Jonathan A Fletcher

Summary

Affiliation: Massachusetts General Hospital
Country: USA

Publications

  1. ncbi request reprint KIT mutations in GIST
    Jonathan A Fletcher
    Brigham and Women s Hospital, 75 Francis Street, Thorn 5, Boston, MA 02115, USA
    Curr Opin Genet Dev 17:3-7. 2007
  2. pmc USP6 and CDH11 oncogenes identify the neoplastic cell in primary aneurysmal bone cysts and are absent in so-called secondary aneurysmal bone cysts
    Andre M Oliveira
    Department of Pathology, Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
    Am J Pathol 165:1773-80. 2004
  3. ncbi request reprint Aneurysmal bone cyst variant translocations upregulate USP6 transcription by promoter swapping with the ZNF9, COL1A1, TRAP150, and OMD genes
    Andre M Oliveira
    Department of Pathology, Brigham and Women s Hospital, Boston, MA 02115, USA
    Oncogene 24:3419-26. 2005
  4. ncbi request reprint 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
  5. ncbi request reprint KIT-negative gastrointestinal stromal tumors: proof of concept and therapeutic implications
    Fabiola 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
  6. pmc Molecular target modulation, imaging, and clinical evaluation of gastrointestinal stromal tumor patients treated with sunitinib malate after imatinib failure
    George D Demetri
    Center for Sarcoma and Bone Oncology, Ludwig Center at Dana Farber Harvard Cancer Center, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Clin Cancer Res 15:5902-9. 2009
  7. doi request reprint Imatinib targeting of KIT-mutant oncoprotein in melanoma
    Xiaofeng Jiang
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
    Clin Cancer Res 14:7726-32. 2008
  8. pmc Efficacy and safety of regorafenib in patients with metastatic and/or unresectable GI stromal tumor after failure of imatinib and sunitinib: a multicenter phase II trial
    Suzanne George
    Center for Sarcoma and Bone Oncology, Dana Farber Cancer Institute D1212, 450 Brookline Ave, Boston, MA, USA
    J Clin Oncol 30:2401-7. 2012
  9. ncbi request reprint Clonal evolution of resistance to imatinib in patients with metastatic gastrointestinal stromal tumors
    Jayesh Desai
    Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
    Clin Cancer Res 13:5398-405. 2007
  10. doi request reprint Protein kinase C inhibitor AEB071 targets ocular melanoma harboring GNAQ mutations via effects on the PKC/Erk1/2 and PKC/NF-κB pathways
    XinQi Wu
    Department of Medical Oncology, Melanoma Disease Center, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02215, USA
    Mol Cancer Ther 11:1905-14. 2012

Detail Information

Publications88

  1. ncbi request reprint KIT mutations in GIST
    Jonathan A Fletcher
    Brigham and Women s Hospital, 75 Francis Street, Thorn 5, Boston, MA 02115, USA
    Curr Opin Genet Dev 17:3-7. 2007
    ..Alternately, the mutant kinase proteins can be targeted using HSP90 inhibitors, which result in degradation of activated KIT and/or PDGFRA, or using KIT transcriptional repressors, such as flavopiridol...
  2. pmc USP6 and CDH11 oncogenes identify the neoplastic cell in primary aneurysmal bone cysts and are absent in so-called secondary aneurysmal bone cysts
    Andre M Oliveira
    Department of Pathology, Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
    Am J Pathol 165:1773-80. 2004
    ..By contrast, secondary ABC lack CDH11 and USP6 rearrangements, and although morphological mimics of primary ABC, appear to represent a non-specific morphological pattern of a diverse group of non-ABC neoplasms...
  3. ncbi request reprint Aneurysmal bone cyst variant translocations upregulate USP6 transcription by promoter swapping with the ZNF9, COL1A1, TRAP150, and OMD genes
    Andre M Oliveira
    Department of Pathology, Brigham and Women s Hospital, Boston, MA 02115, USA
    Oncogene 24:3419-26. 2005
    ..In summary, these studies show that USP6 oncogenic activation results from heterogeneous genomic mechanisms involving USP6 transcriptional upregulation by juxtaposition with ectopic promoters...
