Genomes and Genes
Gene Symbol: C-kit
Description: KIT proto-oncogene receptor tyrosine kinase
Alias: C-Kit, CD117, PBT, SCFR, mast/stem cell growth factor receptor Kit, c-Kit protooncogene, p145 c-kit, piebald trait protein, proto-oncogene c-Kit, proto-oncogene tyrosine-protein kinase Kit, soluble KIT variant 1, tyrosine-protein kinase Kit, v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog, v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene-like protein
Publications366 found, 100 shown here
- Identification of a point mutation in the catalytic domain of the protooncogene c-kit in peripheral blood mononuclear cells of patients who have mastocytosis with an associated hematologic disorderH Nagata
Allergic Diseases Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 92:10560-4. 1995....
- Familial gastrointestinal stromal tumours with germline mutation of the KIT geneT Nishida
Nat Genet 19:323-4. 1998
- KIT pathway alterations in mucosal melanomas of the vulva and other sitesKatarina Omholt
Department of Oncology Pathology, Karolinska Institutet, Karolinska University Hospital Solna, Stockholm, Sweden
Clin Cancer Res 17:3933-42. 2011....
- PDGFRA activating mutations in gastrointestinal stromal tumorsMichael C Heinrich
Department of Medicine, Department of Pathology, Oregon Health and Science University Cancer Institute and Portland VA Medical Center, Portland, OR 97201, USA
Science 299:708-10. 2003..Thus, KIT and PDGFRA mutations appear to be alternative and mutually exclusive oncogenic mechanisms in GISTs...
- Association of paediatric mastocytosis with a polymorphism resulting in an amino acid substitution (M541L) in the transmembrane domain of c-KITR Foster
School of Biomedical Sciences, The University of Newcastle, Callaghan, New South Wales 2308, Australia
Br J Dermatol 159:1160-9. 2008..The receptor tyrosine kinase c-KIT plays a key role in normal mast cell development. Point mutations in c-KIT have been associated with sporadic or familial mastocytosis...
- Deletions affecting codons 557-558 of the c-KIT gene indicate a poor prognosis in patients with completely resected gastrointestinal stromal tumors: a study by the Spanish Group for Sarcoma Research (GEIS)Javier Martin
Department of Oncology, Hospital Universitario de Son Dureta, C Andrea Doria 55, 07014 Palma de Mallorca Baleares, Spain
J Clin Oncol 23:6190-8. 2005..We have investigated the prognostic relevance of the type and position of the mutations, in addition to other clinicopathologic factors, in a large series of patients with GIST...
- Clonal analysis of NRAS activating mutations in KIT-D816V systemic mastocytosisTodd M Wilson
Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, 20892 1881, USA
Haematologica 96:459-63. 2011..Unlike other mature lineages, mast cell survival is dependent on KIT and the presence of these two activating mutations may have a greater impact on the expansion of this cell compartment and in resultant disease severity...
- The meaning of the c-kit proto-oncogene product in malignant transformation in human mammary epitheliumChang Dae Ko
Department of Surgery, University of Ulsan College of Medicine and Asan Medical Center, Seoul, South Korea
Clin Exp Metastasis 20:593-7. 2003..This result suggests that the loss of expression of this protein might correlate with malignant breast cancer progression, but it is most likely involved at an early stage of human breast cancer development...
- Clinical implications of C-kit gene mutation in patients with large gastrointestinal stromal tumorsShee Chan Lin
Division of Gastroenterology, Department of Internal Medicine, Mackay Memorial Hospital and Mackay Medicine, Nursing and Management College, Taipei, Taiwan
J Gastroenterol Hepatol 21:1604-8. 2006..To evaluate the clinical implications of C-kit gene mutation in patients with gastrointestinal stromal tumors (GIST) greater than 10 cm in size...
- Prediction of KIT mutation in gastrointestinal stromal tumors by the immunoprofile of the tumor cellsChu Chung Chou
Department of Emergency Medicine, Changhua Christian Hospital, Changhua, Taiwan
J Formos Med Assoc 109:25-31. 2010..Standardized mutation analysis is not available in many countries; therefore, we aimed to determine if the presence of KIT mutation in GIST can be predicted by the immunoprofile of the tumor cells...
- Monitoring of minimal residual disease in patients with core binding factor acute myeloid leukemia and the impact of C-KIT, FLT3, and JAK2 mutations on clinical outcomeJana Markova
Institute of Hematology and Blood Transfusion, Prague 2, Czech Republic
Leuk Lymphoma 50:1448-60. 2009..These results need validation in even larger patient cohorts than ours. For routine clinical practice, it may be meaningful to screen for C-KIT mutations in AML1/ETO-positive patients, as well as for FLT3(D835) mutations in CBF-AML...
- Preferential localization of c-kit product in tissue mast cells, basal cells of skin, epithelial cells of breast, small cell lung carcinoma and seminoma/dysgerminoma in human: immunohistochemical study on formalin-fixed, paraffin-embedded tissuesY Tsuura
Department of Pathology, Fukushima Medical College, Japan
Virchows Arch 424:135-41. 1994..The c-kit product may be a useful marker in diagnostic pathology of seminoma/dysgerminoma and SCLC among human solid tumours, and in distinction of SCLC from non-pulmonary small cell carcinoma...
- Phosphatidylinositol 3-kinase and Src family kinases are required for phosphorylation and membrane recruitment of Dok-1 in c-Kit signalingXiquan Liang
Cell Biology Program and the Molecular Pharmacology and Therapeutics Program, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
J Biol Chem 277:13732-8. 2002..Taken together, these data indicate that activation of PI 3-kinase by KL promotes binding of the Dok pleckstrin homology domain and Dok-1 recruitment to the plasma membrane where Dok-1 is phosphorylated by Src and/or Tec family kinases...
- Expression of the c-kit receptor characterizes a subset of neuroblastomas with favorable prognosisMatthias Krams
Department of Pediatric Pathology, University of Kiel, Germany
Oncogene 23:588-95. 2004..Assessment of c-kit may improve prognostic models for neuroblastoma and provide a basis for new therapy concepts...
- Expression and mutational analysis of c-kit in ovarian surface epithelial tumorsDong Ja Kim
Department of Pathology, Fatima Hospital, Daegu, Korea
J Korean Med Sci 21:81-5. 2006..Although, KIT protein expression showed higher incidence in mucinous tumors than serous tumors, they lack KIT-activating mutations in exon 11. Thus, ovarian surface epithelial tumors are unlikely to respond to imatinib mesylate...
- Diagnostic utility of CD117, CD133, SALL4, OCT4, TCL1 and glypican-3 in malignant germ cell tumors of the ovaryDat Tien Trinh
Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan
J Obstet Gynaecol Res 38:841-8. 2012..Immunohistochemistry can help in the diagnosis and development of new management strategies. The aim of this study was to investigate the frequency of CD117, CD133, SALL4, OCT4, TCL1 and glypican-3 marker expression in OMGCTs.
