Evidence map›Paper›PMID 24011769›Full record

ReviewBreast (Edinburgh, Scotland)2013

Biology and therapeutic potential of PI3K signaling in ER+/HER2-negative breast cancer.

Xiaoyong Fu, C Kent Osborne, Rachel Schiff

Open access · bronzeAbstract readComparative StudyReview
In one paragraph

Review in Breast (Edinburgh, Scotland), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
6.0field-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

43 citing papers in PubMed, 86 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Advances in systemic therapy for metastatic breast cancer: future perspectives.Medical oncology (Northwood, London, England) · 2017
    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

3 authors at 1 institution in 1 country.

Xiaoyong FuLester and Sue Smith Breast Center, Baylor College of Medicine, Houston, TX 77030, USA; Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA; Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA; Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.
C Kent Osborne
Rachel Schiff
Baylor College of Medicine · US

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
TUMOR SUPPRESSOR GENES IN BREAST CANCER DEVELOPMENTP50CA058183 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI OSBORNE, C KENT · 1992 to 2012
$30.9M
Translational Research in Breast Cancer (SPORE)P50CA186784 · NCI · BAYLOR COLLEGE OF MEDICINE · PI Xiang Zhang · 2014 to 2026
$24.5M
NCI NIH HHS P30 CA125123NCI NIH HHS P50 CA058183NCI NIH HHS P50 CA186784NCI NIH HHS P50 CA58183
6 · The paper itself

Abstract

PI3K is a central node mediating growth factor receptor signaling. With its downstream effectors such as AKT and mTOR, and its crosstalk with the RAS/RAF/MEK/MAPK pathway, it plays a vital role in cancer cell proliferation, metabolism, and survival. Recent breast cancer (BC) molecular portraits delineate PI3K as the most frequently altered pathway, with recurrent PIK3CA mutations mostly found in the luminal subtypes of BC. The transcriptomic and proteomic signatures of PI3K pathway activation associate with reduced estrogen receptor α (ER) levels and activity, and with the luminal B subtype of BC that has a relatively poor outcome. However, oncogenic transforming PIK3CA mutations have been shown to predict a better outcome in ER+/HER2-negative BC treated with endocrine therapy. In this review, we summarize the recent findings in the cause-and-effect of PI3K pathway aberration and endocrine sensitivity, especially the crosstalk with the ER pathway. Potential therapeutic approaches based on these findings are also discussed.

Indexed as

AdultAgedAntineoplastic Agents, HormonalBreast NeoplasmsClass I Phosphatidylinositol 3-KinasesFemaleGenes, erbB-2Genetic Predisposition to DiseaseHumansMiddle AgedMolecular Targeted TherapyMutationPhosphatidylinositol 3-KinasesPrognosisProteomicsReceptors, EstrogenAntineoplastic Agents, HormonalClass I Phosphatidylinositol 3-KinasesMTOR protein, humanPhosphatidylinositol 3-KinasesPIK3CA protein, humanReceptors, EstrogenTOR Serine-Threonine KinasesBreast cancerCrosstalkEstrogen receptorFeedback loopPI3KPIK3CA mutation

Identifiers

PMID24011769
PMCPMC3808116
OpenAlexW1983007007

What OpenQuestion holds

Textmetadata
LicenceTDM
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.