  4. ncbi request reprint 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...
  5. ncbi request reprint KIT-negative gastrointestinal stromal tumors: proof of concept and therapeutic implications
    Fabiola 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...
  6. pmc Molecular target modulation, imaging, and clinical evaluation of gastrointestinal stromal tumor patients treated with sunitinib malate after imatinib failure
    George D Demetri
    Center for Sarcoma and Bone Oncology, Ludwig Center at Dana Farber Harvard Cancer Center, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Clin Cancer Res 15:5902-9. 2009
    ....
  7. doi request reprint Imatinib targeting of KIT-mutant oncoprotein in melanoma
    Xiaofeng Jiang
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
    Clin Cancer Res 14:7726-32. 2008
    ..Biological effects of KIT inhibition in these melanomas remain poorly understood. We sought to investigate further the effects of imatinib in these melanoma subsets...
  8. pmc Efficacy and safety of regorafenib in patients with metastatic and/or unresectable GI stromal tumor after failure of imatinib and sunitinib: a multicenter phase II trial
    Suzanne George
    Center for Sarcoma and Bone Oncology, Dana Farber Cancer Institute D1212, 450 Brookline Ave, Boston, MA, USA
    J Clin Oncol 30:2401-7. 2012
    ....
  9. ncbi request reprint Clonal evolution of resistance to imatinib in patients with metastatic gastrointestinal stromal tumors
    Jayesh 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...
  10. doi request reprint Protein kinase C inhibitor AEB071 targets ocular melanoma harboring GNAQ mutations via effects on the PKC/Erk1/2 and PKC/NF-κB pathways
    XinQi Wu
    Department of Medical Oncology, Melanoma Disease Center, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02215, USA
    Mol Cancer Ther 11:1905-14. 2012
    ..Targeted PKC inhibition with drugs such as AEB071 offers novel therapeutic potential for uveal melanoma harboring GNAQ mutations...
  11. ncbi request reprint Midline carcinoma of children and young adults with NUT rearrangement
    Christopher A French
    Department of Pathology, Brigham and Women s Hospital, 75 Francis St, Boston, MA 02115, USA
    J Clin Oncol 22:4135-9. 2004
    ..We sought to amass a more definitive series of tumors with NUT and/or BRD4 gene rearrangements and to determine distinct clinicopathologic features...
  12. doi request reprint Reporting of diagnostic cytogenetic results
    Azra H Ligon
    Brigham and Women s Hospital, Boston, Massachusetts, USA
    Curr Protoc Hum Genet . 2011
    ..Multi-specimen usage macros are included that can be applied to two or more specimen types...
  13. ncbi request reprint USP6 (Tre2) fusion oncogenes in aneurysmal bone cyst
    Andre M Oliveira
    Department of Pathology, Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
    Cancer Res 64:1920-3. 2004
    ..CDH11 is expressed strongly in bone, and our findings implicate a novel oncogenic mechanism in which deregulated USP6 transcription results from juxtaposition to the highly active CDH11 promoter...
  14. ncbi request reprint Identification of chromosomal aberrations associated with disease progression and a novel 3q13.31 deletion involving LSAMP gene in osteosarcoma
    Chueh Chuan Yen
    Department of Pathology, Brigham and Women s Hospital, Boston, MA 02115, USA
    Int J Oncol 35:775-88. 2009
    ..The study also demonstrated that CN and LOH analyses were able to detect distinct subsets of genetic abnormalities in OS...
  15. doi request reprint Absence of BRAF, NRAS, KRAS, HRAS mutations, and RET/PTC gene rearrangements distinguishes dominant nodules in Hashimoto thyroiditis from papillary thyroid carcinomas
    Peter M Sadow
    Pathology Service, WRN219, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114, USA
    Endocr Pathol 21:73-9. 2010
    ....
