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

c-myc-induced hepatocarcinogenesis in the absence of IGF-I receptor.

International journal of cancer - 20 Apr 2005

Cadoret Axelle, Desbois-Mouthon Christèle, Wendum Dominique, Leneuve Patricia, Perret Christine, Tronche François, Housset Chantal, Holzenberger Martin

Abstract excerpt

Numerous tumours, including hepatocarcinomas, produce IGFs, and some depend on these growth factors in a paracrine or autocrine fashion. We have shown that c-myc-induced experimental hepatocarcinogenesis is associated with enhanced production of IGF-II. To assess the role of the IGF-I receptor (IGF-IR) in hepatocarcinogenesis, we generated conditional mutant mice that overexpressed c-myc and were knocked out for...

Read the complete abstract on PubMed

Topics

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

Share to Blotting, Western
Share to Cell Proliferation

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Hepatocytes

Share to Liver Neoplasms

Share to Proto-Oncogene Proteins c-myc

Share to Receptor, IGF Type 1

Share to Recombination, Genetic

Source

Identifiers

PMID: 15609331
DOI: 10.1002/ijc.20805

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

c-myc-induced hepatocarcinogenesis in the absence of IGF-I receptor.PMID 15609331Read ↗

Igf1r as a therapeutic target in a mouse model of basal-like breast cancerSemantic proximity Read ↗

Evolution of neoplastic development in the liver of transgenic mice co-expressing c-myc and transforming growth factor-alpha.Semantic proximity Read ↗

Lack of p53 accelerates hepatocarcinogenesis in transgenic mice constitutively overexpressing c-myc in the liver.Semantic proximity Read ↗

Insulin receptor functionally enhances multistage tumor progression and conveys intrinsic resistance to IGF-1R targeted therapySemantic proximity Read ↗

The insulin-like growth factor (IGF) signaling axis and hepatitis C virus-associated carcinogenesis (Review)Semantic proximity Read ↗

Molecular analyses of liver tumors in c-myc transgenic mice and c-myc and TGF-alpha double transgenic mice.Semantic proximity Read ↗

Induction of ribosomal genes and hepatocyte hypertrophy by adenovirus-mediated expression of c-Myc <i>in vivo</i>Semantic proximity Read ↗

Molecular Mechanisms of Hepatocarcinogenesis in Transgenic Mouse Models of Liver CancerSemantic proximity Read ↗

Conditional deletion of c-myc does not impair liver regeneration.Semantic proximity Read ↗

An evaluation of the role of insulin-like growth factors (IGF) and of type-I IGF receptor signalling in hepatocarcinogenesis and in the resistance of hepatocarcinoma cells against drug-induced apoptosisSemantic proximity Read ↗

Minimal cooperation between mutant Hras and c-myc or TGFα in the regulation of mouse hepatocyte growth or transformation in vivo.Semantic proximity Read ↗

Insulin-like growth factor 2 is a key mitogen driving liver repopulation in miceSemantic proximity Read ↗

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