Evidence map›Paper›PMID 32894420›Full record

ReviewDrugs2020

Targeting the PI3K/AKT/mTOR Pathway in Hormone-Positive Breast Cancer.

Sara E Nunnery, Ingrid A Mayer

Open access · greenAbstract readReview
In one paragraph

Review in Drugs, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 3 pooled it
6.7field-weighted citation impact, top 2% 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

133 citing papers in PubMed, 3 syntheses or guidelines pooled it, 192 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Clinical Significance of PIK3CA and ESR1 Mutations in Circulating Tumor DNA: Analysis from the MONARCH 2 Study of Abemaciclib plus Fulvestrant.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Trial
  6. Article
  7. Review
  8. Review
  9. Article
  10. Multi-omic Profiling of Recurrence Risk Across Breast Cancer Subtypes.medRxiv : the preprint server for health sciences · 2026
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Feasibility ofGeburtshilfe und Frauenheilkunde · 2026
    Article
  16. Review
  17. Article
  18. Review
  19. Bufalin Inhibits the PI3K/AKT Pathway by Targeting GTF3C4 to Impede Breast Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  20. Review

73 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

2 authors at 1 institution in 1 country.

Sara E NunneryBreast Cancer Program, Division of Hematology/Oncology, Department of Medicine, Vanderbilt-Ingram Cancer Center (VICC), Vanderbilt University Medical Center, 2220 Pierce Avenue, 777 PRB, Nashville, TN, 37232-6307, USA.
Ingrid A MayerBreast Cancer Program, Division of Hematology/Oncology, Department of Medicine, Vanderbilt-Ingram Cancer Center (VICC), Vanderbilt University Medical Center, 2220 Pierce Avenue, 777 PRB, Nashville, TN, 37232-6307, USA. Ingrid.mayer@vumc.org.
Vanderbilt University Medical Center · US

Funding

TISSUE CoreP50CA098131 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PARK, BEN HO, PIETENPOL, JENNIFER A · 2003 to 2024
$48.7M
VOLT (Vanderbilt Oncology Training Program)T32CA217834 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Debra L. Friedman, Douglas B Johnson · 2018 to 2026
$2.7M
NCI NIH HHS P50 CA098131NCI NIH HHS T32 CA217834
6 · The paper itself

Abstract

Approximately 70% of invasive breast cancers have some degree of dependence on the estrogen hormone for cell proliferation and growth. These tumors have estrogen and/or progesterone receptors (ER/PR+), generally referred to as hormone receptor positive (HR+) tumors, as indicated by the presence of positive staining and varying intensity levels of estrogen and/or progesterone receptors on immunohistochemistry. Therapies that inhibit ER signaling pathways, such as aromatase inhibitors (letrozole, anastrozole, exemestane), selective ER modulators (tamoxifen), and ER down-regulators (fulvestrant), are the mainstays of treatment for hormone-receptor-positive breast cancers. However, de novo or acquired resistance to ER targeted therapies is present in many tumors, leading to disease progression. The PI3K/AKT/mTOR pathway is implicated in sustaining endocrine resistance and has become the target of many new drugs for ER+ breast cancer. This article reviews the function of the phosphoinositide 3-kinase (PI3K)/AKT/mTOR pathway and the various classes of PI3K pathway inhibitors that have been developed to disrupt this pathway signaling for the treatment of hormone-receptor-positive breast cancer.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsBreast NeoplasmsClass I Phosphatidylinositol 3-KinasesDNA Mutational AnalysisDrug Resistance, NeoplasmFemaleHumansMutationNeoplasm Recurrence, LocalNeoplasm StagingPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktReceptors, EstrogenReceptors, ProgesteroneSignal TransductionTOR Serine-Threonine KinasesAKT1 protein, humanClass I Phosphatidylinositol 3-KinasesMTOR protein, humanPhosphoinositide-3 Kinase InhibitorsPIK3CA protein, humanProto-Oncogene Proteins c-aktReceptors, EstrogenReceptors, ProgesteroneTOR Serine-Threonine Kinases

Identifiers

PMID32894420
PMCPMC7572750
OpenAlexW3083789602

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.