Evidence map›Paper›PMID 33433737›Full record

ReviewCurrent oncology reports2021

Clinical and Biological Features of Neuroendocrine Prostate Cancer.

Yasutaka Yamada, Himisha Beltran

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Current oncology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 195 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
195citing papers in PubMed, 2 pooled it
29.8field-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

195 citing papers in PubMed, 2 syntheses or guidelines pooled it, 295 citations in OpenAlex.

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135 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

2 authors at 1 institution in 1 country.

Yasutaka YamadaDepartment of Medical Oncology, Dana Farber Cancer Institute, 450 Brookline Avenue, Sm 758, Boston, MA, 02115, USA.
Himisha BeltranDepartment of Medical Oncology, Dana Farber Cancer Institute, 450 Brookline Avenue, Sm 758, Boston, MA, 02115, USA. himisha_beltran@dfci.harvard.edu.ORCID 0000-0003-3259-2226
Dana-Farber Cancer Institute · US

Funding

Molecular mechanisms underlying lineage plasticity in prostate cancerR37CA241486 · NCI · DANA-FARBER CANCER INST · PI Himisha Beltran · 2020 to 2026
$4.1M
NCI NIH HHS R37 CA241486
6 · The paper itself

Abstract

purpose of reviewNeuroendocrine prostate cancer (NEPC) is an aggressive histologic subtype of prostate cancer that most commonly arises in later stages of prostate cancer as a mechanism of treatment resistance. The poor prognosis of NEPC is attributed in part to late diagnosis and a lack of effective therapeutic agents. Here, we review the clinical and molecular features of NEPC based on recent studies and outline future strategies and directions. RECENT

findingsNEPC can arise "de novo" but most commonly develops as a result of lineage plasticity whereby prostate cancer cells adopt alternative lineage programs as a means to bypass therapy. Dependence on androgen receptor (AR) signaling is lost as tumors progress from a prostate adenocarcinoma to a NEPC histology, typically manifested by the downregulation of AR, PSA, and PSMA expression in tumors. Genomic analyses from patient biopsies combined with preclinical modeling have pointed to loss of tumor suppressors RB1 and TP53 as key facilitators of lineage plasticity. Activation of oncogenic drivers combined with significant epigenetic changes (e.g., EZH2 overexpression, DNA methylation) further drives tumor proliferation and expression of downstream neuronal and neuroendocrine lineage pathways controlled in part by pioneer and lineage determinant transcription factors (e.g., SOX2, ASCL1, BRN2). These biologic insights have provided a framework for the study of this subgroup of advanced prostate cancers and have started to provide rationale for the development of biomarker-driven therapeutic strategies. Further study of the dynamic process that leads to NEPC is required for the development of effective strategies to identify and treat patients developing lineage plasticity as a mechanism of treatment resistance.

Indexed as

Drug Resistance, NeoplasmCarcinoma, NeuroendocrineDisease ProgressionHumansMaleProstatic NeoplasmsAR indifferenceCastration resistanceEpigeneticsLineage plasticityNeuroendocrine prostate cancer

Identifiers

PMID33433737
PMCPMC7990389
OpenAlexW3118537036

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.