- Gastrointestinal stromal tumors with KIT exon 11 deletions are associated with poor prognosisJohanna Andersson
Department of Pathology at the Sahlgrenska Academy, Lundberg Laboratory for Cancer Research, Goteborg University, Goteborg, Sweden
Gastroenterology 130:1573-81. 2006..We investigated the correlation among mutation type, phenotype, and clinical course in a preimatinib, population-based series of GIST with long-term follow-up...
- Structural basis for activation of the receptor tyrosine kinase KIT by stem cell factorSatoru Yuzawa
Department of Pharmacology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA
Cell 130:323-34. 2007....
- Deletion of the c-kit protooncogene in the human developmental defect piebald traitR A Fleischman
Department of Medicine, University of Texas Southwestern Medical Center, Dallas 75235
Proc Natl Acad Sci U S A 88:10885-9. 1991....
- Correlation of kinase genotype and clinical outcome in the North American Intergroup Phase III Trial of imatinib mesylate for treatment of advanced gastrointestinal stromal tumor: CALGB 150105 Study by Cancer and Leukemia Group B and Southwest Oncology GrMichael C Heinrich
Division of Hematology Oncology, Department of Medicine and Cell and Developmental Biology, Portland Veterans Affairs Medical Center and Oregon Health and Science University Cancer Institute, Portland, OR 97239, USA
J Clin Oncol 26:5360-7. 2008..In previous studies, GIST genotype correlated with treatment outcome and optimal imatinib dosing...
- Identification of proapoptotic Bim as a tumor suppressor in neoplastic mast cells: role of KIT D816V and effects of various targeted drugsKarl J Aichberger
Department of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of Vienna, Vienna, Austria
Blood 114:5342-51. 2009..Targeting of Bcl-2 family members by drugs promoting Bim (re)-expression, or by BH3-mimetics such as obatoclax, may be an attractive therapy concept in SM...
- Presence of homozygous KIT exon 11 mutations is strongly associated with malignant clinical behavior in gastrointestinal stromal tumorsJerzy Lasota
Department of Soft Tissue Pathology, Armed Forces Institute of Pathology, Washington, DC 20306 6000, USA
Lab Invest 87:1029-41. 2007..4 months. Based on these findings, we conclude that presence of homozygous KIT exon 11 mutations is associated with malignant course of disease and should be considered an adverse prognostic marker in GISTs...
- KIT mutations are common in testicular seminomasKathleen Kemmer
Division of Hematology and Oncology, Oregon Health and Science University Cancer Institute and Portland Veterans Affairs Medical Center, Portland, Oregon 97239, USA
Am J Pathol 164:305-13. 2004..These findings suggest that activating KIT mutations may contribute to tumorigenesis in a subset of seminomas, but are not involved in NSGCT...
- Kit as a human oncogenic tyrosine kinaseY Kitamura
Shionogi Pharmaceutical Company, 3 1 1 Futaba cho, Toyonaka, Osaka 561 0825, Japan
Cell Mol Life Sci 61:2924-31. 2004..The interrelationship between the type of Kit gain-of-function mutations and the therapeutic effect of imatinib mesylate has been well characterized in GISTs. Kit is interesting from both a biological and clinical view-point...
- Mechanisms of sunitinib resistance in gastrointestinal stromal tumors harboring KITAY502-3ins mutation: an in vitro mutagenesis screen for drug resistanceTianhua Guo
Departments of Pathology, Medicine, and Surgery, Memorial Sloan Kettering Cancer Center, Sloan Kettering Institute, New York, NY 10021, USA
Clin Cancer Res 15:6862-70. 2009..The clinical benefit of sunitinib is genotype-dependent in regards to both primary and secondary mutations, with GIST patients harboring the KIT(AY502-3ins) exon 9 mutation being the most sensitive...
- Induction of stem cell factor/c-Kit/slug signal transduction in multidrug-resistant malignant mesothelioma cellsAlfonso Catalano
Department of Molecular Pathology and Innovative Therapies, Polytechnic University of Marche, Ancona 60131, Italy
J Biol Chem 279:46706-14. 2004....
- Multiple novel alterations in Kit tyrosine kinase in patients with gastrointestinally pronounced systemic mast cell activation disorderGerhard J Molderings
Institut fur Pharmakologie und Toxikologie, Universitatsklinikum Bonn, Germany
Scand J Gastroenterol 42:1045-53. 2007....
- Gab2 is involved in differential phosphoinositide 3-kinase signaling by two splice forms of c-KitJianmin Sun
Experimental Clinical Chemistry, Department of Laboratory Medicine, Malmo University Hospital, Lund University, SE 205 02 Malmo, Sweden
J Biol Chem 283:27444-51. 2008....
- Analysis of the activating mutations within the activation loop of leukemia targets Flt-3 and c-Kit based on protein homology modelingMaricel Torrent
Departments of Molecular Systems, Merck Research Laboratories, Merck Co, Sumneytown Pike, West Point, PA 19486, USA
J Mol Graph Model 23:153-65. 2004..The reason why the equilibrium is shifted towards the gate-open conformation of the protein is because, at least in these models, the mutations are found to critically destabilize the inactive conformational state of the kinase...
- Grb2 mediates negative regulation of stem cell factor receptor/c-Kit signaling by recruitment of CblJianmin Sun
Experimental Clinical Chemistry, Department of Laboratory Medicine, Lund University, Malmo University Hospital, SE 205 02 Malmo, Sweden
Exp Cell Res 313:3935-42. 2007....
- C-kit protein expression correlated with activating mutations in KIT gene in oral mucosal melanomaRosario S Rivera
Department of Oral Pathology and Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan
Virchows Arch 452:27-32. 2008..C-kit protein expression correlated with activating mutations indicating the pertinent role of the proto-oncogene KIT in the tumorigenesis of OMM...
- MicroRNA-dependent regulation of cKit in cutaneous melanomaO Igoucheva
Department of Dermatology and Cutaneous Biology, Jefferson Medical College, Thomas Jefferson University, 233 S 10th Street, Philadelphia, PA 19107, USA
Biochem Biophys Res Commun 379:790-4. 2009..They also suggest that regulation of expression and functional activity of identified up-regulated miRNAs should be further studied in the context of malignant melanoma...
- A Variant in a MicroRNA complementary site in the 3' UTR of the KIT oncogene increases risk of acral melanomaS E Godshalk
Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, CT, USA
Oncogene 30:1542-50. 2011..This work identifies a novel genetic marker for increased heritable risk of melanoma...
- Gene expression in gastrointestinal stromal tumors is distinguished by KIT genotype and anatomic siteCristina R Antonescu
Departments of Pathology, Memorial Sloan Kettering Cancer Center, and Molecular Biology, Computational Biology Center, Sloan Kettering Institute, New York, New York 10021, USA
Clin Cancer Res 10:3282-90. 2004..We tested the hypothesis that the gene expression profile in GISTs might be related to KIT genotype and possibly to other clinicopathological factors...
