Evidence map›Paper›PMID 31859348›Full record

ReviewAnnals of oncology : official journal of the European Society for Medical Oncology2019

Overview of the relevance of PI3K pathway in HR-positive breast cancer.

N Vasan, E Toska, M Scaltriti

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Annals of oncology : official journal of the European Society for Medical Oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07387861 (Immunohistochemical Evaluation of p-AKT and p-S6 as Surrogate Markers of PI3K/AKT/mTOR Pathway Activation in ER-Positive, HER2-Negative Breast Carcinoma), which is not on this map. Cited by 99 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 1 pooled it
6.3field-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.

NCT07387861 not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Immunohistochemical Evaluation of p-AKT and p-S6 as Surrogate Markers of PI3K/AKT/mTOR Pathway Activation in ER-Positive, HER2-Negative Breast Carcinoma

TypeobservationalSponsorAssiut UniversityRan2026 to 2028Enrolled70ConditionsBreast Cancer - ER+, HER2-, PIK3CA Gene MutationArmsNot applicable- observational study
3 · Its place in the literature

Who cites it

99 citing papers in PubMed, 1 synthesis or guideline pooled it, 155 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Bufalin Inhibits the PI3K/AKT Pathway by Targeting GTF3C4 to Impede Breast Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  11. Phase separation of DDHD2 remodels lipid metabolism to dictate treatment sensitivity in luminal breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

39 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

N VasanHuman Oncology and Pathogenesis Program, New York, USA.
E ToskaHuman Oncology and Pathogenesis Program, New York, USA.
M ScaltritiHuman Oncology and Pathogenesis Program, New York, USA.
New York Oncology Hematology · USMemorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Unraveling resistance to PI3K-alpha inhibitors in breast cancerR01CA190642 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI SCALTRITI, MAURIZIO · 2015 to 2019
$2.2M
Mechanisms of action of dual compound oncogenic PIK3CA mutationsR21CA223789 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI SCALTRITI, MAURIZIO · 2018 to 2019
$414k
NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA190642NCI NIH HHS R21 CA223789
6 · The paper itself

Abstract

One of the hallmarks of hormone receptor (HR)-positive breast cancer is its dependence on the phosphatidylinositol-3-kinase (PI3K) pathway. Here, we review the epidemiologic, functional, and pharmacologic interactions between oncogenic PI3K and the estrogen receptor (ER). We discuss the epidemiology of PI3K pathway alterations, mechanisms of resistance to PI3K inhibitors, and the current mechanistic landscape of crosstalk between PI3K and ER, which provide the rationale for dual ER and PI3K inhibition and is now a standard of care in the treatment of ER+ PIK3CA-mutant metastatic breast cancer. We outline newer studies in this field that delineate the clinically relevant overlaps between PI3K and parallel signaling pathways, insulin signaling, and ER epigenetic modifiers. We also identify several caveats with the current data and propose new strategies to overcome these bottlenecks.

Indexed as

AnimalsBreast NeoplasmsDrug Resistance, NeoplasmEstrogen Receptor ModulatorsFemaleHumansMolecular EpidemiologyMolecular Targeted TherapyPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsReceptors, EstrogenSignal TransductionEstrogen Receptor ModulatorsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsReceptors, EstrogenAKTbreast cancerestrogen receptorPI3K inhibitorsPI3K pathwayPIK3CA

Identifiers

PMID31859348
PMCPMC6923788
OpenAlexW2994724934

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

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.