Evidence map›Paper›PMID 29605661›Full record

ArticleTrends in endocrinology and metabolism: TEM2018

A Novel Mechanism to Drive Castration-Resistant Prostate Cancer.

Salma Kaochar, Nicholas Mitsiades

Abstract readComment
In one paragraph

Article in Trends in endocrinology and metabolism: TEM, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Salma KaocharDepartment of Medicine, Baylor College of Medicine, Houston, TX 77030, USA; Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.
Nicholas MitsiadesDepartment of Medicine, Baylor College of Medicine, Houston, TX 77030, USA; Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA. Electronic address: mitsiade@bcm.edu.

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI Michael M Ittmann · 2007 to 2026
$73.9M
TUMOR SUPPRESSOR GENES IN BREAST CANCER DEVELOPMENTP50CA058183 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI GUTIERREZ, CAROLLINA · 1992 to 2012
$30.9M
Translational Research in Breast Cancer (SPORE)P50CA186784 · NCI · BAYLOR COLLEGE OF MEDICINE · PI MATTHEW J ELLIS · 2014 to 2026
$24.5M
BCM Oncology Scholars Training ProgramT32CA174647 · NCI · BAYLOR COLLEGE OF MEDICINE · PI LIN, WEEI-CHIN · 2014 to 2018
$1.2M
NCI NIH HHS P30 CA125123NCI NIH HHS P50 CA058183NCI NIH HHS P50 CA186784NCI NIH HHS T32 CA174647
6 · The paper itself

Abstract

Androgen receptor signaling is critical for prostate adenocarcinoma, even after androgen deprivation therapy. Persistence of intratumoral androgens has been found in castration-resistant prostate cancer and attributed to increased in situ synthesis. Recently, Sharifi and colleagues reported an additional mechanism that can enhance local androgenic exposure: downregulation of an androgen-inactivating enzyme.

Indexed as

AndrogensDown-RegulationHumansMalePeroxisomal Multifunctional Protein-2Prostatic NeoplasmsProstatic Neoplasms, Castration-ResistantProtein IsoformsReceptors, AndrogenAndrogensHSD17B4 protein, humanPeroxisomal Multifunctional Protein-2Protein IsoformsReceptors, Androgenandrogen receptor (AR) signalingcastration-resistant prostate cancerDHTHSD17B4 variant 2testosterone

Identifiers

PMID29605661
PMCPMC5960430

What OpenQuestion holds

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LicenceTDM
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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.