Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Prostate cancer castrate resistant progression usage of non-canonical androgen receptor signaling and ketone body fuel

28 Sept 2021

Abstract excerpt

Prostate cancer (PCa) that progresses after androgen deprivation therapy (ADT) remains incurable. The underlying mechanisms that account for the ultimate emergence of resistance to ADT, progressing to castrate-resistant prostate cancer (CRPC), include those that reactivate androgen receptor (AR), or those that are entirely independent or cooperate with androgen signaling to underlie PCa progression. The intricacy...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cancer, Hypoxia, and Metabolism
Share to Cancer, Lipids, and Metabolism
Share to Diet and metabolism studies

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 34584218
DOI: 10.1038/s41388-021-02008-9

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Prostate cancer castrate resistant progression usage of non-canonical androgen receptor signaling and ketone body fuelPMID 34584218Read ↗

Multi-Omics Profiling Exposes a Metabolic Void in Prostate Cancer Models That Drives Precursor Dependence and Clinical ProgressionSemantic proximity Read ↗

Precursor-dependent steroid conversion sustains androgen receptor signaling and lineage-state divergence in prostate cancerSemantic proximity Read ↗

Subtype and Site Specific–Induced Metabolic Vulnerabilities in Prostate CancerSemantic proximity Read ↗

Integrated metabolic and transcriptomic landscapes reveal an obligate reliance on exogenous steroid conversion for prostate cancer survivalSemantic proximity Read ↗

Personalized Medicine for Prostate Cancer: Is Targeting Metabolism a Reality?Semantic proximity Read ↗

Metabolic deregulation in prostate cancerSemantic proximity Read ↗

Reactivation of androgen receptor-regulated lipid biosynthesis drives the progression of castration-resistant prostate cancerSemantic proximity Read ↗

MYC is a regulator of androgen receptor inhibition-induced metabolic requirements in prostate cancerSemantic proximity Read ↗

Loss of an Androgen-Inactivating and Isoform-Specific HSD17B4 Splice Form Enables Emergence of Castration-Resistant Prostate CancerSemantic proximity Read ↗

Chronic hypoxia favours adoption to a castration-resistant cell state in prostate cancerSemantic proximity Read ↗

Chronic hypoxia favours adoption to a castration-resistant cell state in prostate cancerSemantic proximity Read ↗

Novel Target Opportunities in Non-Metastatic Castrate Resistant Prostate CancerSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.