  16. ncbi request reprint Familial gastrointestinal stromal tumor syndrome: phenotypic and molecular features in a kindred
    Frederick 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...
  17. doi request reprint Reporting of diagnostic cytogenetic results
    Azra H Ligon
    Brigham and Women s Hospital, Boston, Massachusetts, USA
    Curr Protoc Hum Genet . 2010
    ..Multi-specimen usage macros are included that can be applied to two or more specimen types...
  18. pmc Targeted inhibition of multiple receptor tyrosine kinases in mesothelioma
    Wen bin Ou
    Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Neoplasia 13:12-22. 2011
    ..These compelling proapoptotic and antiproliferative responses indicate that HSP90 inhibition warrants clinical evaluation as a novel therapeutic strategy in mesothelioma...
  19. ncbi request reprint Role of KIT and platelet-derived growth factor receptors as oncoproteins
    Jonathan A Fletcher
    Department of Pathology, Brigham and Women s Hospital, Boston, MA 02115, USA
    Semin Oncol 31:4-11. 2004
    ..For example, imatinib efficacy for malignancies arising from constitutively activating point mutations in tyrosine kinases depends on the exact location of the mutation in the kinase molecule...
  20. ncbi request reprint An in vitro cytologic assay for evaluation of the KIT signaling pathway in gastrointestinal stromal tumors
    Brian S Chang
    Department of Pathology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Mod Pathol 20:579-83. 2007
    ..Such approaches will be enhanced by the development of additional activation state-specific antibodies, particularly those optimized for use in cytologic preparations...
  21. ncbi request reprint Biology of gastrointestinal stromal tumors: KIT mutations and beyond
    Anette 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...
  22. ncbi request reprint Heat shock protein 90 inhibition in imatinib-resistant gastrointestinal stromal tumor
    Sebastian Bauer
    Department of Pathology, Brigham and Women s Hospital, Center for Sarcoma and Bone Oncology, Dana Farber Cancer Institute, and Ludwig Center at Dana Farber Harvard Cancer Center, Boston, Massachusetts 02115, USA
    Cancer Res 66:9153-61. 2006
    ..The dramatic inactivation of imatinib-resistant KIT oncoproteins suggests that HSP90 inhibition provides a therapeutic solution to the challenge of heterogeneous imatinib resistance mutations in GIST patients...
  23. ncbi request reprint Mechanisms of oncogenic KIT signal transduction in primary gastrointestinal stromal tumors (GISTs)
    Anette Duensing
    Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA
    Oncogene 23:3999-4006. 2004
    ....
  24. doi request reprint Molecular detection of PPAR gamma rearrangements and thyroid carcinoma in preoperative fine-needle aspiration biopsies
    Christopher A French
    Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    Endocr Pathol 19:166-74. 2008
    ..The application of specific mutations to preoperative diagnosis of thyroid carcinoma is predicted to improve the accuracy and reduce the costs of treating patients with thyroid tumors...
  25. doi request reprint The clinicopathologic features of YWHAE-FAM22 endometrial stromal sarcomas: a histologically high-grade and clinically aggressive tumor
    Cheng Han Lee
    Department of Pathology, Brigham and Women s Hospital, Boston, MA, USA
    Am J Surg Pathol 36:641-53. 2012
    ..Thus, their distinction from typical JAZF1 ESS is important for prognostic and therapeutic purposes...
  26. pmc 14-3-3 fusion oncogenes in high-grade endometrial stromal sarcoma
    Cheng Han Lee
    Department of Pathology, Brigham and Women s Hospital, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 109:929-34. 2012
    ..These discoveries reveal diagnostically and therapeutically relevant models for characterizing aberrant 14-3-3 oncogenic functions...
