Research Topics
Genomes and Genes
| M C HeinrichSummaryAffiliation: Oregon Health and Science University Country: USA Publications
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Detail Information
Publications
Crenolanib inhibits the drug-resistant PDGFRA D842V mutation associated with imatinib-resistant gastrointestinal stromal tumorsMichael C Heinrich
Portland VA Medical Center, Portland, OR, USA
Clin Cancer Res 18:4375-84. 2012..To determine the potential of crenolanib, a potent inhibitor of PDGFRA, to treat malignancies driven by mutant PDGFRA...- Sorafenib inhibits many kinase mutations associated with drug-resistant gastrointestinal stromal tumorsMichael C Heinrich
Division of Hematology Oncology, Department of Medicine, Portland VA Medical Center and OHSU Knight Cancer Institute, Oregon Health and Science University, R and D 19 3710 U S Veterans Hospital Road, Portland, OR 97239, USA
Mol Cancer Ther 11:1770-80. 2012..These results have implications for the further development of treatments for drug-resistant GIST... - 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... - Phase II, open-label study evaluating the activity of imatinib in treating life-threatening malignancies known to be associated with imatinib-sensitive tyrosine kinasesMichael C Heinrich
Department of Hematology and Medical Oncology, Oregon Health and Science University Cancer Institute and Portland VA Medical Center, Portland, Oregon 97239 3098, USA
Clin Cancer Res 14:2717-25. 2008..To evaluate the activity of imatinib in treating advanced, life-threatening malignancies expressing one or more imatinib-sensitive tyrosine kinases... - Molecular correlates of imatinib resistance in gastrointestinal stromal tumorsMichael C Heinrich
Division of Hematology Oncology, Department of Pathology, Oregon Health and Science University Cancer Institute, Oregon Health and Science University, Portland, OR, USA
J Clin Oncol 24:4764-74. 2006..In clinical studies, 75% to 90% of patients with advanced GISTs experience clinical benefit from imatinib. However, imatinib resistance is an increasing clinical problem... - Targeting FLT3 kinase in acute myelogenous leukemia: progress, perils, and prospectsMichael C Heinrich
Division of Hematology and Medical Oncology, Oregon Health and Science University Cancer Institute and Portland VA Medical Center, Portland, OR 97201, USA
Mini Rev Med Chem 4:255-71. 2004..Inhibition of FLT3 kinase activity by small molecule inhibitors has been proposed as a novel therapeutic approach AML. The pre-clinical and clinical development of candidate FLT3 inhibitors will be reviewed... - Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumorMichael C Heinrich
R and D 19 3710 SW US Veterans Hospital Rd, Portland, OR 97207, USA
J Clin Oncol 21:4342-9. 2003..The relationship between mutations in these kinases and clinical response to imatinib was examined in a group of patients with advanced GIST... - Clinical and molecular studies of the effect of imatinib on advanced aggressive fibromatosis (desmoid tumor)Michael C Heinrich
Oregon Health and Science University Cancer Institute and Portland VA Medical Center, Portland, OR, USA
J Clin Oncol 24:1195-203. 2006..To determine the clinical efficacy of imatinib in patients with advanced aggressive fibromatosis (AF) and to identify the molecular basis of response/nonresponse to this agent... - Is KIT an important therapeutic target in small cell lung cancer?Michael C Heinrich
Oregon Health and Science University Cancer Institute and Portland Veterans Affairs Medical Center, Portland, Oregon 97201, USA
Clin Cancer Res 9:5825-8. 2003 - 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... - Primary and secondary kinase genotypes correlate with the biological and clinical activity of sunitinib in imatinib-resistant gastrointestinal stromal tumorMichael 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 26:5352-9. 2008..We evaluated the impact of primary and secondary kinase genotype on sunitinib activity... - Inhibition of KIT tyrosine kinase activity: a novel molecular approach to the treatment of KIT-positive malignanciesMichael C Heinrich
Department of Medicine, Division of Hematology Oncology, Oregon Health and Science University, USA
J Clin Oncol 20:1692-703. 2002..In this review, we discuss the rationale for and development of KIT tyrosine kinase inhibitors for the treatment of human malignancies... - Posttranscriptional cell cycle-dependent regulation of human FANCC expressionM C Heinrich
Department of Medicine, Division of Hematology and Medical Oncology, Oregon Health Sciences University and Portland Veterans Affairs Medical Center, Portland, OR 97207, USA
