Evidence map›Paper›PMID 33263560›Full record

ReviewEndocrine-related cancer2021

Overcoming oncogene addiction in breast and prostate cancers: a comparative mechanistic overview.

Eliot B Blatt, Noa Kopplin, Shourya Kumar, Ping Mu, Suzanne D Conzen, Ganesh V Raj

Open access · bronzeAbstract readComparative StudyReview
In one paragraph

Review in Endocrine-related cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.4field-weighted citation impact, top 32% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Game of clones: decipher lineage plasticity in hormone-driven cancers.Cellular and molecular life sciences : CMLS · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
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

6 authors at 1 institution in 1 country.

Eliot B BlattDepartment of Urology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Noa KopplinDepartment of Urology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Shourya KumarDepartment of Urology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Ping MuDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Suzanne D ConzenDepartment of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Ganesh V RajDepartment of Urology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
The University of Texas Southwestern Medical Center · US

Funding

Therapeutic agents targeting nuclear receptor signaling in distinct molecular subtypes of breast cancerR01CA223828 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI RAJ, GANESH V, VADLAMUDI, RATNA K · 2018 to 2022
$3.0M
Development of small molecules for ERG ablation in prostate cancerR01CA200787 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI KITTLER, RALF · 2016 to 2020
$1.8M
Metabolic alterations contributing to enzalutamide resistance in prostate cancerF31CA243276 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI BLATT, ELIOT · 2020 to 2022
$113k
NCI NIH HHS F31 CA243276NCI NIH HHS R01 CA200787NCI NIH HHS R01 CA223828
6 · The paper itself

Abstract

Prostate cancer (PCa) and breast cancer (BCa) are both hormone-dependent cancers that require the androgen receptor (AR) and estrogen receptor (ER, ESR1) for growth and proliferation, respectively. Endocrine therapies that target these nuclear receptors (NRs) provide significant clinical benefit for metastatic patients. However, these therapeutic strategies are seldom curative and therapy resistance is prevalent. Because the vast majority of therapy-resistant PCa and BCa remain dependent on the augmented activity of their primary NR driver, common mechanisms of resistance involve enhanced NR signaling through overexpression, mutation, or alternative splicing of the receptor, coregulator alterations, and increased intracrine hormonal synthesis. In addition, a significant subset of endocrine therapy-resistant tumors become independent of their primary NR and switch to alternative NR or transcriptional drivers. While these hormone-dependent cancers generally employ similar mechanisms of endocrine therapy resistance, distinct differences between the two tumor types have been observed. In this review, we compare and contrast the most frequent mechanisms of antiandrogen and antiestrogen resistance, and provide potential therapeutic strategies for targeting both advanced PCa and BCa.

Indexed as

Breast NeoplasmsProstatic NeoplasmsBreastDrug Resistance, NeoplasmHumansMaleOncogene AddictionReceptors, AndrogenReceptors, EstrogenReceptors, AndrogenReceptors, Estrogenandrogen receptorendocrine therapy resistanceestrogen receptoroncogene

Identifiers

PMID33263560
PMCPMC8218927
OpenAlexW3110288667

What Socratic 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 Socratic graph.