Evidence map›Paper›PMID 24621249›Full record

ArticleBMC genomics2014

Immunomic, genomic and transcriptomic characterization of CT26 colorectal carcinoma.

John C Castle, Martin Loewer, Sebastian Boegel, Jos de Graaf, Christian Bender, Arbel D Tadmor, Valesca Boisguerin, Thomas Bukur, Patrick Sorn, Claudia Paret and 4 more

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 240 papers.

0numbers the graph read from it
0cells of the map it votes in
240citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

240 citing papers in PubMed, 381 citations in OpenAlex.

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  10. CEUS with VEGFR2-targeted microbubbles for monitoring of early immunotherapy effects in a colorectal cancer model.Cancer imaging : the official publication of the International Cancer Imaging Society · 2026
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180 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

14 authors at 3 institutions in 1 country.

John C CastleTRON gGmbH - Translational Oncology, Johannes Gutenberg-University Medical Center gGmbH, Langenbeckstr, 1, Building 708, 55131 Mainz, Germany. john.castle@tron-mainz.de.
Martin Loewer
Sebastian Boegel
Jos de Graaf
Christian Bender
Arbel D Tadmor
Valesca Boisguerin
Thomas Bukur
Patrick Sorn
Claudia Paret
Mustafa Diken
Sebastian Kreiter
Özlem Türeci
Ugur Sahin
Johannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DEBioNTech (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumor models are critical for our understanding of cancer and the development of cancer therapeutics. Here, we present an integrated map of the genome, transcriptome and immunome of an epithelial mouse tumor, the CT26 colon carcinoma cell line.

resultsWe found that Kras is homozygously mutated at p.G12D, Apc and Tp53 are not mutated, and Cdkn2a is homozygously deleted. Proliferation and stem-cell markers, including Top2a, Birc5 (Survivin), Cldn6 and Mki67, are highly expressed while differentiation and top-crypt markers Muc2, Ms4a8a (MS4A8B) and Epcam are not. Myc, Trp53 (tp53), Mdm2, Hif1a, and Nras are highly expressed while Egfr and Flt1 are not. MHC class I but not MHC class II is expressed. Several known cancer-testis antigens are expressed, including Atad2, Cep55, and Pbk. The highest expressed gene is a mutated form of the mouse tumor antigen gp70. Of the 1,688 non-synonymous point variations, 154 are both in expressed genes and in peptides predicted to bind MHC and thus potential targets for immunotherapy development. Based on its molecular signature, we predicted that CT26 is refractory to anti-EGFR mAbs and sensitive to MEK and MET inhibitors, as have been previously reported.

conclusionsCT26 cells share molecular features with aggressive, undifferentiated, refractory human colorectal carcinoma cells. As CT26 is one of the most extensively used syngeneic mouse tumor models, our data provide a map for the rationale design of mode-of-action studies for pre-clinical evaluation of targeted- and immunotherapies.

Indexed as

TranscriptomeAnimalsAntigens, NeoplasmCarcinomaCell Line, TumorColonic NeoplasmsCyclin-Dependent Kinase Inhibitor p16High-Throughput Nucleotide SequencingMiceMice, Inbred BALB CPolymorphism, Single NucleotideProto-Oncogene Proteins p21(ras)Sequence Analysis, DNAAntigens, NeoplasmCyclin-Dependent Kinase Inhibitor p16Hras protein, mouseProto-Oncogene Proteins p21(ras)

Identifiers

PMID24621249
PMCPMC4007559
OpenAlexW1977315768

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.