Blood 95:3970-7. 2000..Our observation of dynamic control of FANCC expression by the proteasome has important implications for understanding the molecular regulation of the multiprotein complex. (Blood. 2000;95:3970-3977).. - Inhibition of c-kit receptor tyrosine kinase activity by STI 571, a selective tyrosine kinase inhibitorM C Heinrich
Division of Hematology and Medical Oncology, Department of Medicine, Oregon Health Sciences University, and Portland Veterans Affairs Medical Center, USA
Blood 96:925-32. 2000..This compound may be useful in treating cancers associated with increased c-kit kinase activity... - Gastric GI stromal tumors (GISTs): the role of surgery in the era of targeted therapyMichael C Heinrich
OHSU Cancer Institute, Oregon Health and Science University and VA Medical Center, Portland, Oregon 97239, USA
J Surg Oncol 90:195-207; discussion 207. 2005..The importance of a multi-disciplinary approach using both surgery and imatinib therapy is emphasized... - PDGFRA mutations in gastrointestinal stromal tumors: frequency, spectrum and in vitro sensitivity to imatinibChristopher L Corless
Department of Pathology, Division of Hematology and Oncology, Oregon Health and Science University Cancer Institute, Portland, OR 97201, USA
J Clin Oncol 23:5357-64. 2005..Little is known of the other types of PDGFRA mutations that occur in GISTs... - Mutations of the BCR-ABL-kinase domain occur in a minority of patients with stable complete cytogenetic response to imatinibD W Sherbenou
Cell and Developmental Biology, Oregon Health and Science University, Portland, OR 97239, USA
Leukemia 21:489-93. 2007..BCR-ABL-kinase domain mutations in patients with a stable CCR are infrequent, and their detection does not consistently predict relapse. Alternative mechanisms must be responsible for disease persistence in the majority of patients... - Transforming growth factor beta 1 inhibits expression of the gene products for steel factor and its receptor (c-kit)M C Heinrich
Department of Medicine, Oregon Health Sciences University, Portland, USA
Blood 85:1769-80. 1995.... - Germ cell defects and hematopoietic hypersensitivity to gamma-interferon in mice with a targeted disruption of the Fanconi anemia C geneM A Whitney
Department of Molecular and Medical Genetics, Vollum Institute, Oregon Regional Primate Center, Portland, USA
Blood 88:49-58. 1996..Progenitor cells from fac knock-out mice were hypersensitive to interferon gamma. This previously unrecognized phenotype may form the basis for BM failure in human FA... - The Fanconi anemia group C gene product is located in both the nucleus and cytoplasm of human cellsM E Hoatlin
Division of Hematology and Medical Oncology, Oregon Health Sciences University, Portland, OR 97201, USA
Blood 91:1418-25. 1998..Therefore, while cytoplasmic localization of this protein appears to be functionally important, it may also exert some essential nuclear function... - Dasatinib (BMS-354825), a dual SRC/ABL kinase inhibitor, inhibits the kinase activity of wild-type, juxtamembrane, and activation loop mutant KIT isoforms associated with human malignanciesMarcus M Schittenhelm
Department of Medicine, Division of Hematology/Oncology, Oregon Health and Science University, Portland, USA
Cancer Res 66:473-81. 2006..Our studies suggest that dasatinib may have clinical efficacy against human neoplasms that are associated with gain-of-function KIT mutations... - Fine-needle aspiration biopsy diagnosis of gastrointestinal stromal tumors using morphology, immunocytochemistry, and mutational analysis of c-kitA E Rader
Department of Pathology, Oregon Health Sciences University, Portland, Oregon 97201 3098, USA
Cancer 93:269-75. 2001..The aim of the current study was to employ immunocytochemistry and mutational analysis of the c-kit gene to aid in the diagnosis of GISTs on FNAB... - Heterogeneity of kinase inhibitor resistance mechanisms in GISTB Liegl
Department of Pathology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
J Pathol 216:64-74. 2008..Our observations underscore the heterogeneity of clinical TKI resistance, and highlight the therapeutic challenges involved in salvaging patients after clinical progression on TKI monotherapies... - Activating alleles of JAK3 in acute megakaryoblastic leukemiaDenise K Walters
Howard Hughes Medical Institute, Portland, Oregon 97239, USA
Cancer Cell 10:65-75. 2006..These findings illustrate the biological importance of gain-of-function JAK3 mutations in leukemogenesis and demonstrate the utility of proteomic approaches to identifying clinically relevant mutations... - A functional genomics approach to Kaposi's sarcomaAshlee V Moses
Vaccine and Gene Therapy Institute and Department of Molecular Microbiology and Immunology, Oregon Health Science University, Portland, Oregon 97239, USA
