Genomes and Genes
fusion oncogene proteins
Summary: The GENETIC TRANSLATION products of the fusion between an ONCOGENE and another gene. The latter may be of viral or cellular origin.
Publications277 found, 100 shown here
- Gene fusions between TMPRSS2 and ETS family genes in prostate cancer: frequency and transcript variant analysis by RT-PCR and FISH on paraffin-embedded tissuesJiangling J Tu
Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY 10021, USA
Mod Pathol 20:921-8. 2007..004). These morphological correlates, and more importantly the potential correlation of such fusions to clinical outcome and treatment responses, should be further explored...
- Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancerScott A Tomlins
Department of Pathology, University of Michigan Medical School, 1301 Catherine Street, Ann Arbor, MI 48109 0602, USA
Science 310:644-8. 2005..These results have implications in the development of carcinomas and the molecular diagnosis and treatment of prostate cancer...
- Distinct classes of chromosomal rearrangements create oncogenic ETS gene fusions in prostate cancerScott A Tomlins
Michigan Center for Translational Pathology, Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA
Nature 448:595-9. 2007..Furthermore, the identification of androgen-repressed and insensitive 5' fusion partners may have implications for the anti-androgen treatment of advanced prostate cancer...
- Role of the TMPRSS2-ERG gene fusion in prostate cancerScott A Tomlins
Michigan Center for Translational Pathology, Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA
Neoplasia 10:177-88. 2008..Our results support previous work suggesting that TMPRSS2-ERG fusions mediate invasion, consistent with the defining histologic distinction between PIN and prostate cancer...
- TMPRSS2:ETV4 gene fusions define a third molecular subtype of prostate cancerScott A Tomlins
Department of Pathology, University of Michigan Medical School, 1301 Catherine Street, Ann Arbor, MI 48109, USA
Cancer Res 66:3396-400. 2006..This result defines a third molecular subtype of prostate cancer and supports the hypothesis that dysregulation of ETS family members through fusions with TMRPSS2 may be an initiating event in prostate cancer development...
- EML4-ALK fusion gene and efficacy of an ALK kinase inhibitor in lung cancerJussi P Koivunen
Lowe Center for Thoracic Oncology, Dana Farber Cancer Institute, D820A, 44 Binney Street, Boston, MA 02115, USA
Clin Cancer Res 14:4275-83. 2008..We determined the frequency of EML4-ALK in Caucasian NSCLC and in NSCLC cell lines. We also determined whether TAE684, a specific ALK kinase inhibitor, would inhibit the growth of EML4-ALK-containing cell lines in vitro and in vivo...
- TMPRSS2:ERG fusion-associated deletions provide insight into the heterogeneity of prostate cancerSven Perner
Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, EBRC 442A, 221 Longwood Avenue, Boston, MA 02115 6110, USA
Cancer Res 66:8337-41. 2006..The deletion as cause of TMPRSS2:ERG fusion is associated with clinical features for prostate cancer progression compared with tumors that lack the TMPRSS2:ERG rearrangement...
- Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancerManabu Soda
Division of Functional Genomics, Jichi Medical University, Tochigi 329 0498, Japan
Nature 448:561-6. 2007..Our data demonstrate that a subset of NSCLC patients may express a transforming fusion kinase that is a promising candidate for a therapeutic target as well as for a diagnostic molecular marker in NSCLC...
- TMPRSS2:ERG gene fusion associated with lethal prostate cancer in a watchful waiting cohortF Demichelis
Department of Pathology, Brigham and Women s Hospital, Boston, MA 02115 6110, USA
Oncogene 26:4596-9. 2007..005). These data suggest that TMPRSS2:ERG fusion prostate cancers may have a more aggressive phenotype, possibly mediated through increased ERG expression...
- Duplication of the fusion of TMPRSS2 to ERG sequences identifies fatal human prostate cancerG Attard
Institute of Cancer Research, Male Urological Cancer Research Centre, Surrey, UK
Oncogene 27:253-63. 2008..We conclude that determination of ERG gene status, including duplication of the fusion of TMPRSS2 to ERG sequences in 2+Edel, allows stratification of prostate cancer into distinct survival categories...
