Evidence map›Paper›PMID 28196852›Full record

ArticleMolecular cancer research : MCR2017

INPP4B and PTEN Loss Leads to PI-3,4-P2 Accumulation and Inhibition of PI3K in TNBC.

Darien E Reed, Kevan M Shokat

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

Article in Molecular cancer research : MCR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. PIPFEBS letters · 2022
    Article
  5. Article
  6. Article
  7. Review
  8. Proteomics and its applications in breast cancer.American journal of cancer research · 2021
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Regulation and modulation of PTEN activity.Molecular biology reports · 2018
    Review
  16. PTEN Regulates PI(3,4)PMolecular cell · 2017
    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

2 authors at 1 institution in 1 country.

Darien E ReedDepartment of Cellular and Molecular Pharmacology, University of California, San Francisco, California.
Kevan M ShokatDepartment of Cellular and Molecular Pharmacology, University of California, San Francisco, California. kevan.shokat@ucsf.edu.
Howard Hughes Medical Institute · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007618 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ANDERSON, MARK S · 1985 to 2020
$29.6M
The PIP2-virus interface and PI 4-kinase: novel biology and validation targetsR01AI099245 · NIAID · STANFORD UNIVERSITY · PI GLENN, JEFFREY S · 2012 to 2016
$5.2M
NIAID NIH HHS R01 AI099245NIGMS NIH HHS T32 GM007618
6 · The paper itself

Abstract

Triple-negative breast cancer [TNBC, lacks expression of estrogen receptor (ER), progesterone receptor (PR), and amplification of HER2/Neu] remains one of the most aggressive subtypes, affects the youngest patients, and still lacks an effective targeted therapy. Both phosphatidylinositol-3-kinase (PI3K)-α and -β contribute to oncogenesis of solid tumors, including the development of breast cancer. Inositol polyphosphate-4-phosphatase type II (INPP4B) catalyzes the removal of the 4'-phosphate of phosphatidylinositol-(3, 4)-bisphosphate (PI-3,4-P2), creating phosphatidylinositol-3-phosphate. There is debate concerning whether PI-3,4-P2 contributes to Akt and downstream effector activation with the known canonical signaling second messenger, phosphatidylinositol-(3, 4, 5)-trisphosphate (PIP3). If PI-3,4-P2 is a positive effector, INPP4B would be a negative regulator of PI3K signaling, and there is some evidence to support this. Utilizing phosphatase and tensin homolog deleted on chromosome ten (PTEN)-null triple-negative breast tumor cell lines, it was unexpectedly found that silencing INPP4B decreased basal phospho-Akt (pAkt) and cellular proliferation, and in most cases sensitized cells to PI3K-α and PI3K-β isoform-specific inhibitors. Conversely, overexpression of INPP4B desensitized cells to PI3K inhibitors in a phosphatase activity-dependent manner. In summary, the current investigation of INPP4B in PTEN-null TNBC suggests new mechanistic insight and the potential for targeted therapy for this aggressive subset of breast cancer.

Indexed as

Cell Line, TumorCell ProliferationEnzyme InhibitorsFemaleHumansIndazolesPhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesPhosphoinositide-3 Kinase InhibitorsPhosphoric Monoester HydrolasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionSulfonamidesTriple Negative Breast Neoplasms2-(1H-indazol-4-yl)-6-(4-methanesulfonylpiperazin-1-ylmethyl)-4-morpholin-4-ylthieno(3,2-d)pyrimidineEnzyme InhibitorsIndazolesphosphatidylinositol-3,4-bisphosphate 4-phosphatasephosphatidylinositol 3,4-diphosphatePhosphatidylinositol 3-Kinasesphosphatidylinositol 3-phosphatePhosphatidylinositol PhosphatesPhosphoinositide-3 Kinase InhibitorsPhosphoric Monoester HydrolasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanSulfonamides

Identifiers

PMID28196852
PMCPMC5502826
OpenAlexW2588750958

What OpenQuestion holds

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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.