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

Therapeutic effect of imatinib in gastrointestinal stromal tumors: AKT signaling dependent and independent mechanisms.

Cancer research - 15 May 2006

Tarn Chi, Skorobogatko Yuliya V, Taguchi Takahiro, Eisenberg Burton, von Mehren Margaret, Godwin Andrew K

Abstract excerpt

Most gastrointestinal stromal tumors (GISTs) possess a gain-of-function mutation in c-KIT. Imatinib mesylate, a small-molecule inhibitor against several receptor tyrosine kinases, including KIT, platelet-derived growth factor receptor-alpha, and BCR-ABL, has therapeutic benefit for GISTs both via KIT and via unknown mechanisms. Clinical evidence suggests that a potential therapeutic benefit of imatinib might...

Read the complete abstract on PubMed

Topics

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

Share to Benzamides
Share to Chromones

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gastrointestinal Stromal Tumors

Share to Glucose Transporter Type 4

Share to Imatinib Mesylate

Share to Morpholines

Share to Piperazines

Share to Proto-Oncogene Proteins c-kit

Source

Identifiers

PMID: 16707477
DOI: 10.1158/0008-5472.CAN-05-3906

Genes

KIT
AKT1
AKT2
BCR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Therapeutic effect of imatinib in gastrointestinal stromal tumors: AKT signaling dependent and independent mechanisms.PMID 16707477Read ↗

Mitochondrial Inhibition Augments the Efficacy of Imatinib by Resetting the Metabolic Phenotype of Gastrointestinal Stromal TumorSemantic proximity Read ↗

ACRIN 6665/RTOG 0132 phase II trial of neoadjuvant imatinib mesylate for operable malignant gastrointestinal stromal tumor: monitoring with 18F-FDG PET and correlation with genotype and GLUT4 expression.Semantic proximity Read ↗

Linsitinib (OSI-906) for the Treatment of Adult and Pediatric Wild-Type Gastrointestinal Stromal Tumors, a SARC Phase II Study.Semantic proximity Read ↗

Combined Inhibition of AKT and KIT Restores Expression of Programmed Cell Death 4 (PDCD4) in Gastrointestinal Stromal TumorSemantic proximity Read ↗

A potent combination of the novel PI3K Inhibitor, GDC-0941, with imatinib in gastrointestinal stromal tumor xenografts: long-lasting responses after treatment withdrawal.Semantic proximity Read ↗

Akt up-regulation increases resistance to microtubule-directed chemotherapeutic agents through mammalian target of rapamycin.Semantic proximity Read ↗

Modulation of energy metabolism to overcome drug resistance in chronic myeloid leukemia cells through induction of autophagySemantic proximity Read ↗

A kinase-independent biological activity for insulin growth factor-1 receptor (IGF-1R): Implications for Inhibition of the IGF-1R signalSemantic proximity Read ↗

Intracellular concentration of the tyrosine kinase inhibitor imatinib in gastrointestinal stromal tumor cells.Semantic proximity Read ↗

Increased drug resistance is associated with reduced glucose levels and an enhanced glycolysis phenotype.Semantic proximity Read ↗

Metabolic response by FDG-PET to imatinib correlates with exon 11 KIT mutation and predicts outcome in patients with mucosal melanoma.Semantic proximity Read ↗

Differing roles of Akt and serum- and glucocorticoid-regulated kinase in glucose metabolism, DNA synthesis, and oncogenic activity.Semantic proximity Read ↗

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