Evidence map›Paper›PMID 24469059›Full record

ArticleOncogene2015

A chromatin modifier genetic screen identifies SIRT2 as a modulator of response to targeted therapies through the regulation of MEK kinase activity.

P K Bajpe, A Prahallad, H Horlings, I Nagtegaal, R Beijersbergen, R Bernards

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Article
  3. Sirtuin 1 and Sirtuin 2 Gene Expressions in Colorectal Cancers.Journal of clinical practice and research · 2025
    Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
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  12. Drugging the Epigenome: Overcoming Resistance to Targeted and Immunotherapies in Melanoma.JID innovations : skin science from molecules to population health · 2022
    Review
  13. Review
  14. Article
  15. Article
  16. Review
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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

6 authors at 3 institutions in 1 country.

P K BajpeDivision of Molecular Carcinogenesis, Cancer Genomics Center, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
A PrahalladDivision of Molecular Carcinogenesis, Cancer Genomics Center, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
H Horlings1] Division of Molecular Carcinogenesis, Cancer Genomics Center, The Netherlands Cancer Institute, Amsterdam, The Netherlands [2] Department of Pathology, Academisch Medisch Centrum, Amsterdam, The Netherlands.
I NagtegaalDepartment of Pathology, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.
R BeijersbergenDivision of Molecular Carcinogenesis, Cancer Genomics Center, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
R BernardsDivision of Molecular Carcinogenesis, Cancer Genomics Center, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
The Netherlands Cancer Institute · NLCancer Genomics Centre · NLRadboud University Nijmegen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resistance to targeted therapies is a major problem in cancer treatment. The epidermal growth factor receptor (EGFR) antibody drugs are effective in a subset of colorectal cancers, but the molecular mechanisms of resistance are understood poorly. Genes involved in epigenetic regulation are frequently deregulated in cancer, raising the possibility that such genes also contribute to drug resistance. Using a focused RNA interference library for genes involved in epigenetic regulation, we identify sirtuin2 (SIRT2), an NAD(+)-dependent deacetylase, as a modulator of the response to EGFR inhibitors in colon and lung cancer. SIRT2 loss also conferred resistance to BRAF and MEK inhibitors in BRAF mutant melanoma and KRAS mutant colon cancers, respectively. These results warrant further investigation into the potential role of SIRT2 in resistance to drugs that act in the receptor tyrosine kinase-RAS-RAF-MEK-ERK signaling pathway.

Indexed as

Molecular Targeted TherapyAcetylationCell ProliferationChromatinDrug Resistance, NeoplasmEpigenesis, GeneticErbB ReceptorsExtracellular Signal-Regulated MAP KinasesHumansMitogen-Activated Protein Kinase KinasesNeoplasmsProtein Kinase InhibitorsProto-Oncogene Proteins B-rafSirtuin 2ChromatinErbB ReceptorsExtracellular Signal-Regulated MAP KinasesMitogen-Activated Protein Kinase KinasesProtein Kinase InhibitorsProto-Oncogene Proteins B-rafSIRT2 protein, humanSirtuin 2

Identifiers

PMID24469059
OpenAlexW2027189297

What OpenQuestion holds

Textmetadata
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.