Evidence map›Paper›PMID 34118355›Full record

ReviewCancer letters2021

Androgen receptor (AR) heterogeneity in prostate cancer and therapy resistance.

Anmbreen Jamroze, Gurkamal Chatta, Dean G Tang

Open access · hybridAbstract readReview
In one paragraph

Review in Cancer letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 1 pooled it
13.2field-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.

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

82 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.

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  7. Functional dissection ofProceedings of the National Academy of Sciences of the United States of America · 2026
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  10. Comparison of mCRPC [European journal of nuclear medicine and molecular imaging · 2026
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22 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 1 institution in 1 country.

Anmbreen JamrozeDepartment of Pharmacology & Therapeutics, Roswell Park Comprehensive Cancer Center, Buffalo, NY, 14263, USA. Electronic address: anmbreen.jamroze@roswellpark.org.
Gurkamal ChattaDepartment of Medicine, Roswell Park Comprehensive Cancer Center, Buffalo, NY, 14263, USA.
Dean G TangDepartment of Pharmacology & Therapeutics, Roswell Park Comprehensive Cancer Center, Buffalo, NY, 14263, USA; Experimental Therapeutics (ET) Graduate Program, University at Buffalo & Roswell Park Comprehensive Cancer Center, NY, 14263, USA. Electronic address: dean.tang@roswellpark.org.
Roswell Park Comprehensive Cancer Center · US

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI Dean G. Tang · 1985 to 2026
$116.6M
Novel Therapeutic Strategies to Co-Target Undifferentiated Prostate Cancer (PCa) Stem Cells and Bulk PCa CellsR01CA240290 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI Dean G. Tang · 2019 to 2026
$3.1M
Tumor-Suppressive Functions and Molecular Regulation of LRIG1 in Prostate Cancer and CRPCR01CA237027 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI TANG, DEAN G. · 2019 to 2023
$2.2M
Correlative efficacy, biomarker, and mechanistic studies associated with a phase Ib/II clinical trial of treating mCRPC patients with enzalutamide and VenetoclaxR21CA237939 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI TANG, DEAN G. · 2020 to 2021
$449k
Slow-cycling cells, therapy resistance and clinical implications in prostate cancerR21CA218635 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI TANG, DEAN G. · 2018 to 2019
$404k
NCI NIH HHS P30 CA016056NCI NIH HHS R01 CA237027NCI NIH HHS R01 CA240290NCI NIH HHS R21 CA218635NCI NIH HHS R21 CA237939
6 · The paper itself

Abstract

Androgen receptor (AR), a ligand-dependent nuclear transcription factor and a member of steroid hormone receptor family, plays an important role in prostate organogenesis by regulating epithelial differentiation and restricting cell proliferation. Although rarely mutated or amplified in treatment-naïve prostate cancer (PCa), AR signaling drives tumor growth and as a result, therapies that aim to inhibit AR signaling, called ARSIs (AR signaling inhibitors), have been in clinical use for >70 years. Unfortunately, the clinical efficacy of ARSIs is short-lived and the majority of treated patients develop castration-resistant PCa (CRPC). Numerous molecular mechanisms have been proposed for castration resistance; however, the cellular basis for CRPC emergence has remained obscure. One under-appreciated cellular mechanism for CRPC development is the AR heterogeneity that pre-exists in treatment-naive primary tumors, i.e., although most PCa cells express AR (i.e., AR

Indexed as

Cell ProliferationDrug Resistance, NeoplasmHumansMaleProstateProstatic NeoplasmsReceptors, AndrogenSignal TransductionReceptors, AndrogenAndrogen receptorCancer cell heterogeneityCancer stem cellsCastration-resistant prostate cancerProstate cancerTherapy resistance

Identifiers

PMID34118355
PMCPMC8355210
OpenAlexW3169645397

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.