Evidence map›Paper›PMID 26929372›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Pten loss promotes MAPK pathway dependency in HER2/neu breast carcinomas.

Saya H Ebbesen, Maurizio Scaltriti, Carl U Bialucha, Natasha Morse, Edward R Kastenhuber, Hannah Y Wen, Lukas E Dow, José Baselga, Scott W Lowe

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. HER2-Positive Breast Cancer Treatment and Resistance.Advances in experimental medicine and biology · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Effect ofMicroorganisms · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
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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

9 authors at 4 institutions in 1 country.

Saya H EbbesenWatson School of Biological Sciences, Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724; Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065;
Maurizio ScaltritiHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065; Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY 10065;
Carl U BialuchaCold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724;
Natasha MorseHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065;
Edward R KastenhuberCancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065; Louis V. Gerstner Jr. Graduate School of Biomedical Sciences, Memorial Sloan Kettering Cancer Center, New York, NY 10065;
Hannah Y WenDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY 10065;
Lukas E DowCancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065;
José BaselgaHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065; Department of Medicine, Weill Cornell Medicine, New York, NY 10065;
Scott W LoweCancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065; Howard Hughes Medical Institute, New York, NY 10065 lowes@mskcc.org.
Memorial Sloan Kettering Cancer Center · USCold Spring Harbor Laboratory · USCornell University · USHoward Hughes Medical Institute · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
The Role of Id Proteins in Breast TumorigenesisP01CA094060 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI BENEZRA, ROBERT I · 2002 to 2018
$39.4M
Making hypomorphic tumor supressors in vivo using RNAiU01CA105388 · NCI · COLD SPRING HARBOR LABORATORY · PI LOWE, SCOTT W. · 2004 to 2013
$8.8M
COMPUTATIONAL AND FUNCTIONAL APPROACHES TO VALIDATING CANCER GENOME TARGETSU01CA168409 · NCI · COLD SPRING HARBOR LABORATORY · PI POWERS, SCOTT · 2012 to 2016
$7.3M
CSHL Watson School of Biological SciencesT32GM065094 · NIGMS · COLD SPRING HARBOR LABORATORY · PI GANN, ALEXANDER · 2002 to 2021
$4.8M
A scalable platform for target validation in GEMM models of gastrointestinal malignancies.R01CA195787 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI LOWE, SCOTT W. · 2015 to 2017
$2.0M
The possible role of the novel Akt 3 R247C mutation in opposing to anti-HER2 therR03CA187094 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI SCALTRITI, MAURIZIO · 2014 to 2015
$176k
Intratumoral Heterogeneity and Tumor Evolution in LymphomaF31CA192835 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI KASTENHUBER, EDWARD R · 2015 to 2018
$157k
Howard Hughes Medical InstituteNCI NIH HHS 01-CA195787NCI NIH HHS F31 CA192835NCI NIH HHS P01 CA094060NCI NIH HHS P01-CA094060NCI NIH HHS P30 CA008748NCI NIH HHS P30-CA008748NCI NIH HHS R01 CA195787NCI NIH HHS R03 CA187094NCI NIH HHS R03-CA187094NCI NIH HHS U01 CA105388NCI NIH HHS U01 CA168409NCI NIH HHS U01-CA168409NIGMS NIH HHS T32 GM065094
6 · The paper itself

Abstract

Loss of the tumor suppressor gene PTEN is implicated in breast cancer progression and resistance to targeted therapies, and is thought to promote tumorigenesis by activating PI3K signaling. In a transgenic model of breast cancer, Pten suppression using a tetracycline-regulatable short hairpin (sh)RNA cooperates with human epidermal growth factor receptor 2 (HER2/neu), leading to aggressive and metastatic disease with elevated signaling through PI3K and, surprisingly, the mitogen-activated protein kinase (MAPK) pathway. Restoring Pten function is sufficient to down-regulate both PI3K and MAPK signaling and triggers dramatic tumor regression. Pharmacologic inhibition of MAPK signaling produces similar effects to Pten restoration, suggesting that the MAPK pathway contributes to the maintenance of advanced breast cancers harboring Pten loss.

Indexed as

AnimalsErb-b2 Receptor Tyrosine KinasesExtracellular Signal-Regulated MAP KinasesFemaleGenes, erbB-2HumansMammary Neoplasms, ExperimentalMammary Tumor Virus, MouseMAP Kinase Kinase 1MAP Kinase Signaling SystemMiceMice, NudeMice, TransgenicNeoplasm MetastasisNeoplasm ProteinsPhosphatidylinositol 3-KinasesAkt1 protein, mouseERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesExtracellular Signal-Regulated MAP KinasesMAP2K1 protein, humanMAP Kinase Kinase 1Neoplasm ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouseRNA, Small Interferingbreast cancermouse modelsRNAitargeted therapiestumor suppressors

Identifiers

PMID26929372
PMCPMC4801318
OpenAlexW2288482051

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.