- EWS/FLI-1 silencing and gene profiling of Ewing cells reveal downstream oncogenic pathways and a crucial role for repression of insulin-like growth factor binding protein 3Alexandre Prieur
Laboratoire de Pathologie Moléculaire des Cancers, INSERM U509, Section de Recherche, Institut Curie, 75248 Paris, France
Mol Cell Biol 24:7275-83. 2004..Finally, IGFBP-3-induced Ewing cell apoptosis relies on both IGF-1-dependent and -independent pathways. These findings therefore identify the repression of IGFBP-3 as a key event in the development of Ewing's sarcoma...
- Sequence-specific knockdown of EWS-FLI1 by targeted, nonviral delivery of small interfering RNA inhibits tumor growth in a murine model of metastatic Ewing's sarcomaSiwen Hu-Lieskovan
Department of Pathology, Children s Hospital Los Angeles, Los Angeles, California 90027, USA
Cancer Res 65:8984-92. 2005..These data provide strong evidence for the safety and efficacy of this targeted, nonviral siRNA delivery system...
- NR0B1 is required for the oncogenic phenotype mediated by EWS/FLI in Ewing's sarcomaMichelle Kinsey
The Department of Oncological Sciences, University of Utah, Salt Lake City, Utah, USA
Mol Cancer Res 4:851-9. 2006..These studies define a new role for NR0B1 in oncogenic transformation and emphasize the utility of analyzing the function of EWS/FLI in Ewing's sarcoma cells...
- Transcriptome sequencing to detect gene fusions in cancerChristopher A Maher
Michigan Center for Translational Pathology, Ann Arbor, USA
Nature 458:97-101. 2009..Taken together, this study establishes a robust pipeline for the discovery of novel gene chimaeras using high-throughput sequencing, opening up an important class of cancer-related mutations for comprehensive characterization...
- PML is essential for multiple apoptotic pathwaysZ G Wang
Department of Human Genetics and Molecular Biology Program, Memorial Sloan Kettering Cancer Center, Graduate School of Medical Sciences, Cornell University, New York, New York 10021, USA
Nat Genet 20:266-72. 1998..These results demonstrate that Pml is a mediator of multiple apoptotic signals, and implicate inhibition of apoptosis in the pathogenesis of APL...
- Characterization of TMPRSS2:ETV5 and SLC45A3:ETV5 gene fusions in prostate cancerBeth E Helgeson
Michigan Center for Translational Pathology, Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109 0602, USA
Cancer Res 68:73-80. 2008..Together, our results suggest that the family of 5' partners previously identified in ETV1 gene fusions can fuse with other ETS family members, suggesting numerous rare gene fusion permutations in prostate cancer...
- EML4-ALK rearrangement in non-small cell lung cancer and non-tumor lung tissuesMaria Paola Martelli
Institute of Hematology, University of Perugia, Perugia, Italy
Am J Pathol 174:661-70. 2009..The EML4-ALK transcript cannot be regarded as a specific diagnostic tool for NSCLC. Our results show therefore that the causal role and value of EML4-ALK as a therapeutic target remain to be defined...
- TMPRSS2-ERG fusion, a common genomic alteration in prostate cancer activates C-MYC and abrogates prostate epithelial differentiationC Sun
Department of Surgery, Center for Prostate Disease Research, Uniformed Services University of the Health Sciences, Rockville, MD 20852, USA
Oncogene 27:5348-53. 2008....
- Megakaryoblastic leukemia 1, a potent transcriptional coactivator for serum response factor (SRF), is required for serum induction of SRF target genesBo Cen
Department of Biological Sciences, Columbia University, 1212 Amsterdam Avenue, New York, NY 10027, USA
Mol Cell Biol 23:6597-608. 2003....
- TMPRSS2:ERG fusion identifies a subgroup of prostate cancers with a favorable prognosisOuti R Saramäki
Institute of Medical Technology, University of Tampere, FIN 33014 Tampere, Finland
Clin Cancer Res 14:3395-400. 2008..Our aim was to assess the frequency of ERG overexpression and TMPRSS2:ERG rearrangement in prostate cancer and their association with clinicopathologic variables and outcome...
