Recruitment of Stem and Progenitor Cells from the Bone Marrow Niche Requires MMP-9 Mediated Release of Kit-Ligand
- B. Heissig, K. Hattori, S. Rafii
- 31 May 2002
Imatinib potentiates anti-tumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido
- V. Balachandran, M. Cavnar, R. DeMatteo
- Biology, MedicineNature Network Boston
- 28 August 2011
It is found that the immune system contributes substantially to the antitumor effects of imatinib in GIST, and concomitant immunotherapy may further improve outcomes in human cancers treated with targeted agents.
Acquired Resistance to Imatinib in Gastrointestinal Stromal Tumor Occurs Through Secondary Gene Mutation
- C. Antonescu, P. Besmer, R. DeMatteo
- Medicine, BiologyClinical Cancer Research
- 1 June 2005
That acquired resistance to imatinib in GIST commonly occurs via secondary gene mutation in the KIT kinase domain has implications for strategies to delay or preventImatinib resistance and to employ newer targeted therapies.
Differential expression and processing of two cell associated forms of the kit-ligand: KL-1 and KL-2.
It is shown that the soluble form of KL is generated by efficient proteolytic cleavage from a transmembrane precursor, KL-1, and that Sld, a viable steel allele, is shown to encode a biologically active secreted mutant KL protein, indicating an important function for both the soluble and the cell associate form of Kl.
The hematopoietic growth factor KL is encoded by the SI locus and is the ligand of the c-kit receptor, the gene product of the W locus
Point mutation in Kit receptor tyrosine kinase reveals essential roles for Kit signaling in spermatogenesis and oogenesis without affecting other Kit responses
- H. Kissel, I. Timokhina, P. Besmer
- BiologyEMBO Journal
- 15 March 2000
A block in Kit receptor‐mediated PI 3‐kinase signaling may be compensated for in hematopoiesis, melano‐genesis and primordial germ cell development, but is critical in spermatogenesis and oogenesis.
Kit signaling through PI 3‐kinase and Src kinase pathways: an essential role for Rac1 and JNK activation in mast cell proliferation
- I. Timokhina, H. Kissel, Greg Stella, P. Besmer
- BiologyEMBO Journal
- 2 November 1998
It is demonstrated that the PI 3‐kinase and Src kinase signaling pathways converge to activate Rac1 and JNK, and that elimination of both pathways abolishes them.
Gonadal expression of c-kit encoded at the W locus of the mouse.
- K. Manova, K. Nocka, P. Besmer, R. Bachvarova
- 1 December 1990
It was concluded that the period of expression of c-kit extends from at least as early as type A2 spermatogonia through type B sperMatogonia and into preleptotene sperMATocytes.
Novel V600E BRAF mutations in imatinib‐naive and imatinib‐resistant gastrointestinal stromal tumors
- Narasimhan P. Agaram, Grace C. Wong, C. Antonescu
- Biology, MedicineGenes, Chromosomes and Cancer
- 1 October 2008
It is hypothesis following the melanoma model that mutations in BRAF or NRAS may play a role in wild‐type GIST pathogenesis, and a primary BRAF V600E mutations in 7% of adult GIST patients, lacking KIT/PDGFRA mutations are identified.
The kit-ligand (steel factor) and its receptor c-kit/W: pleiotropic roles in gametogenesis and melanogenesis.
- P. Besmer, K. Manova, R. Bachvarova
- 1 December 1993
It is proposed that the ectopic c-kit expression in Wsh mice affects early melanogenesis in a dominant fashion and the "sash" or white belt of Wsh/+ animals and some other mutant mice is explained by the varying density of melanoblasts along the body axis of wild-type embryos.