Ann N Y Acad Sci 975:180-91. 2002..J. Virol. 76(16): 8383-8399). These data demonstrate that microarrays are useful for the identification of pharmacological targets essential for KS tumorigenesis... - KIT-negative gastrointestinal stromal tumors: proof of concept and therapeutic implicationsFabiola Medeiros
Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA
Am J Surg Pathol 28:889-94. 2004..Notably, some KIT-negative GISTs contain imatinib-sensitive KIT or PDGFRA mutations; therefore, patients with KIT-negative GISTs should not, a priori, be denied imatinib therapy... - SU5416 and SU5614 inhibit kinase activity of wild-type and mutant FLT3 receptor tyrosine kinaseKevin W H Yee
Department of Medicine, Division of Hematology and Medical Oncology, Oregon Health and Science University, and Portland Veterans Affairs Medical Center, Portland, OR 97201, USA
Blood 100:2941-9. 2002..We conclude that SU5416 and SU5614 are potent inhibitors of FLT3. Our finding that inhibition of FLT3 induces apoptosis of leukemic cells supports the feasibility of targeting FLT3 as a novel treatment strategy for AML... - 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... - Gastrointestinal stromal tumorsC D Blanke
Division of Hematology and Medical Oncology, Department of Medicine, Oregon Health and Science University and Portland Veterans Affairs Medical Center, MC OP28, 3181 S W Sam Jackson Park Road, Portland, OR 97201, USA
Curr Treat Options Oncol 2:485-91. 2001..Its use can serve as a paradigm for designing molecularly targeted therapies for other malignancies... - Protein Kinase C theta (PKCtheta) expression and constitutive activation in gastrointestinal stromal tumors (GISTs)Anette Duensing
Department of Pathology, Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
Cancer Res 64:5127-31. 2004..PKCtheta is strongly activated in most GISTs and hence may serve, along with KIT/PDGFRA, as a novel therapeutic target... - Effects of MLN518, a dual FLT3 and KIT inhibitor, on normal and malignant hematopoiesisIan J Griswold
Howard Hughes Medical Institute, Oregon Health and Science University Cancer Institute, Portland 97239, USA
Blood 104:2912-8. 2004..In analogy to imatinib mesylate in BCR-ABL-positive acute leukemia, MLN518-induced remissions may not be durable. Our studies provide the basis for integrating this compound into chemotherapy and transplantation protocols... - FLT3 K663Q is a novel AML-associated oncogenic kinase: Determination of biochemical properties and sensitivity to Sunitinib (SU11248)M M Schittenhelm
Department of Pathology and Medicine, Oregon Health and Science University Cancer Institute and Portland Veterans Affairs Medical Center, Portland, OR 97239, USA
Leukemia 20:2008-14. 2006..We conclude that FLT3 mutations in AML can involve novel regions of the TK1. Future studies are needed to define the incidence and prognostic significance of FLT3 mutations outside the well-established JM and AL regions... - Pediatric KIT wild-type and platelet-derived growth factor receptor alpha-wild-type gastrointestinal stromal tumors share KIT activation but not mechanisms of genetic progression with adult gastrointestinal stromal tumorsKatherine A Janeway
Department of Medicine, Children s Hospital Boston, MA, USA
Cancer Res 67:9084-8. 2007..KIT activation levels in pediatric KIT-wild-type GISTs are comparable with those in KIT-mutant GISTs. Therapies that inhibit KIT activation, or crucial KIT signaling intermediates, should be explored in pediatric KIT-wild-type GIST... - In vitro and in vivo activity of ATP-based kinase inhibitors AP23464 and AP23848 against activation-loop mutants of KitAmie S Corbin
Oregon Health and Science University, Cancer Institute, L592, 3181 SW Sam Jackson Park Rd, Portland, OR 97239, USA
Blood 106:227-34. 2005..Thus, AP23464 and AP23848 potently and selectively target activation-loop mutants of Kit in vitro and in vivo and could have therapeutic potential against D816V-expressing malignancies... - Biology of gastrointestinal stromal tumorsChristopher L Corless
Oregon Health and Science University Cancer Institute, Department of Pathology, Portland, OR, USA
J Clin Oncol 22:3813-25. 2004..In addition, the role of mutation screening in KIT and PDGFRA as a diagnostic and prognostic aid is emphasized in this review... - Primary extragastrointestinal stromal tumor of the pleura: report of a unique case with genetic confirmationKevin B Long
Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Am J Surg Pathol 34:907-12. 2010..This seems to be the first EGIST arising above the diaphragm. This case shows a potential diagnostic pitfall with therapeutic consequences... - Biology of gastrointestinal stromal tumors: KIT mutations and beyondAnette Duensing
