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

FTO-mediated DSP m6A demethylation promotes an aggressive subtype of growth hormone-secreting pituitary neuroendocrine tumors

20 Sept 2024

Abstract excerpt

Growth hormone-secreting pituitary neuroendocrine tumors can be pathologically classified into densely granulated (DGGH) and sparsely granulated types (SGGH). SGGH is more aggressive and associated with a poorer prognosis. While epigenetic regulation is vital in tumorigenesis and progression, the role of N 6 -methyladenosine (m 6 A) in aggressive behavior has yet to be elucidated. We performed m 6 A-sequencing on...

Read the complete abstract on PubMed

Topics

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

Share to Cardiac tumors and thrombi
Share to Peptidase Inhibition and Analysis
Share to RNA modifications and cancer

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 39304899
DOI: 10.1186/s12943-024-02117-5

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

FTO-mediated DSP m6A demethylation promotes an aggressive subtype of growth hormone-secreting pituitary neuroendocrine tumorsPMID 39304899Read ↗

RNA N6-Methyladenosine (m6A) regulates the cell cycle in Diffuse Midline Glioma (DMG) and confers sensitivity to FTO inhibitionSemantic proximity Read ↗

Single-cell transcriptome and genome analyses of pituitary neuroendocrine tumorsSemantic proximity Read ↗

The Epigenomics of Pituitary AdenomaSemantic proximity Read ↗

Longitudinal multiomics analysis of aggressive pituitary neuroendocrine tumors: comparing primary and recurrent tumors from the same patient, reveals genomic stability and heterogeneous transcriptomic profiles with alterations in metabolic pathwaysSemantic proximity Read ↗

Transcriptome and methylome analysis reveals three cellular origins of pituitary tumorsSemantic proximity Read ↗

Whole Genome Sequencing and single-cell transcriptomics identify<i>KMT2D</i>as a potential new driver for pituitary adenomasSemantic proximity Read ↗

Splicing Machinery is Dysregulated in Pituitary Neuroendocrine Tumors and is Associated with Aggressiveness FeaturesSemantic proximity Read ↗

Transcriptomic Profiles of Normal Pituitary Cells and Pituitary Neuroendocrine Tumor CellsSemantic proximity Read ↗

Developmental Plasticity and Stromal Co-option Shape a Pituitary Neuroendocrine Tumor Transcriptional ContinuumSemantic proximity Read ↗

Splicing diversity enhances the molecular classification of pituitary neuroendocrine tumorsSemantic proximity Read ↗

Harnessing m6A-regulated cholesterol biosynthesis helps impede tumor burden and stemness in high-garde serous ovarian carcinoma mesenchymal phenotype.Semantic proximity Read ↗

Transcriptomic classification of pituitary neuroendocrine tumors causing acromegalySemantic proximity Read ↗

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