Evidence map›Paper›PMID 30231850›Full record

ArticleBMC genetics2018

Exome scale map of genetic alterations promoting metastasis in colorectal cancer.

Krzysztof Goryca, Maria Kulecka, Agnieszka Paziewska, Michalina Dabrowska, Marta Grzelak, Magdalena Skrzypczak, Krzysztof Ginalski, Andrzej Mroz, Andrzej Rutkowski, Katarzyna Paczkowska and 2 more

Open access · diamondAbstract read
In one paragraph

Article in BMC genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 32 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

12 authors at 3 institutions in 1 country.

Krzysztof GorycaDepatment of Genetics, Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Roentgena 5, 02-781, Warsaw, Poland. kgoryca@gmail.com.ORCID 0000-0003-1250-1008
Maria KuleckaDepartment of Gastroenterology, Hepatology and Clinical Oncology, Medical Center for Postgraduate Education, Warsaw, Poland.
Agnieszka PaziewskaDepartment of Gastroenterology, Hepatology and Clinical Oncology, Medical Center for Postgraduate Education, Warsaw, Poland.
Michalina DabrowskaDepatment of Genetics, Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Roentgena 5, 02-781, Warsaw, Poland.
Marta GrzelakLaboratory of Bioinformatics and Systems Biology, Center of New Technologies, University of Warsaw, Warsaw, Poland.
Magdalena SkrzypczakLaboratory of Bioinformatics and Systems Biology, Center of New Technologies, University of Warsaw, Warsaw, Poland.
Krzysztof GinalskiLaboratory of Bioinformatics and Systems Biology, Center of New Technologies, University of Warsaw, Warsaw, Poland.
Andrzej MrozDepartment of Patomorphology, Medical Center for Postgraduate Education, Warsaw, Poland.
Andrzej RutkowskiDepartment of Oncological Gastroenterology, Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Warsaw, Poland.
Katarzyna PaczkowskaDepatment of Genetics, Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Roentgena 5, 02-781, Warsaw, Poland.
Michal MikulaDepatment of Genetics, Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Roentgena 5, 02-781, Warsaw, Poland.
Jerzy OstrowskiDepatment of Genetics, Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Roentgena 5, 02-781, Warsaw, Poland.
The Maria Sklodowska-Curie National Research Institute of Oncology · PLPostgraduate School of Molecular Medicine · PLUniversity of Warsaw · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundApproximately 90% of colorectal cancer (CRC) deaths are caused by tumors ability to migrate into the adjacent tissues and metastase into distant organs. More than 40 genes have been causally linked to the development of CRC but no mutations have been associated with metastasis yet. To identify molecular basis of CRC metastasis we performed whole-exome and genome-scale transcriptome sequencing of 7 liver metastases along with their matched primary tumours and normal tissue. Multiple, spatially separated fragments of primary tumours were analyzed in each case. Uniformly malignant tissue specimen were selected with macrodissection, for three samples followed with laser microdissection.

results> 100 sequencing coverage allowed for detection of genetic alterations in subpopulation of tumour cells. Mutations in KRAS, APC, POLE, and PTPRT, previously associated with CRC development, were detected in most patients. Several new associations were identified, including PLXND1, CELSR3, BAHD1 and PNPLA6.

conclusionsWe confirm the essential role of inflammation in CRC progression but question the mechanism of matrix metalloproteinases activation described in other work. Comprehensive sequencing data made it possible to associate genome-scale mutation distribution with gene expression patterns. To our knowledge, this is the first work to report such link in CRC metastasis context.

Indexed as

MutationColorectal NeoplasmsDNA Mutational AnalysisExomeGene Expression ProfilingHumansLiver NeoplasmsNeoplasm MetastasisSequence Analysis, RNAColorectal cancerExomeGene expressionMetastasisSequencing

Identifiers

PMID30231850
PMCPMC6146521
OpenAlexW2889577155

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.