Department of Pathology, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115, USA
Cancer Invest 22:106-16. 2004..This review focuses on the biological and molecular genetic principles of GISTs, and particularly the role of mutant KIT as a therapeutic target... - Targeting mutant kinases in gastrointestinal stromal tumors: a paradigm for molecular therapy of other sarcomasMichael C Heinrich
Department of Medicine, Oregon Health Science University Cancer Institute, Portland VA Medical Center, 3710 SW US Veterans Hospital Road, Portland, OR 97201, USA
Cancer Treat Res 120:129-50. 2004 - Biology and genetic aspects of gastrointestinal stromal tumors: KIT activation and cytogenetic alterationsMichael C Heinrich
Department of Medicine, Division of Hematology/Oncology, Oregon Health Sciences University and Portland VA Medical Center, USA
Hum Pathol 33:484-95. 2002..These cytogenetic aberrations are undoubtedly important in GIST pathogenesis, but currently they do not play a key role as diagnostic adjuncts... - A single nucleotide polymorphism in the coding region of ABL and its effects on sensitivity to imatinibL C Crossman
Oregon Health and Science University Cancer Institute, Portland, OR, USA
Leukemia 19:1859-62. 2005..Clinicians should be aware that possession of the arginine allele of K247R does not reflect a mutation that necessitates a change in the therapeutic strategy, unless there are other signs of inadequate response to drug... - Detection of ABL kinase domain mutations with denaturing high-performance liquid chromatographyM W N Deininger
Oregon Health and Science University Cancer Institute, Portland, OR 97201 L592, USA
Leukemia 18:864-71. 2004..Early detection of emerging mutant clones may aid in guiding decisions regarding alternative treatment options... - The gene expression profile of extraskeletal myxoid chondrosarcomaSubbaya Subramanian
Department of Pathology, Stanford University Medical Center, Stanford, CA 94035, USA
J Pathol 206:433-44. 2005..Small molecule inhibitors for PPARG exist and PPARG could be a potential therapeutic target for EMC... - 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... - Phase II study of imatinib mesylate in chemotherapy refractory germ cell tumors expressing KITLawrence H Einhorn
Department of Medicine, Division of Hematology Oncology, Indiana University, Indianapolis, Indiana and Walther Cancer Institute, Indianapolis, IN, USA
Am J Clin Oncol 29:12-3. 2006..This phase II study was conducted to determine the activity of imatinib (gleevec) in heavily pretreated patients with KIT-positive metastatic germ cell tumor... - Sensitivity of oncogenic KIT mutants to the kinase inhibitors MLN518 and PD180970Amie S Corbin
Oregon Health and Science University Cancer Institute, Portland, OR 97239, USA
Blood 104:3754-7. 2004..As phase 1 clinical trials of MLN518 in AML have shown little toxicity, our data suggest MLN518 is a promising candidate for the treatment of SM or AML with KIT mutations... - BRAF in papillary thyroid carcinoma of ovary (struma ovarii)Jason Schmidt
Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Am J Surg Pathol 31:1337-43. 2007..In this study, we explored the possible role of these genes in the development of BSO and MSO... - Repression of Fanconi anemia gene (FACC) expression inhibits growth of hematopoietic progenitor cellsG M Segal
Department of Medicine, Oregon Health Sciences University, Portland 97201 3098
J Clin Invest 94:846-52. 1994..We conclude that, while the FACC gene product plays a role in defining cellular tolerance to cross-linking agents, it also functions to regulate growth, differentiation, and/or survival of normal hematopoietic progenitor cells... - Allele-specific polymerase chain reaction for the imatinib-resistant KIT D816V and D816F mutations in mastocytosis and acute myelogenous leukemiaChristopher L Corless
OHSU Dept of Pathology L471, 3181 SW Sam Jackson Park Rd, Portland, OR 97239, USA
J Mol Diagn 8:604-12. 2006..Thus, the assay may be useful in confirming the diagnosis of SM... - Molecular pathobiology of gastrointestinal stromal sarcomasChristopher L Corless
Department of Pathology, Oregon Health and Science University Cancer Institute, Portland, OR 97239, USA
Annu Rev Pathol 3:557-86. 2008.... - Long-term results from a randomized phase II trial of standard- versus higher-dose imatinib mesylate for patients with unresectable or metastatic gastrointestinal stromal tumors expressing KITCharles D Blanke
Oregon Health and Science University Cancer Center and Portland Veterans Affairs Hospital, Portland, OR, USA