- A mouse model for EML4-ALK-positive lung cancerManabu Soda
Divisions of Functional Genomics and Pulmonary Medicine, Jichi Medical University, Tochigi 329 0498, Japan
Proc Natl Acad Sci U S A 105:19893-7. 2008..These data together reinforce the pivotal role of EML4-ALK in the pathogenesis of NSCLC in humans, and they provide experimental support for the treatment of this intractable cancer with ALK inhibitors...
- EML4-ALK fusion transcripts, but no NPM-, TPM3-, CLTC-, ATIC-, or TFG-ALK fusion transcripts, in non-small cell lung carcinomasKazuya Shinmura
1st Department of Pathology, Hamamatsu University School of Medicine, 1 20 1 Handayama, Higashi Ward, Hamamatsu 431 3192, Japan
Lung Cancer 61:163-9. 2008..These results suggested that the EML4-ALK fusion gene product is involved in the carcinogenesis of a subset of NSCLCs...
- Expression profiling of EWS/FLI identifies NKX2.2 as a critical target gene in Ewing's sarcomaRichard Smith
The Center for Children, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112, USA
Cancer Cell 9:405-16. 2006..Thus, we developed a highly validated transcriptional profile for the EWS/FLI fusion protein and identified a critical target gene in Ewing's sarcoma development...
- Identification of novel isoforms of the EML4-ALK transforming gene in non-small cell lung cancerYoung Lim Choi
Division of Functional Genomics and Pulmonary Medicine, Jichi Medical University, Shimotsukeshi, Tochigi, Japan
Cancer Res 68:4971-6. 2008..These data increase the frequency of EML4-ALK-positive NSCLC tumors and bolster the clinical relevance of this oncogenic kinase...
- Frequency of the TMPRSS2:ERG gene fusion is increased in moderate to poorly differentiated prostate cancersAshish B Rajput
Genetic Pathology Evaluation Centre, Vancouver General Hospital, British Columbia Cancer Agency, University of British Columbia, Vancouver, British Columbia, Canada
J Clin Pathol 60:1238-43. 2007..2) to the 3' end of either ERG (21q22.3) or ETV1 (7p21.3). The consequence of these rearrangements is aberrant androgen receptor-driven expression of the potential oncogenes, ETV1 or ERG...
- Detection of TMPRSS2-ERG fusion transcripts and prostate cancer antigen 3 in urinary sediments may improve diagnosis of prostate cancerDaphne Hessels
Experimental Urology, Nijmegen Center for Molecular Life Sciences, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands
Clin Cancer Res 13:5103-8. 2007..We studied the diagnostic usefulness of TMPRSS2-ERG fusion transcripts as well as the combination of prostate cancer antigen 3 (PCA3) RNA and TMPRSS2-ERG fusion transcripts in urinary sediments after digital rectal examination (DRE)...
- The Ewing's sarcoma oncoprotein EWS/FLI induces a p53-dependent growth arrest in primary human fibroblastsStephen L Lessnick
Department of Pediatric Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Cancer Cell 1:393-401. 2002..These data support a role for p53 as a tumor suppressor in Ewing's sarcoma and demonstrate the use of transcriptional profiling of model systems in the identification of cooperating mutations in human cancer...
- A fluorescence in situ hybridization screen for E26 transformation-specific aberrations: identification of DDX5-ETV4 fusion protein in prostate cancerBo Han
Michigan Center for Translational Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA
Cancer Res 68:7629-37. 2008..Fourth, we identified a ubiquitously expressed, androgen-insensitive gene, DDX5, fused in frame with ETV4, leading to the expression of a DDX5-ETV4 fusion protein...
- Expression of the EWS/FLI-1 oncogene in murine primary bone-derived cells Results in EWS/FLI-1-dependent, ewing sarcoma-like tumorsYeny Castillero-Trejo
Hamon Center for Therapeutic Oncology Research, Department of Pathology, Division of Hematology Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, USA
Cancer Res 65:8698-705. 2005..This Ewing sarcoma animal model will be a useful tool for dissecting the molecular pathogenesis of Ewing sarcoma and provides rationale for the broader use of organ-specific progenitor cell populations for the study of human sarcoma...