- Mechanisms of resistance to imatinib mesylate in gastrointestinal stromal tumors and activity of the PKC412 inhibitor against imatinib-resistant mutantsMaria Debiec-Rychter
Center for uman Genetics, Catholic University of Leuven, Leuven, Belgium
Gastroenterology 128:270-9. 2005..We investigated the mechanisms of resistance in patients with progressive GISTs with primary KIT mutations and the efficacy of the kinase inhibitor PKC412 for the inhibition of imatinib-resistant mutants...
- JAK2 is associated with the c-kit proto-oncogene product and is phosphorylated in response to stem cell factorS R Weiler
Division of Cancer Treatment, and Biological Carcinogenesis and Development Program, SAIC Frederick, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702, USA
Blood 87:3688-93. 1996..These data demonstrate that SCF induces tyrosine phosphorylation of JAK2 and suggest that JAK2 is a component of the SCF signal transduction pathway...
- The complexity of KIT gene mutations and chromosome rearrangements and their clinical correlation in gastrointestinal stromal (pacemaker cell) tumorsJohanna Andersson
Department of Pathology, Lundberg Laboratory for Cancer Research, Sahlgrenska University Hospital, Goteborg University, Goteborg, Sweden
Am J Pathol 160:15-22. 2002..Collectively, these findings indicate that the role of KIT mutations and chromosomal rearrangements in the pathogenesis of GIST/GIPACTs are more complex than previously recognized...
- Updates on the cytogenetics and molecular genetics of bone and soft tissue tumors. gastrointestinal stromal tumorsAvery A Sandberg
Department of DNA Diagnostics, St Joseph s Hospital and Medical Center, 350 West Thomas Road, Phoenix, AZ 85013, USA
Cancer Genet Cytogenet 135:1-22. 2002
- Evidence for the involvement of a hematopoietic progenitor cell in systemic mastocytosis from single-cell analysis of mutations in the c-kit geneA Selim Yavuz
Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases NIAMS, and Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases NIAID, National Institutes of Health, Bethesda, MD 20892, USA
Blood 100:661-5. 2002....
- Overexpression of KIT in chromophobe renal cell carcinomaKen Yamazaki
Cancer Genomics Division, National Cancer Center Research Institute, Tokyo, Japan
Oncogene 22:847-52. 2003..As overexpression of KIT might be involved in tumor growth, KIT could be a new therapeutic target in this special type of RCC...
- A conserved quadruplex motif located in a transcription activation site of the human c-kit oncogeneHimesh Fernando
Department of Chemistry, University of Cambridge, Lensfield Road, Cambridge, CB2 1EW, United Kingdom
Biochemistry 45:7854-60. 2006..Collectively, the evidence suggests that this quadruplex is a serious target for a detailed functional investigation at the cell-biology level...
- Molecular alterations of KIT and PDGFRA in GISTs: evaluation of a Portuguese seriesA L Gomes
Life and Health Sciences Research Institute ICVS, School of Health Sciences, University of Minho, Braga, Portugal
J Clin Pathol 61:203-8. 2008..To assess KIT and PDGFRA mutations frequencies in a Portuguese series of gastrointestinal stromal tumours (GISTs)...
- Tumour microvessel endothelial cell KIT and stem cell factor expression in human solid tumoursHarri Sihto
Laboratory of Molecular Oncology, Biomedicum Helsinki, Helsinki, Finland
Histopathology 55:544-53. 2009..To assess KIT receptor tyrosine kinase and stem cell factor (SCF, KIT ligand) expression in tumour microvessel endothelial cells...
- KIT overexpression and amplification in gastrointestinal stromal tumors (GISTs)Séverine Tabone
Biochemistry and Molecular Biology Department, Paul Brousse Hospital, AP HP, INSERM U602, Paris Sud University, Villejuif 94804, France
Biochim Biophys Acta 1741:165-72. 2005..03 respectively). In conclusion, contrasting with the regulation of other tyrosine kinase receptors, KIT overexpression in GISTs is rarely related to a gene amplification, which suggests a deregulation of KIT gene transcription...
- KIT (c-kit oncogene product) pathway is constitutively activated in human testicular germ cell tumorsYasutomo Nakai
Department of Urology, Osaka University Graduate School of Medicine, Japan
Biochem Biophys Res Commun 337:289-96. 2005..These findings suggest that the KIT-PI3K-Akt pathway is constitutively activated in testicular germ cell tumors, due to overexpression of KIT protein and/or gain-of-function mutations in the c-kit gene...
- c-Kit/PDGFRA gene status alterations possibly related to primary imatinib resistance in gastrointestinal stromal tumorsFrancesca C Miselli
Experimental Molecular Pathology, Fondazione IRCCS, Istituto Nazionale dei Tumori, Milan, Italy
Clin Cancer Res 13:2369-77. 2007..To correlate morphologic changes with molecular, biochemical, and cytogenetic profiles in gastrointestinal stromal tumor (GIST) patients before and after imatinib treatment...
- Novel, activating KIT-N822I mutation in familial cutaneous mastocytosisBartosz Wasag
Department of Biology and Genetics, Medical University of Gdansk, Gdansk, Poland
Exp Hematol 39:859-65.e2. 2011..In the children, tryptase measurement and skin histopathological examination were performed...
- Increased gene copy number of KIT and VEGFR2 at 4q12 in primary breast cancer is related to an aggressive phenotype and impaired prognosisIda Johansson
Department of Oncology, Clinical Sciences and CREATE Health Strategic Center for Translational Cancer Research, Lund University, Lund, Sweden
Genes Chromosomes Cancer 51:375-83. 2012..Increased copy number of VEGFR2 and KIT thus has the potential of functioning as a novel predictive biomarker for selected targeted therapy particularly in the difficult-to-treat TNBC patient category...
- Kit signaling through PI 3-kinase and Src kinase pathways: an essential role for Rac1 and JNK activation in mast cell proliferationI Timokhina
Molecular Biology Program, Memorial Sloan Kettering Cancer Center, Cornell University Graduate School of Medical Sciences, New York, NY 10021, USA
EMBO J 17:6250-62. 1998..In addition, KL was shown to inhibit sustained activation of JNK induced by gamma-irradiation and concomitant irradiation-induced apoptosis...
- STAT protein recruitment and activation in c-Kit deletion mutantsM F Brizzi
Department of Internal Medicine, University of Turin, Turin 10126, Italy
J Biol Chem 274:16965-72. 1999..These results indicate that different intracellular domains of c-Kit are involved in activation of the various STAT proteins...
- Activating c-kit gene mutations in human germ cell tumorsQ Tian
Departments of Pathology, University of Virginia Health Sciences Center, Charlottesville, USA
Am J Pathol 154:1643-7. 1999..This is the first description of an activating c-kit mutation in GCTs and is evidence that the KIT signal transduction pathway is important in the pathogenesis of neoplasms with seminoma differentiation...