J Clin Oncol 26:620-5. 2008..We conducted a long-term analysis of patients treated on the trial, including patients followed during an extension phase, to evaluate survival, patterns of failure, and potential prognostic factors, including tumor mutational status... - KIT mutations are common in incidental gastrointestinal stromal tumors one centimeter or less in sizeChristopher L Corless
Department of Pathology, Division of Hematology Oncology, Oregon Health and Science University, Portland, 97201, USA
Am J Pathol 160:1567-72. 2002..The findings suggest that KIT mutations per se are of little prognostic importance in GISTs... - Phosphatidylinositol-3-kinase and AKT1 mutations occur early in breast carcinomaJennifer Dunlap
Department of Pathology, Oregon Health and Science University, L471, 3181 SW Sam Jackson Park Rd, Portland, OR, 97239, USA
Breast Cancer Res Treat 120:409-18. 2010.... - Kaposi's sarcoma-associated herpesvirus-induced upregulation of the c-kit proto-oncogene, as identified by gene expression profiling, is essential for the transformation of endothelial cellsAshlee V Moses
Vaccine and Gene Therapy Institute, Portland, Oregon 97201, USA
J Virol 76:8383-99. 2002..Furthermore, overexpression studies showed that c-Kit was sufficient to induce spindle cell formation. Together, these data demonstrate an essential role for c-Kit in KS tumorigenesis and reveal a target for pharmacological intervention... - Phosphoproteomic analysis of AML cell lines identifies leukemic oncogenesDenise K Walters
Department of Hematology and Oncology, Howard Hughes Medical Institute, Oregon Health and Science University Cancer Institute, 3181 Sam Jackson Park Road, and Portland VA Medical Center, Portland, OR 97239, USA
Leuk Res 30:1097-104. 2006..This study illustrates the benefit of LC-MS/MS mass spectrometry and siRNA for the identification of novel targets and mutations... - Phase III randomized, intergroup trial assessing imatinib mesylate at two dose levels in patients with unresectable or metastatic gastrointestinal stromal tumors expressing the kit receptor tyrosine kinase: S0033Charles D Blanke
Oregon Health and Science University Cancer Institute, 3181 SW Sam Jackson Park Rd, L 586, Portland, OR 97239, USA
J Clin Oncol 26:626-32. 2008.... - In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutantsThomas O'Hare
Howard Hughes Medical Institute, Oregon Health and Science University Cancer Institute, Portland 97239, USA
Cancer Res 65:4500-5. 2005..Thus, both inhibitors hold promise for treating imatinib-refractory CML... - RNAi screen for rapid therapeutic target identification in leukemia patientsJeffrey W Tyner
Division of Hematology and Medical Oncology, Oregon Health and Science University Knight Cancer Institute, Portland, OR 97239, USA
Proc Natl Acad Sci U S A 106:8695-700. 2009..Combination of this technique with whole-genome sequencing will represent an ideal tool for oncogenic target identification such that specific therapies can be matched with individual patients... - Synergistic effect of SU11248 with cytarabine or daunorubicin on FLT3 ITD-positive leukemic cellsKevin W H Yee
Oregon Health and Sciences University Cancer Institute and Portland Veterans Affairs Medical Center, Portland, OR, USA
Blood 104:4202-9. 2004..These data suggest that the addition of potent FLT3 inhibitors such as SU11248 to AML chemotherapy regimens could result in improved treatment results... - The novel marker, DOG1, is expressed ubiquitously in gastrointestinal stromal tumors irrespective of KIT or PDGFRA mutation statusRobert B West
Department of Pathology, Stanford University Medical Center, 300 Pasteur Drive, Stanford, CA 94305, USA
Am J Pathol 165:107-13. 2004..Reactivity for DOG1 may aid in the diagnosis of GISTs, including PDGFRA mutants that fail to express KIT antigen, and lead to appropriate treatment with imatinib mesylate, an inhibitor of the KIT tyrosine kinase... - KIT gene deletions at the intron 10-exon 11 boundary in GI stromal tumorsChristopher L Corless
Department of Pathology, Oregon Health and Science University Cancer Institute, Portland, OR 97239, USA
J Mol Diagn 6:366-70. 2004..Laboratories that offer clinical screening for KIT mutations in GI stromal tumors should be aware of this class of mutations... - RNAi-induced down-regulation of FLT3 expression in AML cell lines increases sensitivity to MLN518Denise K Walters
Department of Hematology and Oncology, Howard Hughes Medical Institute, Oregon Health and Science University, and Portland Veterans Affairs VA Medical Center, 3181 Sam Jackson Park Rd, Portland, OR 97239, USA
Blood 105:2952-4. 2005..Furthermore, siRNA-induced down-regulation of FLT3 increased the sensitivity of both cell lines to treatment with the FLT3 inhibitor MLN518. This illustrates the potential benefit of combined therapeutic approaches... - MET receptor sequence variants R970C and T992I lack transforming capacityJeffrey W Tyner