  27. doi request reprint Gastrointestinal stromal tumors
    Bernadette Liegl-Atzwanger
    Department of Pathology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA, USA
    Virchows Arch 456:111-27. 2010
    ..This review focuses on GIST pathogenesis, morphologic evaluation, promising new immunohistochemical markers, risk assessment, the role of molecular analysis, and the increasing problem of secondary imatinib resistance and its mechanisms...
  28. pmc Strong expression of IGF1R in pediatric gastrointestinal stromal tumors without IGF1R genomic amplification
    Katherine A Janeway
    Department of Pediatric Hematology Oncology, Dana Farber Cancer Institute and Children s Hospital, Boston, MA 02115, USA
    Int J Cancer 127:2718-22. 2010
    ..Despite the absence of apparent genomic activation mechanisms accounting for overexpression, clinical study of IGF1R-directed therapies in pediatric WT GIST is warranted...
  29. pmc Profiling critical cancer gene mutations in clinical tumor samples
    Laura E MacConaill
    Center for Cancer Genome Discovery, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, USA
    PLoS ONE 4:e7887. 2009
    ..We report the implementation of a genotyping and validation algorithm that enables robust tumor mutation profiling in the clinical setting...
  30. doi request reprint Cytogenetics and fluorescence in situ hybridization as adjuncts to cytology in the diagnosis of malignant mesothelioma
    Rachel E Factor
    Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, USA
    Cancer 117:247-53. 2009
    ..In the current study, the authors investigated the value of karyotyping and fluorescence in situ hybridization (FISH) as adjuncts to conventional cytologic examination in patients with MM...
  31. ncbi request reprint Oncogenic MITF dysregulation in clear cell sarcoma: defining the MiT family of human cancers
    Ian J Davis
    Melanoma Program in Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Cell 9:473-84. 2006
    ..Seemingly unrelated tumors thus employ distinct strategies to oncogenically dysregulate the MiT family, collectively broadening the definition of MiT-associated human cancers...
  32. ncbi request reprint Distinctive cytogenetic profile in benign metastasizing leiomyoma: pathogenetic implications
    Marisa R Nucci
    Department of Pathology, Divisions of Women s and Perinatal Pathology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA, USA
    Am J Surg Pathol 31:737-43. 2007
    ....
  33. doi request reprint c-Jun amplification and overexpression are oncogenic in liposarcoma but not always sufficient to inhibit the adipocytic differentiation programme
    Eric L Snyder
    Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    J Pathol 218:292-300. 2009
    ..Thus, c-Jun amplification is oncogenic in liposarcomas but not always sufficient for inhibition of adipocytic differentiation...
  34. ncbi request reprint Genomic and functional evidence for an ARID1A tumor suppressor role
    Jianmin Huang
    Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Genes Chromosomes Cancer 46:745-50. 2007
    ..These studies provide strong evidence that ARID1A is a tumor suppressor gene. (c) 2007 Wiley-Liss, Inc...
  35. pmc Cloning of an Alpha-TFEB fusion in renal tumors harboring the t(6;11)(p21;q13) chromosome translocation
    Ian J Davis
    Department of Pediatric Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 100:6051-6. 2003
    ..Alpha-TFEB is thus identified as a fusion gene in a subset of pediatric renal neoplasms...
  36. ncbi request reprint 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...
  37. doi request reprint Reporting of diagnostic cytogenetic results
    Azra H Ligon
    Brigham and Women s Hospital, Boston, Massachusetts, USA
    Curr Protoc Hum Genet . 2004
    ..Multi-specimen usage macros are included that can be applied to two or more specimen types...
  38. ncbi request reprint Prognostic value of KIT mutation type, mitotic activity, and histologic subtype in gastrointestinal stromal tumors
    Samuel Singer
    Department of Pathology and Surgery, Brigham and Women s Hospital, Boston, MA, USA
    J Clin Oncol 20:3898-905. 2002
    ..The aim of this study was to evaluate the prognostic relevance for KIT mutations in a series of GISTs in which the mutations were evaluated intensively by genomic and cDNA sequencing...