- Primary mediastinal seminomas: evidence of single and multiple KIT mutationsRonald M Przygodzki
Armed Forces Institute of Pathology, Department of Cellular Pathology and Genetics, Rockville, Maryland 20850, USA
Lab Invest 82:1369-75. 2002..Our findings demonstrate a unique KIT sequence and expression pattern among MS. KIT sequencing may assist in differentiating primary from metastatic MS...
- Molecular cloning of mammalian Spred-3 which suppresses tyrosine kinase-mediated Erk activationReiko Kato
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
Biochem Biophys Res Commun 302:767-72. 2003..The finding of Spred-3 revealed the presence of a novel family of regulators for the Ras/MAP kinase pathway, each member of which may have different specificities for extracellular signals...
- Clinicopathologic, phenotypic, and genotypic characteristics of gastrointestinal mesenchymal tumorsJean Francois Emile
Pathology Department, Ambroise Pare Hospital, Boulogne, France
Clin Gastroenterol Hepatol 2:597-605. 2004..This retrospective multicenter study included 276 patients with gastrointestinal mesenchymal tumors...
- Gastrointestinal stromal tumors (GISTs) with KIT and PDGFRA mutations have distinct gene expression profilesSubbaya Subramanian
Department of Pathology, Stanford University Medical Center, Stanford, CA 94305, USA
Oncogene 23:7780-90. 2004..These gene products could serve as highly selective therapeutic targets in GISTs containing the KIT or PDGFRA mutational types with which they are associated...
- KIT activating mutations: incidence in adult and pediatric acute myeloid leukemia, and identification of an internal tandem duplicationAlessandro Beghini
Department of Biology and Genetics for Medical Sciences, Medical Faculty, University of Milan, Italy
Haematologica 89:920-5. 2004..We evaluated the incidence of KIT mutation in 52 adult patients with de novo CBFL and in 49 FLT3/ITD-negative childhood patients with de novo acute myeloid leukemia (AML), excluding cases of acute promyelocytic leukemia...
- The Kasumi-1 cell line: a t(8;21)-kit mutant model for acute myeloid leukemiaLidia Larizza
Department of Biology and Genetics for Medical Sciences, Medical Faculty, University of Milan, Italy
Leuk Lymphoma 46:247-55. 2005..Independent findings on the same model system provide complementary insights into designing strategies for treatment of CBF leukemia associated with mutations in the KIT catalytic domain...
- KIT (CD117): a review on expression in normal and neoplastic tissues, and mutations and their clinicopathologic correlationMarkku Miettinen
Department of Soft Tissue Pathology, Armed Forces Institute of Pathology, Washington, DC 20306 6000, USA
Appl Immunohistochem Mol Morphol 13:205-20. 2005b>CD117 (KIT) is a type III receptor tyrosine kinase operating in cell signal transduction in several cell types. Normally KIT is activated (phosphorylated) by binding of its ligand, the stem cell factor...
- Polyclonal evolution of multiple secondary KIT mutations in gastrointestinal stromal tumors under treatment with imatinib mesylateEva Wardelmann
Department of Pathology, University of Bonn Medical School, Bonn, Germany
Clin Cancer Res 12:1743-9. 2006..According to our results, the identification of newly acquired KIT mutations in addition to the primary mutation is dependent on the number of tissue samples analyzed and has high implications for further therapeutic strategies...
- KIT and PDGFRA mutations in gastrointestinal stromal tumors (GISTs)Jerzy Lasota
Department of Soft Tissue Pathology, Armed Forces Institute of Pathology, Washington, DC 20306 6000, USA
Semin Diagn Pathol 23:91-102. 2006..Mutation genotyping is a tool in GIST diagnosis and in assessment of sensitivity to kinase inhibitors. This is a US government work. There are no restrictions on its use...
- Cooperating mutations of receptor tyrosine kinases and Ras genes in childhood core-binding factor acute myeloid leukemia and a comparative analysis on paired diagnosis and relapse samplesL Y Shih
Division of Hematology Oncology, Chang Gung Memorial Hospital, Taipei, Taiwan
Leukemia 22:303-7. 2008..Our study showed that 54% of childhood CBF-AML had RTKs and/or Ras mutations; c-KIT but not CSF1R mutations play a role in the leukemogenesis of childhood CBF-AML...
- CD117/KIT expression in pancreatic adenocarcinomaAdrian C Bateman
Department of Cellular Pathology, Southampton General Hospital, Southampton, UK
Pancreas 36:76-9. 2008b>CD117/KIT overexpression is common in neoplasms such as gastrointestinal stromal tumors and predicts clinical response to tyrosine kinase inhibitors...
- Expression of c-kit and platelet-derived growth factor receptors in ovarian granulosa cell tumorsRodney P Rocconi
Department of Obstetrics and Gynecology, University of South Alabama Mitchell Cancer Institute, Mobile, Alabama 36607, USA
Reprod Sci 15:673-7. 2008..This study aimed at evaluating the expression of tyrosine kinase receptors c-kit, (platelet-derived growth factor receptor-alpha (PDGFR-alpha), and PDGFR-beta in ovarian granulosa cell tumors (GCTs)...
- Multiple sporadic gastrointestinal stromal tumors (GISTs) of the proximal stomach are caused by different somatic KIT mutations suggesting a field effectAbbas Agaimy
Institute of Pathology, Nürnberg Clinic Center, Nurnberg, Germany daggerInstitute of Pathology, University of Basel, Basel, Switzerland
Am J Surg Pathol 32:1553-9. 2008....
- Immunohistochemical detection of receptor tyrosine kinases c-kit, EGF-R, and PDGF-R in colorectal adenocarcinomasJan Friederichs
Department of Surgery, Klinikum rechts der Isar, Technische Universitat Munchen, Munich, Germany
Langenbecks Arch Surg 395:373-9. 2010..This study aimed to clarify expression patterns of therapeutically addressable receptor tyrosine kinases in colorectal cancer...
- Prognosis and predictive value of KIT exon 11 deletion in GISTsJ B Bachet
EA4340 Epidémiologie et Oncogénesè des Tumeurs Digestives, Faculté de Médecine PIFO, UVSQ, Guyancourt, France
Br J Cancer 101:7-11. 2009..Our aim was to compare the outcome of patients with deletion of both Tyr568-570 (delTyr) and the most frequent deletion delWK557-558 (delWK)...
- Efficacy evaluation of imatinib treatment in patients with gastrointestinal stromal tumors: a meta-analysisPing Chen
Department of Gastrointestinal Surgery, Subei People s Hospital of Jiangsu Province, Yangzhou 225001, Jiangsu Province, China
World J Gastroenterol 16:4227-32. 2010..To perform a meta-analysis to derive a more precise estimation of imatinib treatment for different genotypes of gastrointestinal stromal tumors (GIST)...