- EWS-FLI-1 expression triggers a Ewing's sarcoma initiation program in primary human mesenchymal stem cellsNicolò Riggi
Division of Experimental Pathology, Institute of Pathology, University of Lausanne, Switzerland
Cancer Res 68:2176-85. 2008..These observations are consistent with our recent findings using mouse mesenchymal progenitor cells and provide compelling evidence that hMSCs are candidate cells of origin of ESFT...
- EML4-ALK fusion is linked to histological characteristics in a subset of lung cancersKentaro Inamura
Department of Pathology, The Cancer Institute, Japanese Foundation for Cancer Research JFCR, Tokyo, Japan
J Thorac Oncol 3:13-7. 2008..Tumors featuring EML4-ALK fusion constitute one subtype of NSCLC that might be highly sensitive to ALK inhibitors. Herein, we present results of a first large scale study of EML4-ALK fusion in lung cancers...
- Similar MLL-associated leukemias arising from self-renewing stem cells and short-lived myeloid progenitorsAntonio Cozzio
Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
Genes Dev 17:3029-35. 2003....
- Development of Ewing's sarcoma from primary bone marrow-derived mesenchymal progenitor cellsNicolò Riggi
Experimental Pathology Division, Institute of Pathology, University of Lausanne, Switzerland
Cancer Res 65:11459-68. 2005..These observations provide the first identification of candidate primary cells from which EFTs originate and suggest that EWS-FLI-1 expression may constitute the initiating event in EFT pathogenesis...
- Caveolin-1 (CAV1) is a target of EWS/FLI-1 and a key determinant of the oncogenic phenotype and tumorigenicity of Ewing's sarcoma cellsOscar M Tirado
Laboratory of Experimental Carcinogenesis, Department of Radiation Medicine, Georgetown University Medical Center, Washington, DC 20057, USA
Cancer Res 66:9937-47. 2006..Overall, these data identify CAV1 as a key determinant of the tumorigenicity of ESFT and imply that targeting CAV1 may allow the development of new molecular therapeutic strategies for ESFT patients...
- Noninvasive detection of TMPRSS2:ERG fusion transcripts in the urine of men with prostate cancerBharathi Laxman
Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA
Neoplasia 8:885-8. 2006..These results demonstrate that TMPRSS2:ERG gene fusions can be detected in the urine of patients with prostate cancer and support larger studies on prospective cohorts for noninvasive detection of prostate cancer...
- EWS-Fli1 antisense oligodeoxynucleotide inhibits proliferation of human Ewing's sarcoma and primitive neuroectodermal tumor cellsK Tanaka
Department of Orthopaedic Surgery, Faculty of Medicine, Kyushu University, Fukuoka, Japan
J Clin Invest 99:239-47. 1997....
- Actin dynamics control SRF activity by regulation of its coactivator MALFrancesc Miralles
Transcription Laboratory, Room 401, Cancer Research UK London Research Institute, Lincolns Inn Fields Laboratories, 44 Lincoln s Inn Fields, London WC2A 3PX, UK
Cell 113:329-42. 2003..Constitutively cytoplasmic MAL derivatives interfere with MAL redistribution and Rho-actin signaling to SRF. MAL associates with several SRF target promoters regulated via the Rho-actin pathway...
- A previously unidentified alternatively spliced isoform of t(8;21) transcript promotes leukemogenesisMing Yan
Department of Molecular and Experimental Medicine, The Scripps Research Institute, MEM L51, 10550 North Torrey Pines Road, La Jolla, California 92037, USA
Nat Med 12:945-9. 2006..These results indicate that fusion proteins from alternatively spliced isoforms of a chromosomal translocation may work together to induce cancer development...
