Evidence map›Paper›PMID 31217297›Full record

ArticleCancer discovery2019

PTEN Methylation by NSD2 Controls Cellular Sensitivity to DNA Damage.

Jinfang Zhang, Yu-Ru Lee, Fabin Dang, Wenjian Gan, Archita Venugopal Menon, Jesse M Katon, Chih-Hung Hsu, John M Asara, Priyanka Tibarewal, Nicholas R Leslie and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer discovery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

52 citing papers in PubMed, 83 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Many faces of mammalian NSD methyltransferases.Cellular & molecular biology letters · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Comprehensive computational analysis of deleterious nsSNPs inMolecular biology research communications · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. PTEN: an emerging target in rheumatoid arthritis?Cell communication and signaling : CCS · 2024
    Review
  18. Article
  19. Review
  20. Article
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

13 authors at 3 institutions in 3 countries.

Jinfang Zhang *Department of Radiation and Medical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, P.R. China.
Yu-Ru Lee *Cancer Research Institute, Beth Israel Deaconess Cancer Center, Boston, Massachusetts.
Fabin Dang *Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Wenjian GanDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Archita Venugopal MenonCancer Research Institute, Beth Israel Deaconess Cancer Center, Boston, Massachusetts.
Jesse M KatonDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Chih-Hung HsuDepartment of Public Health, Women's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, P.R. China.ORCID 0000-0001-8071-0122
John M AsaraDivision of Signal Transduction, Beth Israel Deaconess Medical Center and Department of Medicine, Harvard Medical School, Boston, Massachusetts.
Priyanka TibarewalInstitute of Biological Chemistry, Biophysics and Bioengineering, Heriot Watt University, Edinburgh, United Kingdom.
Nicholas R LeslieInstitute of Biological Chemistry, Biophysics and Bioengineering, Heriot Watt University, Edinburgh, United Kingdom.
Yang ShiDivision of Newborn Medicine and Epigenetics Program, Department of Medicine, Boston Children's Hospital, Boston, Massachusetts.
Pier Paolo PandolfiCancer Research Institute, Beth Israel Deaconess Cancer Center, Boston, Massachusetts. wwei2@bidmc.harvard.edu ppandolf@bidmc.harvard.edu.
Wenyi WeiDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts. wwei2@bidmc.harvard.edu ppandolf@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · USBoston Children's Hospital · USHeriot-Watt University · GB

Funding

Tuberous Sclerosis-Pathway and PathogenesisP01CA120964 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI David J. Kwiatkowski · 2007 to 2026
$35.9M
Novel regulation of PI3K/Akt to direct targeted breast cancer therapiesR01CA177910 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2013 to 2023
$3.9M
Functional analysis of beta-TRCP in cell cycle control and DNA damage responseR01GM094777 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2012 to 2015
$1.3M
Functional analysis of a tissue context-dependent role for beta-TRCP in lipid metabolism and tumorigenesisR01CA229307 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2018 to 2020
$1.1M
Elucidating Novel Akt Regulatory Mechanisms to Overcome Akt-mediated Therapeutic Resistance in Breast CancerR00CA207867 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI GAN, WENJIAN · 2019 to 2021
$747k
High Resolution Mass Spectrometry SystemS10OD010612 · OD · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ASARA, JOHN M · 2012 to 2012
$600k
Elucidating a Novel Mechanism for SPOP in Suppressing Prostate TumorigenesisK99CA212292 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZHANG, JINFANG · 2017 to 2018
$338k
Medical Research Council G0801865NCI NIH HHS K99 CA212292NCI NIH HHS P01 CA120964NCI NIH HHS R00 CA207867NCI NIH HHS R01 CA177910NCI NIH HHS R01 CA229307NIGMS NIH HHS R01 GM094777NIH HHS S10 OD010612
6 · The paper itself

Abstract

The function of PTEN in the cytoplasm largely depends on its lipid-phosphatase activity, though which it antagonizes the PI3K-AKT oncogenic pathway. However, molecular mechanisms underlying the role of PTEN in the nucleus remain largely elusive. Here, we report that DNA double-strand breaks (DSB) promote PTEN interaction with MDC1 upon ATM-dependent phosphorylation of T/S398-PTEN. Importantly, DNA DSBs enhance NSD2 (MMSET/WHSC1)-mediated dimethylation of PTEN at K349, which is recognized by the tudor domain of 53BP1 to recruit PTEN to DNA-damage sites, governing efficient repair of DSBs partly through dephosphorylation of γH2AX. Of note, inhibiting NSD2-mediated methylation of PTEN, either through expressing methylation-deficient PTEN mutants or through inhibiting NSD2, sensitizes cancer cells to combinatorial treatment with a PI3K inhibitor and DNA-damaging agents in both cell culture and

Indexed as

AnimalsBinding SitesCell Line, TumorDNA Breaks, Double-StrandedFemaleHCT116 CellsHistone-Lysine N-MethyltransferaseHistonesHumansMethylationMiceNeoplasmsNIH 3T3 CellsPhosphorylationPTEN PhosphohydrolaseRepressor ProteinsH2AX protein, humanHistone-Lysine N-MethyltransferaseHistonesNSD2 protein, humanPTEN PhosphohydrolasePTEN protein, humanRepressor ProteinsTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1

Identifiers

PMID31217297
PMCPMC6726527
OpenAlexW2949911367

What OpenQuestion holds

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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.