- Large-scale analysis of KIT aberrations in Chinese patients with melanomaYan Kong
Key Laboratory of Carcinogenesis and Translational Research Ministry of Education, Department of Renal Cancer and Melanoma, Peking University Cancer Hospital and Institute, Beijing, China
Clin Cancer Res 17:1684-91. 2011..KIT aberrations were described in acral and mucosal melanomas in largely Caucasian populations. Asian populations are more prone to develop acral and mucosal than cutaneous melanomas, and may harbor a high frequency of KIT aberrations...
- Amplification of the PDGFRA, KIT and KDR genes in glioblastoma: a population-based studySumihito Nobusawa
International Agency for Research on Cancer, Lyon, France
Neuropathology 31:583-8. 2011....
- Importance of c-kit mutation detection method sensitivity in prognostic analyses of t(8;21)(q22;q22) acute myeloid leukemiaS Wakita
Division of Hematology, Department of Internal Medicine, Nippon Medical School, Tokyo, Japan
Leukemia 25:1423-32. 2011..006). We conclude that sensitivity of c-kit mutation detection method is important to predict prognosis for t(8;21) AML...
- Ovarian cancer cells with the CD117 phenotype are highly tumorigenic and are related to chemotherapy outcomeLijing Luo
Department of Obstetrics and Gynecology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
Exp Mol Pathol 91:596-602. 2011..We identified and isolated the tumorigenic cells as CD117(+)Lineage(-) from three different xenografts...
- MicroRNA-494 downregulates KIT and inhibits gastrointestinal stromal tumor cell proliferationWon Kyu Kim
Department of Pathology, Yonsei, University College of Medicine, Seoul 120752, Korea
Clin Cancer Res 17:7584-94. 2011..This study aimed to discover microRNAs (miRNA) that target KIT and reveal the relationship between the discovered miRNAs and KIT expression in GISTs...
- The cancer stem cell antigens CD133, BCRP1/ABCG2 and CD117/c-KIT are not associated with prognosis in resected early-stage non-small cell lung cancerEsther Herpel
Institute of Pathology, University of Heidelberg, Heidelberg, Germany
Anticancer Res 31:4491-500. 2011..In various tumor entities, expression of cancer stem cell (CSC) antigens has been proven to be prognostically unfavorable. However, for lung cancer, the data are scant and conflicting...
- Distinct phenotypic differences associated with differential amplification of receptor tyrosine kinase genes at 4q12 in glioblastomaAnna Burford
Divisions of Molecular Pathology, The Institute of Cancer Research, Sutton, United Kingdom Cancer Therapeutics, The Institute of Cancer Research, Sutton, United Kingdom
PLoS ONE 8:e71777. 2013..Thus we have identified differential patterns of gene amplification and expression of RTKs at the 4q12 locus to be associated with specific phenotypes which may reflect their distinct underlying mechanisms. ..
- Tyrosine residue 719 of the c-kit receptor is essential for binding of the P85 subunit of phosphatidylinositol (PI) 3-kinase and for c-kit-associated PI 3-kinase activity in COS-1 cellsH Serve
Molecular Biology Program, Sloan Kettering Institute, New York, New York
J Biol Chem 269:6026-30. 1994....
- Direct association of Csk homologous kinase (CHK) with the diphosphorylated site Tyr568/570 of the activated c-KIT in megakaryocytesD J Price
Divisions of Experimental Medicine and Hematology Oncology, Beth Israel Deaconess Medical Center, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215, USA
J Biol Chem 272:5915-20. 1997..This indicates that CHK binds to the same site on c-KIT to which FYN binds, possibly bringing the two into proximity on associated c-KIT subunits and leading to the down-regulation of FYN by CHK...
- Gain-of-function mutations of c-kit in human gastrointestinal stromal tumorsS Hirota
Department of Pathology, Osaka University Medical School, Yamada oka 2 2, Suita 565, Japan
Science 279:577-80. 1998..GISTs may originate from the interstitial cells of Cajal (ICCs) because the development of ICCs is dependent on the SCF-KIT interaction and because, like GISTs, these cells express both KIT and CD34...
- Piebaldism with deafness: molecular evidence for an expanded syndromeR A Spritz
Department of Medical Genetics, School of Medicine, University of Wisconsin, Madison 53706, USA
Am J Med Genet 75:101-3. 1998....
- Stem cell factor induces phosphatidylinositol 3'-kinase-dependent Lyn/Tec/Dok-1 complex formation in hematopoietic cellsT B van Dijk
Institute of Hematology, Erasmus University Rotterdam, Rotterdam, The Netherlands
Blood 96:3406-13. 2000..These findings suggest that p62Dok-1 may function as an important scaffold molecule in cKit-mediated signaling...
- Enhanced hematopoiesis by hematopoietic progenitor cells lacking intracellular adaptor protein, LnkSatoshi Takaki
Division of Immunology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo 108 8639, Japan
J Exp Med 195:151-60. 2002..These observations indicate that Lnk plays critical roles in the expansion and function of early hematopoietic progenitors, and provide useful clues for the amplification of hematopoietic progenitor cells...
- Amplification of a novel c-Kit activating mutation Asn(822)-Lys in the Kasumi-1 cell line: a t(8;21)-Kit mutant model for acute myeloid leukemiaAlessandro Beghini
Department of Biology and Genetics, Medical Faculty, University of Milan, Italy
Hematol J 3:157-63. 2002..In rare core binding factor leukemia patients an increased dosage of a mutated Asp816(Tyr/Val) kit allele is achieved through nonrandom duplication of chromosome 4 where the c-kit gene is located...
- The adapter protein APS associates with the multifunctional docking sites Tyr-568 and Tyr-936 in c-KitPatrik Wollberg
Ludwig Institute for Cancer Research, Biomedical Centre, P O Box 595, SE 751 24 Uppsala, Sweden
Biochem J 370:1033-8. 2003..This allowed us to design mutants that selectively failed to associate with APS, while still associating with Src family members, SHP-2 and Grb2, respectively...
- Deletion of Trp-557 and Lys-558 in the juxtamembrane domain of the c-kit protooncogene is associated with metastatic behavior of gastrointestinal stromal tumorsEva Wardelmann
Department of Pathology, University of Bonn Medical Center, Bonn, Germany
Int J Cancer 106:887-95. 2003....
- Immunohistochemical determination of HER-2/neu, c-Kit (CD117), and vascular endothelial growth factor (VEGF) overexpression in malignant melanomaAnil Potti
Department of Medicine, Division of Oncology, University of North Dakota School of Medicine, 58102, USA
J Cancer Res Clin Oncol 130:80-6. 2004....
- c-KIT expression and correlation with chemotherapy resistance in ovarian carcinoma: an immunocytochemical studyM R Raspollini
Department of Human Pathology and Oncology, University of Florence, Florence, Italy
Ann Oncol 15:594-7. 2004..The aim of this study was to determine the incidence and correlation with chemotherapy resistance of c-KIT expression in advanced serous, low grade of differentiation, ovarian carcinoma...
