Evidence map›Paper›PMID 35107853›Full record

ArticleEMBO molecular medicine2022

Can THEM6 targeting stop resistance to prostate cancer treatment?

Mrittika Chattopadhyay, Doris Germain

Abstract readComment
In one paragraph

Article in EMBO molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Mrittika ChattopadhyayTish Cancer Institute, Division of Hematology/Oncology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Doris GermainTish Cancer Institute, Division of Hematology/Oncology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.ORCID 0000-0001-6597-0196

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PCa) clinical management relies heavily on androgen-deprivation therapy (ADT). However, despite experiencing initial clinical benefit, patients getting ADT for non-resectable PCa eventually relapse and develop fatal castration-resistant PCa (CRPC). Multiple mechanisms of acquired resistance to treatment have been reported, including metabolic adaptation (Marine et al, 2020). Notably, activation of the endoplasmic reticulum (ER) unfolded protein response (UPR) has been associated with oncogenic transformation (Hart et al, 2012), tumor progression, metastasis dissemination, and resistance to therapy (Chen & Cubillos-Ruiz, 2021). Targeting different branches of ER UPR has been found to be an effective tool against aggressive PCa (Nguyen et al, 2018; Sheng et al, 2019). Therefore, a better understanding of these pathways may lead to the identification of novel drug targets.

Indexed as

Androgen AntagonistsProstatic Neoplasms, Castration-ResistantHumansMaleNeoplasm Recurrence, LocalSignal TransductionAndrogen Antagonists

Identifiers

PMID35107853
PMCPMC8899918

What OpenQuestion holds

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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.