Division of Hematology and Medical Oncology, Oregon Health and Science University, Portland, Oregon 97239, USA
Cancer Res 70:6233-7. 2010.... - Pure red cell aplasia associated with parvovirus B19 infection occurring late after allogeneic bone marrow transplantationBrandon Hayes-Lattin
Adult Bone Marrow Transplant Program, Division of Hematology and Medical Oncology, Oregon Health and Science University, The OHSU Cancer Institute, Portland, Oregon 97239, USA
Am J Hematol 75:142-5. 2004..Characteristics of parvovirus B19 infection and the immunosuppressed state after allogeneic stem cell transplantation are reviewed... - High prevalence of PIK3CA/AKT pathway mutations in papillary neoplasms of the breastMegan L Troxell
Department of Pathology, Knight Cancer Institute, Oregon Health and Science University, Portland, OR 97239, USA
Mod Pathol 23:27-37. 2010..These findings indicate that approximately two-thirds of papillomas are driven by mutations in the PI3CA/AKT pathway. Some papillary carcinomas may arise from these lesions, but others may have different molecular origins... - Combined Abl inhibitor therapy for minimizing drug resistance in chronic myeloid leukemia: Src/Abl inhibitors are compatible with imatinibThomas O'Hare
Howard Hughes Medical Institute, Oregon Health and Science University, Portland 97239, USA
Clin Cancer Res 11:6987-93. 2005..As combination therapy is frequently used to prevent emergence of resistance, the combination of imatinib with an inhibitor of imatinib-resistant Bcr-Abl mutants (e.g., Src/Abl inhibitors AP23848 and BMS-354825) was investigated... - RNAi screening of the tyrosine kinome identifies therapeutic targets in acute myeloid leukemiaJeffrey W Tyner
Division of Hematology and Medical Oncology, Oregon Health and Science University Cancer Institute, Portland, USA
Blood 111:2238-45. 2008..This technique, with additional development, might eventually offer the potential to match specific therapies with individual patients based on a functional assay... - STI571: a paradigm of new agents for cancer therapeuticsMichael J Mauro
Leukemia Program, Division of Hematology and Medical Oncology, Oregon Health Sciences University, 3181 SW Sam Jackson Park Rd, Portland, OR 97201, USA
J Clin Oncol 20:325-34. 2002..Lastly, the potential use of STI571 in other malignancies and the translation of this paradigm to other malignancies are explored... - Activity of the tyrosine kinase inhibitor PKC412 in a patient with mast cell leukemia with the D816V KIT mutationJason Gotlib
Department of Medicine, Division of Hematology, Stanford University, Stanford Cancer Center, 875 Blake Wilbur Dr, Rm 2327B, Stanford, CA 94305 5821, USA
Blood 106:2865-70. 2005..This case indicates that KIT tyrosine kinase inhibition is a feasible approach in SM, but single-agent clinical efficacy may be limited by clonal evolution in the advanced leukemic phase of this disease... - A novel monoclonal antibody against DOG1 is a sensitive and specific marker for gastrointestinal stromal tumorsInigo Espinosa
Department of Pathology, Stanford University Medical Center, Stanford, CA 94305, USA
Am J Surg Pathol 32:210-8. 2008..5%) synovial sarcomas among the 935 soft tissue tumors examined showed positive immunostaining for DOG1.1. In addition, DOG1.1 immunoreactivity was seen in fewer cases of carcinoma, melanoma, and seminoma as compared with KIT... - A human gene coding for a membrane-associated nucleic acid-binding proteinD C Siess
Departments of Immunology, Pulmonology and Hematology, Veterans Affairs Medical Center, Portland, Oregon 97201, USA
J Biol Chem 275:33655-62. 2000..Characterization of the MNAB protein as a cell-surface DNA-binding protein, critical in binding and internalization of extracellular DNA, awaits confirmation of its localization to cell surfaces... - Dermatofibrosarcoma protuberans: a partial response to imatinib therapyKhosrow Mehrany
Department of Dermatology, Oregon Health and Science University, and Oregon Health and Cancer Institute, Portland, Oregon 97239, USA
Dermatol Surg 32:456-9. 2006 - Ménétrier disease and gastrointestinal stromal tumors: hyperproliferative disorders of the stomachRobert J Coffey
Department of Medicine, Vanderbilt University Medical Center and Nashville Veterans Affairs Medical Center, Nashville, Tennessee, USA
J Clin Invest 117:70-80. 2007.... - Chemotherapy and dasatinib induce long-term hematologic and molecular remission in systemic mastocytosis with acute myeloid leukemia with KIT D816VCelalettin Ustun