- CD117 immunoreactivity in stage I adenocarcinoma and squamous cell carcinoma of the lung: relevance to prognosis in a subset of adenocarcinoma patientsGiuseppe Pelosi
Department of Pathology and Laboratory Medicine, European Institute of Oncology and University of Milan School of Medicine, Milan, Italy
Mod Pathol 17:711-21. 2004b>CD117, a trans-membrane tyrosine kinase receptor, has been immunolocalized in a large variety of human neoplasms...
- Detection of overexpressed and phosphorylated wild-type kit receptor in surgical specimens of small cell lung cancerElena Tamborini
Experimental Molecular Pathology, Department of Pathology, Istituto Nazionale per lo Studio e al Cura dei Tumori, Milan, Italy
Clin Cancer Res 10:8214-9. 2004....
- Expression and mutational analysis of tyrosine kinase receptors c-kit, PDGFRalpha, and PDGFRbeta in ovarian cancersSharon P Wilczynski
Department of Pathology, City of Hope National Medical Center, Duarte, CA 91010, USA
Hum Pathol 36:242-9. 2005..This study demonstrates that PDGFR alpha, PDGFR beta, and c-kit are expressed in a high percentage of epithelial ovarian cancers suggesting that tyrosine kinase inhibitors may be useful in the treatment of these tumors...
- Prognostic value of KIT mutation in gastrointestinal stromal tumorsXiao Hong Liu
Department of Pathology, Changhai Hospital, Second Military Medical University, Changhai Road, Shanghai 200433, China
World J Gastroenterol 11:3948-52. 2005..To examine the prevalence and prognostic significance of C-kit gene mutation and analysis the correlation of C-kit gene mutation and the clinicalpathologic parameters of GISTs...
- Novel germline mutation of KIT associated with familial gastrointestinal stromal tumors and mastocytosisKarin Hartmann
Department of Dermatology, University of Cologne, Cologne, Germany
Gastroenterology 129:1042-6. 2005..Our studies identify a new regulatory region in the KIT molecule and strongly suggest that patients with extracellular KIT mutations respond to tyrosine kinase inhibitors...
- Mutation and expression of PDGFRA and KIT in malignant peripheral nerve sheath tumors, and its implications for imatinib sensitivityNikola Holtkamp
Institute of Neuropathology, Charite Universitatsmedizin Berlin, Germany
Carcinogenesis 27:664-71. 2006..In summary, PDGFRA, PDGF and KIT dysregulation as well as growth inhibition of cell culture S462 by imatinib may suggest that MPNST patients benefit from treatment with imatinib...
- Deletion of the KIT gene is associated with liver metastasis and poor prognosis in patients with gastrointestinal stromal tumor in the stomachSongde Cho
Department of Medicine and Molecular Science, Hiroshima University Graduate School of Biomedical Sciences, Minami Ku, Hiroshima 734 8551, Japan
Int J Oncol 28:1361-7. 2006..Our data indicate that KIT mutations, especially deletions in exon 11, are markers of poor prognosis for gastric GISTs...
- KIT mutation in mast cells and other bone marrow hematopoietic cell lineages in systemic mast cell disorders: a prospective study of the Spanish Network on Mastocytosis (REMA) in a series of 113 patientsAndres C Garcia-Montero
Centro de Investigacion del Cancer, Campus Miguel de Unamuno, 37007 Salamanca, Spain
Blood 108:2366-72. 2006..These results would support the notion that KIT mutation is a hallmark of adult SM where it targets a pluripotent hematopoietic stem cell, and may contribute to explaining previously observed discrepancies in the literature...
- Direct binding of Cbl to Tyr568 and Tyr936 of the stem cell factor receptor/c-Kit is required for ligand-induced ubiquitination, internalization and degradationKristina Masson
Experimental Clinical Chemistry, Department of Laboratory Medicine, Lund University, Malmo University Hospital, SE 205 02 Malmo, Sweden
Biochem J 399:59-67. 2006..Taken together, our findings reveal novel insights into the mechanisms by which Cbl negatively regulates c-Kit-mediated signalling...
- Platelet-derived growth factor receptor family mutations in gastrointestinal stromal tumoursHarri Sihto
Laboratory of Molecular Oncology, Biomedicum, Haartmaninkatu 8, PO Box 700, FIN 00029 Helsinki, Finland
Scand J Gastroenterol 41:805-11. 2006..The type of gene mutation is associated with the aggressiveness of the disease, response to imatinib therapy, and the tumour site in the gastrointestinal tract. However, a subgroup of GISTs does not harbour these mutations...
- Neoplasia driven by mutant c-KIT is mediated by intracellular, not plasma membrane, receptor signalingZhifu Xiang
Washington University School of Medicine, Campus Box 8007, 660 South Euclid Avenue, St Louis, MO 63110, USA
Mol Cell Biol 27:267-82. 2007....
- Protein expression of KIT and gene mutation of c-kit and PDGFRs in Ewing sarcomasIngu Do
Department of Pathology, Kyung Hee University Hospital, 1 Hoegi dong, Dongdaemun Gu, Seoul 130 702, Republic of Korea
Pathol Res Pract 203:127-34. 2007..These findings imply other mechanisms for KIT activity and leave open the question of whether imatinib would be efficacious in the treatment of Ewing sarcoma...
- L576P KIT mutation in anal melanomas correlates with KIT protein expression and is sensitive to specific kinase inhibitionCristina R Antonescu
Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA
Int J Cancer 121:257-64. 2007..These results suggest that a subset of anal melanomas show activating KIT mutations, which are susceptible for therapy with specific kinase inhibitors...
- Clinical significance of oncogenic KIT and PDGFRA mutations in gastrointestinal stromal tumoursJ Lasota
Department of Soft Tissue Pathology, Armed Forces Institute of Pathology, Washington, DC 20306 6000, USA
Histopathology 53:245-66. 2008..GISTs with secondary mutations in exon 13 and 14 are sensitive to sunitinib, another tyrosine kinase inhibitor. KIT and PDGFRA genotyping is important for GIST diagnosis and assessment of sensitivity to tyrosine kinase inhibitors...
- Phenotypic and genotypic characteristics of mastocytosis according to the age of onsetFanny Lanternier
Universite Paris V, Service de Maladies Infectieuses et Tropicales, centre de référence des mastocytoses, Hopital Necker Enfants Malades, Centre d Infectiologie Necker Pasteur, Paris, France
PLoS ONE 3:e1906. 2008..001). In conclusion, pathogenesis of mastocytosis significantly differs according to the age of disease's onset. Our data may have major therapeutic relevance when considering c-kit-targeted therapy...
- Evolution from heterozygous to homozygous KIT mutation in gastrointestinal stromal tumor correlates with the mechanism of mitotic nondisjunction and significant tumor progressionLei L Chen
Department of Internal Medicine, Division of Hematology Oncology, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112, USA
Mod Pathol 21:826-36. 2008....
- KIT GROWTH CONTROL OF MELANOCYTIC TUMORSJames Grichnik; Fiscal Year: 2002..The proposed experiments will define to what extent manipulation of the KIT pathway will be useful for the therapeutic treatment of proliferative melanocytic disease processes. ..