- RET/PTC1 oncogene signaling in PC Cl 3 thyroid cells requires the small GTP-binding protein RhoM V Barone
Centro di Endocrinologia ed Oncologia Sperimentale del CNR, c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, , Via S. Pansini 5, Naples, Italy
Oncogene 20:6973-82. 2001..We conclude that Rho is implicated in the actin reorganization and cell survival mediated by the chimeric RET/PTC1 oncogene in thyroid epithelial cells, both phenotypes being cell type- and oncogene type-specific...
- Chimeric transcript discovery by paired-end transcriptome sequencingChristopher A Maher
Michigan Center for Translational Pathology, Ann Arbor, MI 48109, USA
Proc Natl Acad Sci U S A 106:12353-8. 2009..Together, this study establishes a highly specific and sensitive approach for accurately and comprehensively cataloguing chimeras within a sample using paired-end transcriptome sequencing...
- Standardization and quality control studies of 'real-time' quantitative reverse transcriptase polymerase chain reaction of fusion gene transcripts for residual disease detection in leukemia - a Europe Against Cancer programJ Gabert
Department of Hematology Biology, Institut Paoli Calmettes, France
Leukemia 17:2318-57. 2003..This is likely to prove invaluable to the management of patients entered into multicenter therapeutic trials...
- A RA-dependent, tumour-growth suppressive transcription complex is the target of the PML-RARalpha and T18 oncoproteinsS Zhong
Department of Human Genetics, Molecular Biology Program, Memorial Sloan Kettering Cancer Center, Sloan Kettering Division, Graduate School of Medical Sciences, Cornell University, New York, New York, USA
Nat Genet 23:287-95. 1999..Our data define a new pathway for the control of cell growth and tumorigenesis, and provide a new model for the pathogenesis of acute promyelocytic leukaemia (APL)...
- Analysis of the expression of cell cycle regulators in Ewing cell lines: EWS-FLI-1 modulates p57KIP2and c-Myc expressionL Dauphinot
INSERM U509, , Institut Curie, 26 rue d'Ulm, 75248 Paris Cedex 05, France
Oncogene 20:3258-65. 2001..These results suggest that the modulation of p57(KIP2) expression by EWS-FLI-1 is a fundamental step in Ewing tumorigenesis...
- A transcriptional profiling meta-analysis reveals a core EWS-FLI gene expression signatureJeffrey D Hancock
The Division of Pediatric Hematology Oncology and The Center for Children, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, Utah, USA
Cell Cycle 7:250-6. 2008..15) These results demonstrate the utility of using comparative analysis to validate model systems and emphasize the unique potential of this approach to identify both oncogenic and background cell signatures...
- Gene fusions involving PAX and FOX family members in alveolar rhabdomyosarcomaF G Barr
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, 36th Street and Hamilton Walk, Philadelphia, Pennsylvania, PA 19104 6082, USA
Oncogene 20:5736-46. 2001..This aberrant gene expression program is then hypothesized to contribute to tumorigenic behavior by impacting on the control of growth, apoptosis, differentiation and motility...
- BRD4-NUT fusion oncogene: a novel mechanism in aggressive carcinomaChristopher 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...
- Stat5 is essential for the myelo- and lymphoproliferative disease induced by TEL/JAK2J Schwaller
Division of Hematology and Oncology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
Mol Cell 6:693-704. 2000..These data define a critical role for Stat5a/b and mOSM in the pathogenesis of TEL/JAK2 disease...
- Three-color FISH analysis of TMPRSS2/ERG fusions in prostate cancer indicates that genomic microdeletion of chromosome 21 is associated with rearrangementMaisa Yoshimoto
Applied Molecular Oncology, Ontario Cancer Institute, Princess Margaret Hospital, Toronto, Ontario, Canada
Neoplasia 8:465-9. 2006..Analysis of genomic architecture in the region of genomic rearrangement suggests that tracts of microhomology could facilitate TMPRSS2/ERG fusion events...
- A murine model of CML blast crisis induced by cooperation between BCR/ABL and NUP98/HOXA9Ajeeta B Dash
Division of Hematology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 99:7622-7. 2002..Furthermore, these data indicate that despite acquisition of additional mutations, CML blast crisis cells retain their dependence on BCR/ABL for proliferation and survival...