  39. ncbi request reprint The role of chromosomal translocation (15;19) in the carcinoma of the upper aerodigestive tract in children
    Reza Rahbar
    Department of Otolaryngology, Children s Hospital, Boston, MA 02115, USA
    Otolaryngol Head Neck Surg 129:698-704. 2003
    ..To further evaluate the role of chromosomal translocation (15;19) in the presentation of the carcinoma (CA) of the upper aerodigestive tract...
  40. pmc PKC412 inhibits the zinc finger 198-fibroblast growth factor receptor 1 fusion tyrosine kinase and is active in treatment of stem cell myeloproliferative disorder
    Jing Chen
    Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 101:14479-84. 2004
    ..Therefore, PKC412 may be a useful therapy for treatment of human stem cell leukemia-lymphoma syndrome...
  41. pmc Defects in succinate dehydrogenase in gastrointestinal stromal tumors lacking KIT and PDGFRA mutations
    Katherine A Janeway
    Department of Pediatric Hematology Oncology, Dana Farber Cancer Institute and Children s Hospital, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 108:314-8. 2011
    ..Testing for germline mutations in SDH is recommended in patients with WT GIST. These findings highlight a potential central role of SDH dysregulation in WT GIST oncogenesis...
  42. doi request reprint Osteofibrous dysplasia and adamantinoma in children and adolescents: a clinicopathologic reappraisal
    Briana C Gleason
    Department of Pathology, Children s Hospital Boston, Boston, MA 02115, USA
    Am J Surg Pathol 32:363-76. 2008
    ..OFD, OFD-like adamantinoma, and classic adamantinoma appear to show a progressive complexity of cytogenetic aberrations, perhaps indicative of a multistep neoplastic transformation...
  43. doi request reprint MED12 mutations in leiomyosarcoma and extrauterine leiomyoma
    Gloria Ravegnini
    1 Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA 2 Department of Pharmacology, University of Bologna, Bologna, Italy
    Mod Pathol 26:743-9. 2013
    ..These findings indicate that MED12 has oncogenic roles in a broad range of smooth muscle neoplasia, including tumors arising in extrauterine locations...
  44. pmc Anti-KIT designer T cells for the treatment of gastrointestinal stromal tumor
    Steven C Katz
    Roger Williams Medical Center, Department of Surgery, Providence, RI Boston University School of Medicine, Boston, MA, USA
    J Transl Med 11:46. 2013
    ..The aims of this study were to develop and test novel anti-KIT dTc engineered to target GIST cells...
  45. ncbi request reprint Cytogenetic aberrations in perineurioma: variation with subtype
    Jane E Brock
    Department of Pathology, Children s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Am J Surg Pathol 29:1164-9. 2005
    ..The findings also expand previous assertions that chromosome 22 abnormalities are pathogenetic in perineurioma and suggest that diverse genetic tumorigenic mechanisms may exist, possibly depending on the subtype...
  46. pmc Genetic and biological subgroups of low-stage follicular thyroid cancer
    Christopher A French
    Division of Endocrinology, Department of Pathology, Brigham and Women s Hospital, Boston, Massachusetts, USA
    Am J Pathol 162:1053-60. 2003
    ..The findings support a model in which separate genetic alterations initiate distinct pathways of oncogenesis in thyroid carcinoma subtypes...
  47. doi request reprint Trisomy 18 is a consistent cytogenetic feature in pilomatricoma
    Agoston T Agoston
    Department of Pathology, Children s Hospital, Boston, MA 02115, USA
    Mod Pathol 23:1147-50. 2010
    ....
  48. ncbi request reprint Overexpression, amplification, and androgen regulation of TPD52 in prostate cancer
    Mark A Rubin
    Department of Pathology, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Cancer Res 64:3814-22. 2004
    ..In summary, these findings suggest that dysregulation of TPD52 by genomic amplification and androgen induction may play a role in prostate cancer progression...