- Mechanisms Regulating Reduced c-Kit-Dependent EAE Susceptibility in Male SJL MiceMELISSA ANN BROWN; Fiscal Year: 2013..These mice provide a perfect system to explore the how c-kit signaling, in concert with influences from male sex hormones, confers neuroprotection and may lead to better therapies for this devastating CNS disease. ..
- Rac1 and Rac2 Guanosine Triphosphatases in Erythroid Function and DifferentiationTHEODOSIA ANASTASIOS KALFA; Fiscal Year: 2012..abstract_text> ..
- George E Davis; Fiscal Year: 2014..Specific Aim #3. To determine how SCF, IL-3 and SDF-1[unreadable] act to regulate pericyte-induced EC sprouting responses and vasculogenic EC-pericyte tube coassembly in 3D extracellular matrices. ..
- Structural biology of oncogenic receptor tyrosine kinasesXiaolin He; Fiscal Year: 2010..These studies will elucidate novel structural mechanisms that will lay the groundwork for therapeutic development to treat class III-RTK-related cancers. ..
- STEM CELL FACTOR ACTION IN NEURAL CREST DEVELOPMENTMaya Sieber Blum; Fiscal Year: 2003..However, the newly detected additional roles of SCF in maintaining stem cells, up-regulating neurotrophin receptors and promoting sensory neurogenesis suggest additional defects in human piebaldism that remain to be elucidated. ..
- REGULATION OF MAST CELL DEVELOPMENT AND FUNCTIONSTEPHEN JOSEPH GALLI; Fiscal Year: 2010..abstract_text> ..
- Oncogenic Kit receptor signaling in vivoPeter Besmer; Fiscal Year: 2012..Furthermore we will produce and characterize mice carrying oncogenic imatinib resistant Kit alleles. ..
- Role of Vav and Rac in KIT oncogenesisReuben Kapur; Fiscal Year: 2013..abstract_text> ..
- Peter Besmer; Fiscal Year: 2014..abstract_text> ..
- ZNF-Mediated Resistance to Imatinib Mesylate in Gastrointestinal Stromal TumorLori Rink; Fiscal Year: 2013..This work will establish robust strategies to identify useful combinations in conjunction with predictive biomarkers that identify patients most likely to respond to a specific therapy. ..
- Michael Heinrich; Fiscal Year: 2016..However, the results for this project will also be valuable for the evolving development of molecularly targeted therapies for the more common solid tumors such as lung, colon, prostate, and breast cancer. ..
- Preliminary Evaluation of FDG-PET with anti-IGF-1R Targeted Therapy in GISTsMargaret von Mehren; Fiscal Year: 2013....
- Biomarkers of response to Hsp90 inhibitors in triple-negative breast cancerGabriela Chiosis; Fiscal Year: 2013....
- Phase II Study of Imatinib Mesylate in Patients with Inoperable Melanoma Gary K Schwartz; Fiscal Year: 2010..In addition, correlative studies will be performed on each patient's tumor including immunohistochemistry for CD117 as well as comparative genomic hybridization (CGH) to further assess for amplification at 4q12...
- Epidemiology of Syndromic GI Stromal TumorsJudy Ellen Garber; Fiscal Year: 2010..Our goal is to define the spectrum of syndromic GISTs, and to generate the information that will form the basis for clinical counseling for members of GIST kindreds, with and without germline mutations in KIT or PDGFRA. ..
- The Molecular Actions of Imatinib Mesylate in GISTsMargaret von Mehren; Fiscal Year: 2013..Gastrointestinal stromal tumors (GISTs) are rare but deadly mesenchymal tumors characterized by expression of CD117 and oncogenic gain-of-function mutations in c-KIT and PDGFRa...
- c-Kit Mutations and Their Role in Tumor BiologyCheryl London; Fiscal Year: 2005..abstract_text> ..
- SERGE P NANA-SINKAM; Fiscal Year: 2014....
- Development of a novel whole genome amplification method that mimics natureHuimin Kong; Fiscal Year: 2009....
- Cell signaling as a leukemia biomarkerJAMES WILLIAM JACOBBERGER; Fiscal Year: 2013....
- Paul S Frenette; Fiscal Year: 2016..Here, we will explore further the hypothesis that the retention of hematopoietic stem and progenitor cells in the niche is regulated by differing signals from the sympathetic nervous system and macrophages. ..
- Stem cell-mediated reversal of thymic involution in premature aging modelsKenneth I Weinberg; Fiscal Year: 2010....
- Pro-inflammatory role of megakaryocytes in arthritisPeter A Nigrovic; Fiscal Year: 2013....
- DC-T Cell Interactions in Pulmonary Immune ResponsesAnuradha Ray; Fiscal Year: 2012..These studies will help identify targets for inhibiting undesired immune responses in the lung at the same time promoting those that protect from infectious agents. ..
- NEUROFIBROMATOSIS TYPE 1 GENE REGULATES MYELOPOIESISDAVID W CLAPP; Fiscal Year: 2012..If the hypothesis is correct, we would predict that developing small molecules that inhibit Pak1 function could be useful as a molecular therapy for treatment of plexiform neurofibromas. ..
- Shu Hsia Chen; Fiscal Year: 2016....
- Preclinical Testing of Targeted Therapies for NeurofibromasDAVID W CLAPP; Fiscal Year: 2011..Finally, using a combination of PET and CT imaging, we now have the ability to image the development, growth, and metabolism of plexiform neurofibromas in genetically engineered mice in vivo as a function of time. ..
- Kit Inhibition in Asthma (KIA)Elliot Israel; Fiscal Year: 2012..In an ancillary study, we will examine the contribution of circulating and bone-marrow derived mast cells to the mast cell population resident in the lung. ..
- Targeting c-kit in Dendritic Cells to Control allergic Immune ResponsesPrabir Ray; Fiscal Year: 2011..PUBLIC HEALTH RELEVANCE: The goal of this project is to understand the role of a cell surface molecule, c-kit, in promoting allergic immune response to various common allergens using murine models of allergic asthma. ..
- Mouse models of neuroprotection in dopamine neuronsEric J Huang; Fiscal Year: 2013..Our long-term goal is to use information from these mutants as platforms to identify therapeutic targets that can promote survival of DA neurons under neurodegenerative conditions. ..
- Mechanism of c-Kit-Induced Cell Polarization and Asymmetric Cell DivisionWilliam T Tse; Fiscal Year: 2012..Results from this proposed project should help develop new ways to expand blood cells for clinical treatment and find better ways to eradicate leukemia stem cells. ..
- SIGNALING PATHWAYS IN CHEMICAL INDUCED OVOTOXICITYPatricia B Hoyer; Fiscal Year: 2010..This will lead to an appreciation of the global impact of the environment on the reproductive life span in women. ..
