin, Germany. soulafa.mamlouk@charite.de.ORCID 0000-0001-7285-1320
Tincy SimonInstitute of Pathology, Charité Universitätsmedizin Berlin, Berlin, Germany.
Laura TomásDepartment of Biochemistry, Genetics, and Immunology, University of Vigo, Vigo, Spain.
David C WedgeBig Data Institute, University of Oxford, Oxford, UK.
Alexander ArnoldInstitute of Pathology, Charité Universitätsmedizin Berlin, Berlin, Germany.
Andrea MenneInstitute of Pathology, Charité Universitätsmedizin Berlin, Berlin, Germany.
David HorstInstitute of Pathology, Charité Universitätsmedizin Berlin, Berlin, Germany.
David CapperInstitute of Pathology, Charité Universitätsmedizin Berlin, Berlin, Germany.
Markus MorkelInstitute of Pathology, Charité Universitätsmedizin Berlin, Berlin, Germany.
David PosadaDepartment of Biochemistry, Genetics, and Immunology, University of Vigo, Vigo, Spain.
Christine SersInstitute of Pathology, Charité Universitätsmedizin Berlin, Berlin, Germany.
Hendrik BläkerDepartment für Diagnostik, Institut für Pathologie, Universitätsklinikum Leipzig AöR, Leipzig, Germany.
Charité - Universitätsmedizin Berlin · DEGerman Cancer Research Center · DEGalicia Sur Biomedical Foundation · ESOpen Data Institute · GBUniversity Hospital Leipzig · DE

Funding

H2020 European Research Council 617457Ministerio de Economía y Competitividad BFU2015-63774-P)Xunta de Galicia ED481A-2018/303
6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) development is generally accepted as a sequential process, with genetic mutations determining phenotypic tumor progression. However, matching genetic profiles with histological transition requires the analyses of temporal samples from the same patient at key stages of progression.

resultsHere, we compared the genetic profiles of 34 early carcinomas with their respective adenomatous precursors to assess timing and heterogeneity of driver alterations accompanying the switch from benign adenoma to malignant carcinoma. In almost half of the cases, driver mutations specific to the carcinoma stage were not observed. In samples where carcinoma-specific alterations were present, TP53 mutations and chromosome 20 copy gains commonly accompanied the switch from adenomatous tissue to carcinoma. Remarkably, 40% and 50% of high-grade adenomas shared TP53 mutations and chromosome 20 gains, respectively, with their matched carcinomas. In addition, multi-regional analyses revealed greater heterogeneity of driver mutations in adenomas compared to their matched carcinomas.

conclusionGenetic alterations in TP53 and chromosome 20 occur at the earliest histological stage in colorectal carcinomas (pTis and pT1). However, high-grade adenomas can share these alterations despite their histological distinction. Based on the well-defined sequence of CRC development, we suggest that the timing of genetic changes during neoplastic progression is frequently uncoupled from histological progression.

Indexed as

MutationAdenomaCarcinomaCell Transformation, NeoplasticColorectal NeoplasmsDisease ProgressionHumansAdenomaCancer driver mutationsCancer progressionCarcinomaCopy number alterationsPolypTP53 mutations

Identifiers

PMID32895052
PMCPMC7487684
OpenAlexW3083515706

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.