  49. ncbi request reprint Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors
    George D Demetri
    Dana Farber Cancer Institute and Harvard Cancer Center, Boston, MA 02115, USA
    N Engl J Med 347:472-80. 2002
    ..Imatinib mesylate, a selective tyrosine kinase inhibitor, has been shown in preclinical models and preliminary clinical studies to have activity against such tumors...
  50. doi request reprint ALK rearrangement in sickle cell trait-associated renal medullary carcinoma
    Adrian Mariño-Enríquez
    Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston 02115, MA, USA
    Genes Chromosomes Cancer 50:146-53. 2011
    ..This report widens the spectrum of ALK-related tumors and ALK fusion partners, and provides a rationale for treating RMC with targeted ALK inhibitors...
  51. ncbi request reprint Inhibition of FLT3 in MLL. Validation of a therapeutic target identified by gene expression based classification
    Scott A Armstrong
    Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Cancer Cell 3:173-83. 2003
    ..Finally, we developed a mouse model of MLL and used bioluminescent imaging to determine that PKC412 is active against MLL in vivo...
  52. ncbi request reprint Molecular biology and cytogenetics of soft tissue sarcomas: relevance for targeted therapies
    Jonathan A Fletcher
    Department of Pathology, Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
    Cancer Treat Res 120:99-116. 2004
  53. pmc PPARgamma ligands inhibit primary tumor growth and metastasis by inhibiting angiogenesis
    Dipak Panigrahy
    Surgical Research Laboratory, Children s Hospital, Department of Surgery, Harvard Medical School, Boston, Massachusetts, USA
    J Clin Invest 110:923-32. 2002
    ..These results suggest that PPARgamma ligands may be useful in treating angiogenic diseases such as cancer by inhibiting angiogenesis...
  54. ncbi request reprint Cavernous sinus and leptomeningeal metastases arising from a squamous cell carcinoma of the face: case report
    Jay Jiguang Zhu
    Division of Neurology, Caritas St Elizabeth s Medical Center, Tufts University School of Medicine, 736 Cambridge Street, Boston, MA 02135, USA
    Neurosurgery 54:492-8; discussion 498-9. 2004
    ..Metastasis to the leptomeninges and cauda equina has not been reported. We report a unique case of perineural spread and central dissemination from an epithelial squamous cell carcinoma (SCC) associated with a tumor biomarker...
  55. ncbi request reprint BRD4-NUT fusion oncogene: a novel mechanism in aggressive carcinoma
    Christopher A French
    Department of Pathology, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Cancer Res 63:304-7. 2003
    ..Very few fusion oncogenes have been identified in epithelial tumors, and BRD4-NUT is the first fusion oncogene mechanism identified in a highly lethal form of carcinoma...
  56. ncbi request reprint CHIPing soft tissue tumors: will the paradigms be changed?
    Andre M Oliveira
    Department of Pathology, Brigham and Women s Hospital, 75 Francis Street, Boston, MA 02115, USA
    Adv Anat Pathol 10:1-7. 2003
  57. ncbi request reprint Constitutive activation of insulin receptor substrate 1 is a frequent event in human tumors: therapeutic implications
    Qing Chang
    Department of Pathology, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Cancer Res 62:6035-8. 2002
    ..These studies suggest that constitutive IRS-1 activation is a common phenomenon in tumors and that activated IRS-1 may present an attractive therapeutic target...
  58. ncbi request reprint Chromogenic in situ hybridization and FISH in pathology
    Bae Li Hsi
    Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    Methods Mol Biol 204:343-51. 2002
  59. ncbi request reprint Soft tissue sarcomas of adults: state of the translational science
    Ernest C Borden
    The Cleveland Clinic Foundation, Cleveland, Ohio, 44195, USA
    Clin Cancer Res 9:1941-56. 2003
    ..Finally, multicenter, coordinated trials, such as those that occurred with assessment of imatinib mesylate in metastatic gastrointestinal stromal tumors, will assure the most rapid reductions in morbidity and mortality...