- Analysis of lung cancer stem cell radioresistanceVera Levina; Fiscal Year: 2013..We will generate new knowledge regarding lung CSC biology, and our findings could lead to significant improvements in the efficacy of NSCLC radiation therapy. ..
- Joseph H Nadeau; Fiscal Year: 2014..We also discovered, and propose to characterize spontaneous TGCT metastases in several of our mouse models. ..
- Zebrafish Based Model for Gastrointenstinal PhysiologyADAM J RICH; Fiscal Year: 2010..This AREA proposal will establish the zebrafish as a model system to study the role of ICC in GI motility, and will contribute to a better understanding of the mechanisms that support ICC development in human health and disease. ..
- Inflammation of Myofibroblasts and Loss of Elastic Recoil in Severe AsthmaSally E Wenzel; Fiscal Year: 2010..Completing these aims should lead to an improved understanding of the contribution of inflammation and injury repair in the small airways/alveoli to the development of severe asthma. These findings may improve therapy as well. ..
- Preeti Tandon; Fiscal Year: 2014..The overall goal of this research is to delineate the functions of Ras proteins in NF1 pathogenesis and to identify novel therapeutic strategies based on inhibition of specific Ras proteins. ..
- microRNAs targeting Kit inhibit the development and maintenance of ICCSeungil Ro; Fiscal Year: 2012....
- Gangjian Qin; Fiscal Year: 2015....
- Role of SCF in airway eosinophil inflammationNicholas W Lukacs; Fiscal Year: 2013..Thus, these studies will clarify a number of previously unexplored questions in this novel area of research. ..
- Loren J Field; Fiscal Year: 2015..Ultimately these approaches might be useful to reconstitute myocardial mass following cardiac injury. ..
- RNA aptamers as cell surface receptor agonists and siRNA delivery agentsBRUCE ALAN SULLENGER; Fiscal Year: 2012..Technologies that mediate targeted delivery of small interfering RNAs (siRNAs) are needed to improve the therapeutic efficacy, safety and cost effectiveness of siRNA-based therapeutic agents ..
- Reconstitution of thrombopoiesis by angiogenic factorsShahin Rafii; Fiscal Year: 2009....
- MICROPHTHALMIA IN OSTEOCLAST DEVELOPMENTKatherine Weilbaecher; Fiscal Year: 2002..Dr. David Fisher will supervise the project and head an advisory board of experts in signalling, bone biology, cellular physiology formed to provide additional guidance and aid in my transition to an independent investigator. ..
- THE ROLE OF TR-KIT RECEPTOR IN STEM CELL MAINTENANCE AND DIFFERENTIATIONRoland Jurecic; Fiscal Year: 2007..unreadable] [unreadable] [unreadable]..
- IL-7R and c-kit interactions in thymopoiesisKenneth Weinberg; Fiscal Year: 2006..abstract_text> ..
- Regulation of thymic epithelial cell differentiationNancy Manley; Fiscal Year: 2007..Further, our identification of a new function for the N-terminal domain may have implications for functional domains in other forkhead family transcription factors. ..
- MICROPHTHALMIA--CRITICAL FACTOR IN MAST CELL DEVELOPMENTClifford Takemoto; Fiscal Year: 2001..Dr. David Fisher will supervise the project and head and advisory board of experts in hematopoiesis and mast cell biology formed to provide additional guidance and aid in the candidate's transition to an independent investigator. ..
- CUTANEOUS BIOLOGY OF KIT LIGANDJACK LONGLEY; Fiscal Year: 2005..These studies will determine specific contributions of SCF-KIT signaling to contact dermatitis, an provide support for the hypothesis that inhibitors of KIT may be novel therapeutic agents for human cutaneous inflammation. ..
- ROLES OF MEMBRANE AND SOLUBLE KL IN HEMATOPOIESISPeter Besmer; Fiscal Year: 2002..Furthermore, in order to evaluate the in vivo role of disintegrins in the production of soluble KL and Kit in serum knock-out mouse models will be used. ..
- MECHANISMS OF MAST CELL APOPTOSIS IN LUNG ALLOGRAFTSKenneth Fang; Fiscal Year: 2003..abstract_text> ..
- Cutaneous Biology KIT LigandJACK LONGLEY; Fiscal Year: 2007..unreadable] [unreadable] [unreadable] [unreadable]..
- Genetic analysis of Kit ligand of miceMARY BEDELL; Fiscal Year: 2006..Together, these studies will provide new insights into Kitl function and may lead to novel strategies for the development of more effective cytokines. ..
- BACTERIA INDUCED CYTOKINE PRODUCTION IN THE GUTGary Klimpel; Fiscal Year: 2001....
- The Biology of Prostate Stem CellsE Wilson; Fiscal Year: 2005..These experiments will define the subset of proximal cells in which prostatic stem cells reside and identify the manner in which their growth is regulated. ..
- Phase II Trial of Tiopronin in Aneurysmal Subarachnoid HemorrhageEDWARD SANDER CONNOLLY; Fiscal Year: 2011..This would spark further study that could further explore neuroprotective pre-treatment of cerebral ischemia, and thus help neutralize a major source of morbidity and mortality in this disease process. ..
- Biomarker for liver ischemia/reperfusion-induced injuryMONIKA OLI; Fiscal Year: 2006..The overall goal of this proposal is to develop a prototype ELISA kit for the quantitative determination of ASS as novel diagnostic biomarker in biological fluids including serum or plasma. [unreadable] [unreadable] [unreadable]..
- STI571 Therapy for Gastrointestinal Stromal TumorsRonald DeMatteo; Fiscal Year: 2002..The results are essential to advance our understanding of GIST biology and determine the therapeutic value and limitations of STI571. ..
- Mechanisms of adhesion and growth control in stem cellsReuben Kapur; Fiscal Year: 2010..Our proposed studies will provide unique insights into the physiologic significance of the in vivo interactions between class IA PI3K and phosphatases in regulating growth and survival in SC/Ps. ..
- Discovery of Small Molecule MBT Domain AntagonistsSTEPHEN VERNON FRYE; Fiscal Year: 2010..The chemical probes designed, synthesized and validated in this proposal will have applications in the discovery of molecular targets to treat diseases such as cancer and in the development of safe stem cell based therapeutics. ..
- Present Homologous and Heterologous Antigen with Hepatitis E VirusR Holland Cheng; Fiscal Year: 2012....
- Phosphotyrosine signaling pathways controlling tracheal tube geometryKAI G ZINN; Fiscal Year: 2013..We can also analyze tyrosine phosphorylation of the proteins and determine if they physically interact with each other in the embryo. ..
- Non-viral gene therapy for sickle cell anemiaCLIFFORD JOHN STEER; Fiscal Year: 2012..The ultimate goal of this research project is to develop and evaluate in patients an innovative gene therapy approach that has the potential to treat and correct SCA. ..
- Diagnostic array for aseptic encephalitisDarrell P Chandler; Fiscal Year: 2011..The underlying platform developed herein will likewise find broad application in many areas of infectious disease diagnostics. ..