Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P42345 (mTOR)
 26,049 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The 21st international symposium of the American Association for Cancer Research (AACR), the NCI and the European Organization for Research and Treatment of Cancer (EORTC), held in Boston, included topics covering the development of therapeutics and molecular targets in the field of cancer research. This conference report highlights selected presentations on the development of novel drugs for cancer. Investigational drugs discussed include RO-506876 (F Hoffmann-La Roche Ltd), GDC-0980 (Genentech Inc), EMD-1214063 and EMD-1204831 (Merck Serono SA), AR-mTOR01 and AR-mTOR-26 (Array BioPharma Inc), GSK-2126458 (GlaxoSmithKline plc), EXEL-1415 and EXEL-2008 (Exelixis Inc), FP-1039 (FivePrime Therapeutics Inc), and AV-412 (AVEO Pharmaceuticals Inc).
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PMID:AACR-NCI-EORTC--21st International Symposium. Molecular targets and cancer therapeutics--Part 2. 2002 39

mTOR inhibitors have potent antiangiogenic and anti-lymphangiogenic effects in addition to their growth inhibitory effects in head and neck squamous cell carcinoma (HNSCC). Lymphatogenous spread is much more predominant in HNSCC than hematogenous spread and significantly decreases survival. In this study we evaluated the effects of rapamycin on targeting tumor-stroma crosstalk in HNSCC. HNSCC tumor cells (FaDu) and human lymphatic endothelial cells (HMEC-1A) were co-cultured in various combinations using transwell cell culture inserts to study tumor-stroma crosstalk and the effects of mTOR inhibitor rapamycin. Levels of growth factors and cytokines in cell culture media were measured using Milliplex bead immunoassay (EMD Millipore) and ELISA assay (R&D Systems). We found that conditioned media collected from tumor cells or co-culture with tumor cells significantly increased the invasiveness of lymphatic and blood vascular endothelial cells (P<0.05), while there was no effect of conditioned media collected from endothelial cell cultures or co-culture with endothelial cells on tumor cell invasiveness. There was a significant effect of rapamycin on both baseline and tumor cell stimulated invasiveness of endothelial cells (P<0.05). Importantly the level of IL-6 secreted in media increased significantly in tumor-endothelial cell co-culture compared to monocultures. Rapamycin significantly suppressed secretion of IL-6 by tumor cells (P<0.05). Thus, HNSCC cells produce chemotactic stimuli that promote endothelial cell invasion toward tumor cells that can stimulate lymphangiogenesis. Rapamycin effectively reverted the stimulatory effect of IL-6 secreted by tumor cells on endothelial cell invasiveness.
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PMID:Rapamycin targets Interleukin 6 (IL-6) expression and suppresses endothelial cell invasion stimulated by tumor cells. 2790 83