  60. ncbi request reprint The Her-2/neu gene and protein in breast cancer 2003: biomarker and target of therapy
    Jeffrey S Ross
    Department of Pathology and Laboratory Medicine, Albany Medical College, Albany, New York 12208, USA
    Oncologist 8:307-25. 2003
    ..The review also evaluates the status of serum-based testing for circulating HER-2/neu receptor protein and its ability to predict disease outcome and therapy response...
  61. ncbi request reprint PDGFRA activating mutations in gastrointestinal stromal tumors
    Michael 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...
  62. doi request reprint Phase II, open-label study evaluating the activity of imatinib in treating life-threatening malignancies known to be associated with imatinib-sensitive tyrosine kinases
    Michael 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...
  63. ncbi request reprint Molecular genetic characterization of the EWS/CHN and RBP56/CHN fusion genes in extraskeletal myxoid chondrosarcoma
    Ioannis Panagopoulos
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    Genes Chromosomes Cancer 35:340-52. 2002
    ....
  64. ncbi request reprint Testing for KIT (CD117) in gastrointestinal stromal tumors: another HercepTest?
    Christopher D M Fletcher
    Appl Immunohistochem Mol Morphol 10:197-8. 2002
  65. ncbi request reprint Gastrointestinal stromal tumors (GISTs) with KIT and PDGFRA mutations have distinct gene expression profiles
    Subbaya 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...
  66. ncbi request reprint Biology and genetic aspects of gastrointestinal stromal tumors: KIT activation and cytogenetic alterations
    Michael 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...
  67. ncbi request reprint Peripheral nerve sheath tumors from patients with neurofibromatosis type 1 do not have the chromosomal translocation t(X;18)
    Michael A Liew
    Department of Pediatrics, Division of Medical Genetics, University of Utah, 50 North Medical Drive, Salt Lake City, UT 84132, USA
    Pediatr Dev Pathol 5:165-9. 2002
    ..The results indicate that the t(X;18) translocation is absent in neurofibromas and is not a marker for MPNST in patients with NF1...
  68. ncbi request reprint Gonadotropic pituitary carcinoma: HER-2/neu expression and gene amplification. Report of two cases
    Federico Roncaroli
    Department of Oncology, Bellaria Hospital, Bologna, Italy
    J Neurosurg 99:402-8. 2003
    ..Further studies are needed to determine whether HER-2/neu plays a role in the pathogenesis of pituitary carcinoma...
  69. ncbi request reprint Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumor
    Michael 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...
  70. ncbi request reprint Molecular and clinical analysis of locally advanced dermatofibrosarcoma protuberans treated with imatinib: Imatinib Target Exploration Consortium Study B2225
    Grant 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...
  71. ncbi request reprint 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...
  72. pmc KIT gene deletions at the intron 10-exon 11 boundary in GI stromal tumors
    Christopher 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...
  73. ncbi request reprint Molecular correlates of imatinib resistance in gastrointestinal stromal tumors
    Michael 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...
  74. ncbi request reprint Imatinib mesylate: an attractive alternative in young children with large, surgically challenging dermatofibrosarcoma protuberans
    Victoria E Price
    Department of Pediatrics, Division Hematology Oncology, The Hospital for Sick Children, University of Toronto, Toronto, Canada
    Pediatr Blood Cancer 44:511-5. 2005
    ..The drug was tolerated well without any adverse reactions. Imatinib mesylate offers a non-surgical alternative for the treatment of large DFSP in children...
  75. ncbi request reprint Biology of gastrointestinal stromal tumors
    Christopher 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...
