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

Synergistic effect of oncogenic RET and loss of p18 on medullary thyroid carcinoma development.

Cancer research - 1 Mar 2008

van Veelen Wendy, van Gasteren Carola J R, Acton Dennis S, Franklin David S, Berger Ruud, Lips Cornelis J M, Höppener Jo W M

Abstract excerpt

Activating mutations in the RET proto-oncogene are associated with both familial and sporadic medullary thyroid carcinoma (MTC) development; however, the genetic mechanisms underlying MTC tumorigenesis remain largely unknown. Recently, we have identified somatic inactivating mutations in the cell...

Read the complete abstract on PubMed

Topics

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

Share to Calcitonin
Share to Carcinoma, Medullary
Share to Cell Cycle

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Transformation, Neoplastic

Share to Cyclin-Dependent Kinase Inhibitor p18

Share to Proto-Oncogene Mas

Share to Proto-Oncogene Proteins c-ret

Share to Thyroid Neoplasms

Source

Identifiers

PMID: 18316595
DOI: 10.1158/0008-5472.CAN-07-5754

Genes

RET

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-18316595-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Synergistic effect of oncogenic RET and loss of p18 on medullary thyroid carcinoma development.PMID 18316595Read ↗

P18 is a tumor suppressor gene involved in human medullary thyroid carcinoma and pheochromocytoma development.Semantic proximity Read ↗

p18Ink4c collaborates with Men1 to constrain lung stem cell expansion and suppress non-small-cell lung cancers.Semantic proximity Read ↗

p18Ink4c, but not p27Kip1, collaborates with Men1 to suppress neuroendocrine organ tumors.Semantic proximity Read ↗

Haploinsufficiency of p18(INK4c) sensitizes mice to carcinogen-induced tumorigenesis.Semantic proximity Read ↗

Functional Collaboration between Different Cyclin-Dependent Kinase Inhibitors Suppresses Tumor Growth with Distinct Tissue SpecificitySemantic proximity Read ↗

Tumorigenesis in p27/p53- and p18/p53-double null mice: functional collaboration between the pRb and p53 pathways.Semantic proximity Read ↗

Cooperation between Cdk4 and p27kip1 in tumor development: a preclinical model to evaluate cell cycle inhibitors with therapeutic activity.Semantic proximity Read ↗

The haploinsufficient tumor suppressor p18 upregulates p53 via interactions with ATM/ATR.Semantic proximity Read ↗

p18<sup><i>Ink4c</i></sup> and <i>Pten</i> Constrain a Positive Regulatory Loop between Cell Growth and Cell Cycle ControlSemantic proximity Read ↗

Expression of p18(INK4C) is down-regulated in human pituitary adenomas.Semantic proximity Read ↗

G2/M transition requires multisite phosphorylation of oncoprotein 18 by two distinct protein kinase systems.Semantic proximity Read ↗

Oncoprotein 18 is a phosphorylation-responsive regulator of microtubule dynamics.Semantic proximity Read ↗

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