Medical College of Georgia, Department of Medicine, Section of Hematology Oncology, Augusta, GA 30912 3125, USA
Leuk Res 33:735-41. 2009..Along with chemotherapy, dasatinib should be considered in these patients particularly if they cannot undergo allogeneic stem cell transplantation for this poor prognostic AML... - KIT gene mutations and copy number in melanoma subtypesCarol Beadling
Oregon Cancer Institute, Oregon Health and Science University, Portland, Oregon 97239, USA
Clin Cancer Res 14:6821-8. 2008..To determine the frequency of KIT mutations across melanoma subtypes, we surveyed a large series of tumors... - The effects of the Fanconi anemia zinc finger (FAZF) on cell cycle, apoptosis, and proliferation are differentiation stage-specificMu Shui Dai
Division of Molecular Medicine, Oregon Health and Science University, Portland, Oregon 97201, USA
J Biol Chem 277:26327-34. 2002..These results suggest an essential role for FAZF during the proliferative stages of primitive hematopoietic progenitors, possibly acting in concert with (a subset of) the Fanconi anemia proteins... - MicroRNA expression signature of human sarcomasS Subramanian
Department of Pathology, Stanford University, Stanford, CA 94305, USA
Oncogene 27:2015-26. 2008..The identification of unique miRNA signatures in each tumor type may indicate their role in tumorigenesis and may aid in diagnosis of soft tissue sarcomas... - Absence of BRAF and NRAS mutations in uveal melanomaFrank Cruz
Oregon Health and Science University OHSU Cancer Institute, Department of Pathology, OHSU and Portland Veterans Affairs Medical Center, Portland, Oregon 97239, USA
Cancer Res 63:5761-6. 2003..No NRAS exon 1 mutations were detected in either type of melanoma. We conclude that UMs arise independent of oncogenic BRAF and NRAS mutations, an observation that may have implications for therapies targeted to the NRAS-BRAF pathway... - High-throughput sequencing screen reveals novel, transforming RAS mutations in myeloid leukemia patientsJeffrey W Tyner
Division of Hematology and Medical Oncology, Oregon Health and Science University Knight Cancer Institute, Portland, OR 97239, USA
Blood 113:1749-55. 2009.... - High-throughput sequence analysis of the tyrosine kinome in acute myeloid leukemiaMarc M Loriaux
Division of Hematology and Medical Oncology, Oregon Health and Science University Cancer Institute, Portland, OR 97239, USA
Blood 111:4788-96. 2008.... - Extragastrointestinal stromal tumors presenting as vulvovaginal/rectovaginal septal masses: a diagnostic pitfallMaggie M Lam
Department of Anatomic Pathology, University of Washington Medical Center, Seattle, WA 98195, USA
Int J Gynecol Pathol 25:288-92. 2006..Thus, it is imperative to consider EGISTs in the differential diagnosis of mesenchymal neoplasms in the vulvovaginal/rectovaginal septum... - An innovative phase I clinical study demonstrates inhibition of FLT3 phosphorylation by SU11248 in acute myeloid leukemia patientsAnne Marie O'Farrell
SUGEN Inc, South San Francisco, California, USA
Clin Cancer Res 9:5465-76. 2003..Study drug-related adverse events occurred in 31% of patients, mainly grade 1 or 2 diarrhea and nausea, at higher dose levels... - Gastrointestinal stromal tumors: insights from a new familial GIST kindred with unusual genetic and pathologic featuresCiarán O'Riain
Department of Histopathology, St Vincent s University Hospital, Elm Park, Dublin, Ireland
Am J Surg Pathol 29:1680-3. 2005..Two smaller lesions from this patient were heterozygous for the mutation. This phenomenon has been observed in up to 8% of sporadic malignant GISTs but has not been documented in familial disease... - Novel mode of action of c-kit tyrosine kinase inhibitors leading to NK cell-dependent antitumor effectsChristophe Borg
Department of Clinical Biology, Equipe de Recherche Mixte 0208, INSERM, Institut Gustave Roussy, Villejuif, France
J Clin Invest 114:379-88. 2004..These data point to a novel mode of antitumor action for Gleevec... - Familial gastrointestinal stromal tumor syndrome: phenotypic and molecular features in a kindredFrederick P Li
Dana Farber Cancer Institute, 44 Binney St, Boston, MA 02115, USA
J Clin Oncol 23:2735-43. 2005..A tumor from the proband was analyzed to compare features with sporadic GISTs... - Molecular and clinical analysis of locally advanced dermatofibrosarcoma protuberans treated with imatinib: Imatinib Target Exploration Consortium Study B2225Grant A McArthur
Peter MacCallum Cancer Centre, East Melbourne, Australia
J Clin Oncol 23:866-73. 2005..The purpose of this study was to evaluate molecular, cytogenetic, and kinase activation profiles in a series of DFSPs and to determine whether these biologic parameters are correlated with the clinical responses of DFSP to imatinib... - Serum KIT and KIT ligand levels in patients with gastrointestinal stromal tumors treated with imatinibPetri Bono
