Evidence map›Paper›PMID 20887199›Full record

ReviewAnnual review of medicine2011

Mechanisms of endocrine resistance in breast cancer.

C Kent Osborne, Rachel Schiff

2 registry-linked trialsAbstract readReview
In one paragraph

Review in Annual review of medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 674 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
674citing papers in PubMed, 4 pooled it
26.9field-weighted citation impact, top 1% 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.

NCT04999540 phase2unknown statusnot on this mapstarted 2021, after this paper: background citation

Trial of Tucidinostat in Combination With Fulvestrant in Patients With Hormone-receptor Positive Advanced Breast Cancer

TypeinterventionalSponsorGuangdong Women and Children HospitalRan2021 to 2024Enrolled73ConditionsBreast CancerArmsTucidinostat, Fulvestrant
NCT05181033 phase2recruitingnot on this mapstarted 2021, after this paper: background citation

A Phase II Randomized Trial of Lenvatinib Combined With Letrozole Versus Fulvestrant in Metastatic Estrogen Receptor (ER) Positive, HER2 Negative Breast Cancer, Who Have Progressed on First-line Aromatase Inhibitor + a CDK4/6 Inhibitor.

TypeinterventionalSponsorNational University Hospital, SingaporeRan2021 to 2027Enrolled120ConditionsBreast CancerArmsLenvatinib + Letrozole, Fulvestrant
3 · Its place in the literature

Who cites it

674 citing papers in PubMed, 4 syntheses or guidelines pooled it, 1,162 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Trial
  8. Trial
  9. Trial
  10. Trial
  11. Trial
  12. Selective regulation of βMedical oncology (Northwood, London, England) · 2026
    Article
  13. Recent advances in hormone-based biopharmaceuticals for cancer therapy.Journal of the Egyptian National Cancer Institute · 2026
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

614 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.

C Kent OsborneDan L. Duncan Cancer Center, Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA. kosborne@bcm.edu
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
NCI NIH HHS P30 CA125123NCI NIH HHS P30CA125123NCI NIH HHS P50 CA058183NCI NIH HHS P50CA058183
6 · The paper itself

Abstract

The estrogen receptor (ER) pathway plays a pivotal role in breast cancer development and progression. Endocrine therapy to block the ER pathway is highly effective, but its usefulness is limited by common intrinsic and acquired resistance. Multiple mechanisms responsible for endocrine resistance have been proposed and include deregulation of various components of the ER pathway itself, alterations in cell cycle and cell survival signaling molecules, and the activation of escape pathways that can provide tumors with alternative proliferative and survival stimuli. Among these, increased expression or signaling of growth factor receptor pathways, especially the EGFR/HER2 pathway, has been associated with both experimental and clinical endocrine therapy resistance. New treatment combinations targeting both ER and growth factor receptor signaling to block the crosstalk between these pathways and eliminate escape routes have been proven highly effective in preclinical models. Results of recent clinical studies, while partly supporting this approach, also highlight the need to better identify a priori the patients whose tumors are most likely to benefit from these specific cotargeting strategies.

Indexed as

Drug Resistance, NeoplasmAntineoplastic Agents, HormonalBreast NeoplasmsCell ProliferationClinical Trials as TopicErb-b2 Receptor Tyrosine KinasesErbB ReceptorsEstrogen AntagonistsFemaleHumansReceptors, EstrogenSignal TransductionAntineoplastic Agents, HormonalERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesErbB ReceptorsEstrogen AntagonistsReceptors, Estrogen

Identifiers

PMID20887199
PMCPMC3656649
OpenAlexW2117357260

What OpenQuestion holds

Textmetadata
LicenceTDM
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.