  76. ncbi request reprint Histone H2AX is a mediator of gastrointestinal stromal tumor cell apoptosis following treatment with imatinib mesylate
    Ying Liu
    Molecular Virology Program, University of Pittsburgh Cancer Institute, Pennsylvania 15213, USA
    Cancer Res 67:2685-92. 2007
    ..Our results underscore the importance of H2AX as a human tumor suppressor protein, provide mechanistic insights into imatinib-induced tumor cell apoptosis and establish H2AX as a novel target in cancer therapy...
  77. ncbi request reprint Sustained complete remission of metastatic dermatofibrosarcoma protuberans with imatinib mesylate
    Stefanos V Labropoulos
    First Department of Medical Oncology, Hygeia Hospital, Marousi, Greece
    Anticancer Drugs 16:461-6. 2005
    ..We conclude that sustained complete remission of metastatic DFSP with specific FISH abnormalities involving the PDGFB locus can be obtained with imatinib mesylate with minimal toxicity for the patient...
  78. pmc Activation of the GLI oncogene through fusion with the beta-actin gene (ACTB) in a group of distinctive pericytic neoplasms: pericytoma with t(7;12)
    Anna Dahlén
    Department of Clinical Genetics, University Hospital, Lund, Sweden
    Am J Pathol 164:1645-53. 2004
    ....
  79. pmc KIT mutations are common in testicular seminomas
    Kathleen 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...
  80. ncbi request reprint 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 tumors
    Katherine 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...
  81. ncbi request reprint Genetics of soft tissue tumors
    Matt van de Rijn
    Department of Pathology, Stanford University Medical Center, Stanford, California 94305, USA
    Annu Rev Pathol 1:435-66. 2006
    ..Here we describe the known molecular changes in a number of sarcomas and focus on novel scientific approaches that can be expected to lead to improved diagnosis, prognostication, and therapy of sarcoma...
  82. doi request reprint 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 KIT
    Charles 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...
  83. ncbi request reprint Targeted therapy in breast cancer: the HER-2/neu gene and protein
    Jeffrey S Ross
    Department of Pathology and Laboratory Medicine, Albany Medical College, Albany, NY 12208, USA
    Mol Cell Proteomics 3:379-98. 2004
    ..The review will also evaluate the status of serum-based testing for circulating HER-2/neu receptor protein and its ability to predict disease outcome and therapy response...
  84. pmc KIT gene mutations in gastrointestinal stromal tumors: more complex than previously recognized?
    Jonathan A Fletcher
    Am J Pathol 161:737-8; author reply 738-9. 2002
  85. ncbi request reprint Detection by the fluorescence in situ hybridization technique of MYC translocations in paraffin-embedded lymphoma biopsy samples
    Eugenia Haralambieva
    Leukaemia Research Fund Immunodiagnostics Unit, Nuffield Department of Clinical Laboratory Sciences, John Radcliffe Hospital, Oxford OX3 9DU, UK
    Br J Haematol 121:49-56. 2003
    ....
  86. ncbi request reprint HER-2/neu testing in breast cancer
    Jeffrey S Ross
    Department of Pathology and Laboratory Medicine, Albany Medical College, NY 12208, USA
    Am J Clin Pathol 120:S53-71. 2003
    ....
  87. ncbi request reprint The chimeric FUS/CREB3l2 gene is specific for low-grade fibromyxoid sarcoma
    Ioannis Panagopoulos
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    Genes Chromosomes Cancer 40:218-28. 2004
    ..The results indicated that FUS/CREB3L2 is specifically associated with LGFMS and that RT-PCR or FISH analysis may be useful for the differential diagnosis...
  88. ncbi request reprint Cytogenetic and p53 profiles in congenital cystic adenomatoid malformation: insights into its relationship with pleuropulmonary blastoma
    Sara O Vargas
    Department of Pathology, Children s Hospital Boston, and Department of Pathology, Harvard Medical School, MA, USA
    Pediatr Dev Pathol 9:190-5. 2006
    ..Overall, these findings provide evidence that CCAM is nonneoplastic. Although some may view CCAM as a PPB precursor, it remains biologically distinct in terms of karyotype and p53 status...