- Non-solid oncogenes in solid tumors: EML4-ALK fusion genes in lung cancerHiroyuki Mano
Division of Functional Genomics, Jichi Medical University, 3311 1 Yakushiji, Shimotsukeshi, Tochigi 329 0498, Japan
Cancer Sci 99:2349-55. 2008....
- Histologic grade, but not SYT-SSX fusion type, is an important prognostic factor in patients with synovial sarcoma: a multicenter, retrospective analysisLouis Guillou
Institut Universitaire de Pathologie, Rue du Bugnon 25, 1011 Lausanne, Suisse
J Clin Oncol 22:4040-50. 2004..To assess the prognostic value of SYT-SSX fusion type, in comparison with other factors, in a population of 165 patients with synovial sarcoma (SS)...
- The t(8;22) in chronic myeloid leukemia fuses BCR to FGFR1: transforming activity and specific inhibition of FGFR1 fusion proteinsA Demiroglu
Department of Haematology, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom
Blood 98:3778-83. 2001..The study demonstrates that the BCR-FGFR1 fusion may occur in patients with apparently typical CML. Patients with constitutively active FGFR1 fusion genes may be amenable to treatment with specific FGFR1 inhibitors...
- Ewing's sarcoma oncoprotein EWS-FLI1: the perfect target without a therapeutic agentAykut Uren
Georgetown University School of Medicine, Lombardi Comprehensive Cancer Center, 3970 Reservoir Road North West, New Research Building, Room W316, Washington DC, WA 20057, USA
Future Oncol 1:521-8. 2005..Recent advances in generating recombinant EWS-FLI1 and novel data on the cellular functions of EWS-FLI1 should enhance progress towards understanding and application...
- Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4-ALKAlice T Shaw
Department of Pathology, Massachusetts General Hospital, Warren 501c, 55 Fruit St, Boston, MA 02114, USA
J Clin Oncol 27:4247-53. 2009..To aid in identification and treatment of these patients, we examined the clinical characteristics and treatment outcomes of patients who had NSCLC with and without EML4-ALK...
- KIF5B-ALK, a novel fusion oncokinase identified by an immunohistochemistry-based diagnostic system for ALK-positive lung cancerKengo Takeuchi
The Cancer Institute, Japanese Foundation for Cancer Research, Japan
Clin Cancer Res 15:3143-9. 2009..The sensitivity of EML4-ALK detection by immunohistochemistry should be increased adequately...
- Development of anaplastic lymphoma kinase (ALK) small-molecule inhibitors for cancer therapyRongshi Li
High Throughput Medicinal Chemistry, ChemBridge Research Laboratories, 16981 Via Tazon, Suites K, San Diego, California 92127, USA
Med Res Rev 28:372-412. 2008....
- In utero origin of t(8;21) AML1-ETO translocations in childhood acute myeloid leukemiaJoseph L Wiemels
Laboratory for Molecular Epidemiology, Department of Epidemiology and Biostatistics, University of California San Francisco 94143 0560, USA
Blood 99:3801-5. 2002....
- Fusion in the ETS gene family and prostate cancerS A Narod
Department of Medicine, Womens College Research Institute, University of Toronto, ON, Canada
Br J Cancer 99:847-51. 2008..Studies that examine how individual variants and their associated phenotypes affect prostate cancer presentation and progression are required...
- Expression of EWS-ETS fusions in NIH3T3 cells reveals significant differences to Ewing's sarcomaChi L Braunreiter
The Division of Pediatric Hematology Oncology, Huntsman Cancer Institute, Salt Lake City, Utah 84112, USA
Cell Cycle 5:2753-9. 2006..Thus, data derived from the NIH3T3 model system needs to be appropriately validated before they can be accepted as relevant to the human disease...
- IGF2 is critical for tumorigenesis by synovial sarcoma oncoprotein SYT-SSX1Y Sun
Department of Biomedical Genetics Univeristy of Rochester, Rochester, NY 14642, USA
Oncogene 25:1042-52. 2006..These findings suggest that inhibition of the IGF2/IGF1-R signaling pathway may represent a significant therapeutic modality for treating synovial sarcoma...
