Evidence map›Paper›PMID 35109899›Full record

ReviewJournal of experimental & clinical cancer research : CR2022

Aggressive variants of prostate cancer: underlying mechanisms of neuroendocrine transdifferentiation.

Lina Merkens, Verena Sailer, Davor Lessel, Ella Janzen, Sarah Greimeier, Jutta Kirfel, Sven Perner, Klaus Pantel, Stefan Werner, Gunhild von Amsberg

Abstract readReview
In one paragraph

Review in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
–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

75 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  18. Melanoma to rhabdomyosarcoma plasticity in the setting of immunotherapy.medRxiv : the preprint server for health sciences · 2025
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15 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

10 authors.

Lina MerkensDepartment of Tumor Biology, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany. l.merkens@uke.de.
Verena SailerInstitute of Pathology, University of Luebeck and University Hospital Schleswig-Holstein, Campus Luebeck, Ratzeburger Allee 160, 23538, Luebeck, Germany.
Davor LesselInstitute of Human Genetics, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.
Ella JanzenDepartment of Tumor Biology, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.
Sarah GreimeierDepartment of Tumor Biology, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.
Jutta KirfelInstitute of Pathology, University of Luebeck and University Hospital Schleswig-Holstein, Campus Luebeck, Ratzeburger Allee 160, 23538, Luebeck, Germany.
Sven PernerInstitute of Pathology, University of Luebeck and University Hospital Schleswig-Holstein, Campus Luebeck, Ratzeburger Allee 160, 23538, Luebeck, Germany.
Klaus PantelDepartment of Tumor Biology, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.
Stefan Werner *Department of Tumor Biology, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.
Gunhild von Amsberg *Department of Hematology and Oncology, University Cancer Center Hamburg, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.

Funding

Deutsche Forschungsgemeinschaft Ki 672/6-1Deutsche Forschungsgemeinschaft PA 341/25-1Deutsche Forschungsgemeinschaft PE1179/15-1 SPP µboneDeutsche Forschungsgemeinschaft SA 3254/1-2 SPP µboneDeutsche Forschungsgemeinschaft SPP 2084: μBONEDeutsche Forschungsgemeinschaft WE 5844/5-1Deutsche Krebshilfe 70113304Hansestadt Hamburg LFF-GK10Rudolf Becker Foundation T0321/36080/20207kg
6 · The paper itself

Abstract

Prostate cancer is a hormone-driven disease and its tumor cell growth highly relies on increased androgen receptor (AR) signaling. Therefore, targeted therapy directed against androgen synthesis or AR activation is broadly used and continually improved. However, a subset of patients eventually progresses to castration-resistant disease. To date, various mechanisms of resistance have been identified including the development of AR-independent aggressive variant prostate cancer based on neuroendocrine transdifferentiation (NED). Here, we review the highly complex processes contributing to NED. Genetic, epigenetic, transcriptional aberrations and posttranscriptional modifications are highlighted and the potential interplay of the different factors is discussed. Background Aggressive variant prostate cancer (AVPC) with traits of neuroendocrine differentiation emerges in a rising number of patients in recent years. Among others, advanced therapies targeting the androgen receptor axis have been considered causative for this development. Cell growth of AVPC often occurs completely independent of the androgen receptor signal transduction pathway and cells have mostly lost the typical cellular features of prostate adenocarcinoma. This complicates both diagnosis and treatment of this very aggressive disease. We believe that a deeper understanding of the complex molecular pathological mechanisms contributing to transdifferentiation will help to improve diagnostic procedures and develop effective treatment strategies. Indeed, in recent years, many scientists have made important contributions to unravel possible causes and mechanisms in the context of neuroendocrine transdifferentiation. However, the complexity of the diverse molecular pathways has not been captured completely, yet. This narrative review comprehensively highlights the individual steps of neuroendocrine transdifferentiation and makes an important contribution in bringing together the results found so far.

Indexed as

Cell TransdifferentiationHumansMaleProstatic NeoplasmsAggressive variant prostate cancerNeuroendocrine prostate cancerNeuroendocrine transdifferentiationSmall cell prostate cancer

Identifiers

PMID35109899
PMCPMC8808994

What OpenQuestion holds

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LicenceCC BY
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.