Evidence map›Paper›PMID 28991255›Full record

ArticleNature genetics2017

Patient-derived xenografts undergo mouse-specific tumor evolution.

Uri Ben-David, Gavin Ha, Yuen-Yi Tseng, Noah F Greenwald, Coyin Oh, Juliann Shih, James M McFarland, Bang Wong, Jesse S Boehm, Rameen Beroukhim and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 486 papers.

0numbers the graph read from it
0cells of the map it votes in
486citing papers in PubMed
26.1field-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

486 citing papers in PubMed, 710 citations in OpenAlex.

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426 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

11 authors at 1 institution in 1 country.

Uri Ben-DavidCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.
Gavin HaCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.
Yuen-Yi TsengCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.
Noah F GreenwaldCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.ORCID http://orcid.org/0000-0002-7836-4379
Coyin OhCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.ORCID http://orcid.org/0000-0002-5732-3471
Juliann ShihCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.ORCID http://orcid.org/0000-0002-4086-8651
James M McFarlandCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.
Bang WongCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.
Jesse S BoehmCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.ORCID http://orcid.org/0000-0002-6795-6336
Rameen BeroukhimCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.
Todd R GolubCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.ORCID http://orcid.org/0000-0003-0113-2403
Broad Institute · US

Funding

Genetic evolution of glioblastomas during radiation and temozolomide therapyR01CA188228 · NCI · DANA-FARBER CANCER INST · PI BEROUKHIM, RAMEEN, CHAKRAVARTI, ARNAB · 2015 to 2025
$6.9M
NCI NIH HHS R01 CA188228
6 · The paper itself

Abstract

Patient-derived xenografts (PDXs) have become a prominent cancer model system, as they are presumed to faithfully represent the genomic features of primary tumors. Here we monitored the dynamics of copy number alterations (CNAs) in 1,110 PDX samples across 24 cancer types. We observed rapid accumulation of CNAs during PDX passaging, often due to selection of preexisting minor clones. CNA acquisition in PDXs was correlated with the tissue-specific levels of aneuploidy and genetic heterogeneity observed in primary tumors. However, the particular CNAs acquired during PDX passaging differed from those acquired during tumor evolution in patients. Several CNAs recurrently observed in primary tumors gradually disappeared in PDXs, indicating that events undergoing positive selection in humans can become dispensable during propagation in mice. Notably, the genomic stability of PDXs was associated with their response to chemotherapy and targeted drugs. These findings have major implications for PDX-based modeling of human cancer.

Indexed as

DNA Copy Number VariationsAneuploidyAnimalsAntineoplastic AgentsClonal EvolutionClone CellsDisease Models, AnimalDNA, NeoplasmHeterograftsHumansMiceNeoplasmsSelection, GeneticSpecies SpecificityTumor Cells, CulturedAntineoplastic AgentsDNA, Neoplasm

Identifiers

PMID28991255
PMCPMC5659952
OpenAlexW2737053924

What OpenQuestion holds

Textmetadata
LicenceTDM
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.