Evidence map›Paper›PMID 30662905›Full record

ArticleBioMed research international2018

Challenges in Stratifying the Molecular Variability of Patient-Derived Colon Tumor Xenografts.

Magdalena Cybulska, Tomasz Olesinski, Krzysztof Goryca, Katarzyna Paczkowska, Malgorzata Statkiewicz, Michal Kopczynski, Aleksandra Grochowska, Katarzyna Unrug-Bielawska, Anita Tyl-Bielicka, Marta Gajewska and 8 more

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.9field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

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  4. Personalizing non-small cell lung cancer treatment through patient-derived xenograft models: preclinical and clinical factors for consideration.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
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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

18 authors at 2 institutions in 1 country.

Magdalena CybulskaDepartment of Genetics, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.
Tomasz OlesinskiDepartment of Gastroenterological Oncology, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.
Krzysztof GorycaDepartment of Genetics, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.
Katarzyna PaczkowskaDepartment of Genetics, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.
Malgorzata StatkiewiczDepartment of Genetics, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.
Michal KopczynskiDepartment of Genetics, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.
Aleksandra GrochowskaDepartment of Genetics, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.
Katarzyna Unrug-BielawskaDepartment of Genetics, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.
Anita Tyl-BielickaDepartment of Genetics, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.
Marta GajewskaDepartment of Genetics, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.
Andrzej MrozDepartment of Gastroenterological Oncology, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.
Michalina DabrowskaDepartment of Genetics, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.
Jakub KarczmarskiDepartment of Genetics, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.
Agnieszka PaziewskaDepartment of Gastroenterology, Hepatology and Clinical Oncology, Medical Center for Postgraduate Education, 01-813 Warsaw, Poland.
Leszek ZającDepartment of Gastroenterological Oncology, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.
Mariusz BednarczykDepartment of Gastroenterological Oncology, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.
Michal MikulaDepartment of Genetics, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.ORCID 0000-0003-3447-7328
Jerzy OstrowskiDepartment of Genetics, Maria Sklodowska-Curie Institute-Oncology Centre, 02-781 Warsaw, Poland.ORCID 0000-0002-1450-8564
The Maria Sklodowska-Curie National Research Institute of Oncology · PLPostgraduate School of Molecular Medicine · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is the second most common cancer in Europe and a leading cause of death worldwide. Patient-derived xenograft (PDX) models maintain complex intratumoral biology and heterogeneity and therefore remain the platform of choice for translational drug discovery. In this study, we implanted 37 primary CRC tumors and five CRC cell lines into NU/J mice to develop xenograft models. Primary tumors and established xenografts were histologically assessed and surveyed for genetic variants and gene expression using a panel of 409 cancer-related genes and RNA-seq, respectively. More than half of CRC tumors (20 out of 37, 54%) developed into a PDX. Histological assessment confirmed that PDX grading, stromal components, inflammation, and budding were consistent with those of the primary tumors. DNA sequencing identified an average of 0.14 variants per gene per sample. The percentage of mutated variants in PDXs increased with successive passages, indicating a decrease in clonal heterogeneity. Gene Ontology analyses of 4180 differentially expressed transcripts (adj. p value < 0.05) revealed overrepresentation of genes involved in cell division and catabolic processes among the transcripts upregulated in PDXs; downregulated transcripts were associated with GO terms related to extracellular matrix organization, immune responses, and angiogenesis. Neither a transcriptome-based consensus molecular subtype (CMS) classifier nor three other predictors reliably matched PDX molecular subtypes with those of the primary tumors. In sum, both genetic and transcriptomic profiles differed between donor tumors and PDXs, likely as a consequence of subclonal evolution at the early phase of xenograft development, making molecular stratification of PDXs challenging.

Indexed as

AnimalsCell Line, TumorColonic NeoplasmsDisease Models, AnimalDown-RegulationGene ExpressionGenetic VariationHeterograftsHumansMiceMice, NudeTranscriptomeUp-RegulationXenograft Model Antitumor Assays

Identifiers

PMID30662905
PMCPMC6313970
OpenAlexW2905262120

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.