- Novel markers of subclinical disease for Ewing family tumors from gene expression profilingIrene Y Cheung
Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
Clin Cancer Res 13:6978-83. 2007..Genome-wide expression arrays can uncover novel genes differentially expressed in tumors over normal marrow/blood, which may have potentials as markers of subclinical disease...
- MLL translocations specify a distinct gene expression profile that distinguishes a unique leukemiaScott A Armstrong
Departments of Pediatric Oncology, Dana Farber Cancer Institute, Boston, Massachusetts, USA
Nat Genet 30:41-7. 2002..Establishing that MLL is a unique entity is critical, as it mandates the examination of selectively expressed genes for urgently needed molecular targets...
- Aberrant ERG expression cooperates with loss of PTEN to promote cancer progression in the prostateBrett S Carver
Cancer Biology and Genetics Program, Sloan Kettering Institute, New York, New York, USA
Nat Genet 41:619-24. 2009..Thus, ERG has a distinct role in prostate cancer progression and cooperates with PTEN haploinsufficiency to promote progression of HGPIN to invasive adenocarcinoma...
- The insulin-like growth factor-I receptor is required for EWS/FLI-1 transformation of fibroblastsJ A Toretsky
Pediatric Oncology Branch, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 272:30822-7. 1997..WF cells demonstrated a greater degree of ligand-stimulated insulin receptor substrate-1 phosphorylation when compared with W cells, suggesting that expression of the EWS/FLI-1 fusion protein alters the IGF-IR signaling pathway...
- The Biology of Ewing sarcomaNicolò Riggi
Division of Experimental Pathology, Institute of Pathology, University of Lausanne, Switzerland
Cancer Lett 254:1-10. 2007..This review will highlight some of the most recent discoveries in the field of Ewing sarcoma biology and origins...
- Expression of TMPRSS2:ERG gene fusion in prostate cancer cells is an important prognostic factor for cancer progressionRobert K Nam
Division of Urology, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Canada
Cancer Biol Ther 6:40-5. 2007..Our study indicates that the expression of TMPRSS2:ERG fusion gene among prostate cancer patients treated with surgery is a strong prognostic factor for disease relapse, and may have important clinical implications...
- Microenvironment determines lineage fate in a human model of MLL-AF9 leukemiaJunping Wei
Division of Experimental Hematology, Cincinnati Children s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA
Cancer Cell 13:483-95. 2008..Targeting the Rac signaling pathway by pharmacologic or genetic means resulted in rapid and specific apoptosis of MLL-AF9 cells, suggesting that the Rac signaling pathway may be a valid therapeutic target in MLL-rearranged AML...
- Induction of acute myeloid leukemia in mice by the human leukemia-specific fusion gene NUP98-HOXD13 in concert with Meis1Nicolas Pineault
Terry Fox Laboratory, Vancouver, BC, Canada
Blood 101:4529-38. 2003....
- Molecular mechanisms underlying human synovial sarcoma developmentN R dos Santos
Department of Human Genetics, University Hospital Nijmegen, Nijmegen, The Netherlands
Genes Chromosomes Cancer 30:1-14. 2001..Together, these studies have provided mechanistic clues about how the SYT-SSX fusion proteins may trigger synovial sarcoma development...
- A bcr-3 isoform of RARalpha-PML potentiates the development of PML-RARalpha-driven acute promyelocytic leukemiaJ L Pollock
Washington University School of Medicine, Division of Bone Marrow Transplantation, Department of Internal Medicine, St Louis, MO 63110, USA
Proc Natl Acad Sci U S A 96:15103-8. 1999..These findings suggest that PML-RARalpha drives the development of APML and defines its basic phenotype, whereas RARalpha-PML potentiates this phenotype via mechanisms that are not yet understood...
- The partner gene of AML1 in t(16;21) myeloid malignancies is a novel member of the MTG8(ETO) familyT Gamou
Radiobiology Division, National Cancer Center Research Institute, Tokyo, Japan
Blood 91:4028-37. 1998..Thus, the AML1-MTG16 gene fusion in t(16;21) leukemia results in the production of a protein that is very similar to the AML1-MTG8 chimeric protein...
