Peter Besmer

Avian bic, a gene isolated from a common retroviral site in avian leukosis virus-induced lymphomas that encodes a noncoding RNA, cooperates with c-myc in lymphomagenesis and erythroleukemogenesis.

Recruitment of stem and progenitor cells from the bone marrow niche requires MMP-9 mediated release of kit-ligand.

Gastrointestinal stromal tumors in a mouse model by targeted mutation of the Kit receptor tyrosine kinase.

A role for kit receptor signaling in Leydig cell steroidogenesis.

Association of KIT exon 9 mutations with nongastric primary site and aggressive behavior: KIT mutation analysis and clinical correlates of 120 gastrointestinal stromal tumors.

Pleomorphic characteristics of a germ-line KIT mutation in a large kindred with gastrointestinal stromal tumors, hyperpigmentation, and dysphagia.

Critical role for Kit-mediated Src kinase but not PI 3-kinase signaling in pro T and pro B cell development.

Gene expression in gastrointestinal stromal tumors is distinguished by KIT genotype and anatomic site.

Multiple gastrointestinal stromal tumors in type I neurofibromatosis: a pathologic and molecular study.

Gastrointestinal stromal tumors in children and young adults: a clinicopathologic, molecular, and genomic study of 15 cases and review of the literature.

Acquired resistance to imatinib in gastrointestinal stromal tumor occurs through secondary gene mutation.

Extracellular KIT receptor mutants, commonly found in core binding factor AML, are constitutively active and respond to imatinib mesylate.

Lyn kinase promotes erythroblast expansion and late-stage development.

A distant upstream locus control region is critical for expression of the Kit receptor gene in mast cells.

The scaffolding adapter Gab2, via Shp-2, regulates kit-evoked mast cell proliferation by activating the Rac/JNK pathway.

Oncogenic Kit signaling and therapeutic intervention in a mouse model of gastrointestinal stromal tumor.

Comparative ultrastructural analysis and KIT/PDGFRA genotype in 125 gastrointestinal stromal tumors.

Pathologic and molecular heterogeneity in imatinib-stable or imatinib-responsive gastrointestinal stromal tumors.

Different ADAMs have distinct influences on Kit ligand processing: phorbol-ester-stimulated ectodomain shedding of Kitl1 by ADAM17 is reduced by ADAM19.

Histone H2AX is a mediator of gastrointestinal stromal tumor cell apoptosis following treatment with imatinib mesylate.

L576P KIT mutation in anal melanomas correlates with KIT protein expression and is sensitive to specific kinase inhibition.

Sorafenib inhibits the imatinib-resistant KITT670I gatekeeper mutation in gastrointestinal stromal tumor.

Tumor mitotic rate, size, and location independently predict recurrence after resection of primary gastrointestinal stromal tumor (GIST).

Molecular characterization of pediatric gastrointestinal stromal tumors.

Novel V600E BRAF mutations in imatinib-naive and imatinib-resistant gastrointestinal stromal tumors.

Changes in the structure and function of ICC networks in ICC hyperplasia and gastrointestinal stromal tumors.

A KIT juxtamembrane PY567 -directed pathway provides nonredundant signals for erythroid progenitor cell development and stress erythropoiesis.

Kit signaling via PI3K promotes ovarian follicle maturation but is dispensable for primordial follicle activation.

Mechanisms of sunitinib resistance in gastrointestinal stromal tumors harboring KITAY502-3ins mutation: an in vitro mutagenesis screen for drug resistance.

Kit ligand cytoplasmic domain is essential for basolateral sorting in vivo and has roles in spermatogenesis and hematopoiesis.

Imatinib upregulates compensatory integrin signaling in a mouse model of gastrointestinal stromal tumor and is more effective when combined with dasatinib.

Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido.

CD133 and CD44 are universally overexpressed in GIST and do not represent cancer stem cell markers.