Department of Oncology, University Central Hospital of Helsinki, Helsinki, Finland
Blood 103:2929-35. 2004..1-259-fold). A high serum SCF/KIT ratio may increase SCF-induced cell signaling with prolonged imatinib treatment, at the time when imatinib treatment is withdrawn, and in patients whose GIST has wild-type receptors... - Phase 1 clinical results with tandutinib (MLN518), a novel FLT3 antagonist, in patients with acute myelogenous leukemia or high-risk myelodysplastic syndrome: safety, pharmacokinetics, and pharmacodynamicsDaniel J DeAngelo
Dana Farber Cancer Institute, 44 Binney St, Boston, MA 02115, USA
Blood 108:3674-81. 2006..Tandutinib at the MTD (525 mg twice daily) should be evaluated more extensively in patients with AML with FLT3-ITD mutations to better define its antileukemic activity... - Response to imatinib mesylate of a gastrointestinal stromal tumor with very low expression of KITSebastian Bauer
Department of Internal Medicine Cancer Research, University of Essen Medical School, Germany
Cancer Chemother Pharmacol 51:261-5. 2003..Our experience with this patient suggests that even GISTs with very low levels of KIT expression may respond to imatinib mesylate therapy... - SU11248 is a novel FLT3 tyrosine kinase inhibitor with potent activity in vitro and in vivoAnne Marie O'Farrell
Preclinical Research and Exploratory Development, SUGEN, South San Francisco, CA 94080, USA
Blood 101:3597-605. 2003..These results suggest that further exploration of SU11248 activity in AML patients is warranted... - Clonal evolution of resistance to imatinib in patients with metastatic gastrointestinal stromal tumorsJayesh Desai
Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
Clin Cancer Res 13:5398-405. 2007..The objective of this study was to correlate molecular and radiologic patterns of imitinib-refractory disease with existing conventional criteria for disease progression... - Identification of driver and passenger mutations of FLT3 by high-throughput DNA sequence analysis and functional assessment of candidate allelesStefan Fröhling
Division of Hematology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Cancer Cell 12:501-13. 2007.... - Epithelioid gastric stromal tumours of the antrum in young females with the Carney triad: a report of three new cases with mutational analysis and comparative genomic hybridizationAbbas Agaimy
Institute of Pathology, Klinikum Nürnberg, 90419 Nurnberg, Germany
Oncol Rep 18:9-15. 2007.... - Gastrointestinal stromal tumourBrian P Rubin
Department of Anatomic Pathology, Taussig Cancer Center and the Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
Lancet 369:1731-41. 2007..The important interplay between the molecular genetics of gastrontestinal stromal tumour and responses to targeted therapeutics serves as a model for the study of targeted therapies in other solid tumours... - Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumorsGeorge D Demetri
Dana-Farber Cancer Institute and Harvard Cancer Center, Boston, MA 02115, USA
N Engl J Med 347:472-80. 2002..Inhibition of the KIT signal-transduction pathway is a promising treatment for advanced gastrointestinal stromal tumors, which resist conventional chemotherapy... - Clinicopathologic profile of gastrointestinal stromal tumors (GISTs) with primary KIT exon 13 or exon 17 mutations: a multicenter study on 54 casesJerzy Lasota
Department of Soft Tissue Pathology, Armed Forces Institute of Pathology, Washington, DC 20306 6000, USA
Mod Pathol 21:476-84. 2008..The latter is also true for all KIT exon 17 mutant GISTs... - Clinical management of gastrointestinal stromal tumors: before and after STI-571Ronald P Dematteo
Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA
Hum Pathol 33:466-77. 2002..The advent of STI-571 has markedly altered the clinical approach to GIST. It has proven to be effective in metastatic GIST and is also under investigation as a neoadjuvant and adjuvant therapy... - Efficacy and safety of sunitinib in patients with advanced gastrointestinal stromal tumour after failure of imatinib: a randomised controlled trialGeorge D Demetri
Ludwig Center at Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
Lancet 368:1329-38. 2006.... - Phase II study of imatinib in patients with recurrent gliomas of various histologies: a European Organisation for Research and Treatment of Cancer Brain Tumor Group StudyEric Raymond
Service inter hospitalier de cancérologie, Beaujon University Hospital, Clichy
J Clin Oncol 26:4659-65. 2008..To evaluate the safety and the efficacy of imatinib in recurrent malignant gliomas...