- A variant TMPRSS2 isoform and ERG fusion product in prostate cancer with implications for molecular diagnosisJacques Lapointe
Department of Pathology, Stanford University, Stanford, CA 94305 5176, USA
Mod Pathol 20:467-73. 2007....
- The AML1-MTG8 leukemic fusion protein forms a complex with a novel member of the MTG8(ETO/CDR) family, MTGR1I Kitabayashi
Radiobiology Division, National Cancer Center Research Institute, Tokyo, Japan
Mol Cell Biol 18:846-58. 1998..These results suggest that AML1-MTG8 could function as a complex with MTGR1 and that the complex might be important in promoting leukemogenesis...
- Endogenous retroviral sequence is fused to FGFR1 kinase in the 8p12 stem-cell myeloproliferative disorder with t(8;19)(p12;q13.3)Geraldine Guasch
INSERM U119, the Institut de Cancérologie et d Immunologie de Marseille, France
Blood 101:286-8. 2003..RT-PCR detected only 1 of the 2 possible fusion transcripts, HERV-K/FGFR1...
- AML1-ETO inhibits maturation of multiple lymphohematopoietic lineages and induces myeloblast transformation in synergy with ICSBP deficiencyMaike Schwieger
Department of Cell and Virus Genetics, Heinrich Pette Institut für Experimentelle Virologie und Immunologie, D 20251 Hamburg, Germany
J Exp Med 196:1227-40. 2002..Our findings demonstrate that AML1-ETO synergizes with an ICSBP deficiency to induce myeloblastic transformation in the BM, reminiscent of AML...
- Oligomerization of RAR and AML1 transcription factors as a novel mechanism of oncogenic activationS Minucci
European Institute of Oncology, Department of Experimental Oncology, Milan, Italy
Mol Cell 5:811-20. 2000..These results show that oligomerization of a transcription factor, imposing an altered interaction with transcriptional coregulators, represents a novel mechanism of oncogenic activation...
- In vivo analysis of the molecular pathogenesis of acute promyelocytic leukemia in the mouse and its therapeutic implicationsL Z He
Department of Human Genetics and Molecular Biology Program, Memorial Sloan Kettering Cancer Center, Sloan Kettering Division, Graduate School of Medical Sciences, Cornell University, 1275 York Avenue, New York, NY 10021, USA
Oncogene 18:5278-92. 1999..We will also discuss how this new understanding has allowed to propose, develop and test in these murine leukemia models as well as in human APL patients novel therapeutic strategies...
- Efficacy of trabectedin (ecteinascidin-743) in advanced pretreated myxoid liposarcomas: a retrospective studyFederica Grosso
Cancer Medicine Department, Adult Sarcoma Medical Treatment Unit, IRCCS Foundation National Cancer Institute, Milan, Italy
Lancet Oncol 8:595-602. 2007....
- Genetic heterogeneity in the alveolar rhabdomyosarcoma subset without typical gene fusionsFrederic G Barr
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
Cancer Res 62:4704-10. 2002....
- The EML4-ALK fusion gene is involved in various histologic types of lung cancers from nonsmokers with wild-type EGFR and KRASDaisy Wing Sze Wong
Department of Pathology, University of Hong Kong, Queen Mary Hospital, Hong Kong Special Administrative Region, China
Cancer 115:1723-33. 2009..The authors of this study investigated the frequency, genetic and clinicopathologic profiles of EML4-ALK in Chinese patients with NSCLC...
- Loss of p16 pathways stabilizes EWS/FLI1 expression and complements EWS/FLI1 mediated transformationB Deneen
Molecular Biology Institute, Gwynne Hazen Cherry Memorial Labs, University of California at Los Angeles, Los Angeles, CA 90095, USA
Oncogene 20:6731-41. 2001..While loss of a single tumor suppressor is sufficient to establish expression of EWS/FLI1, cellular transformation requires further genetic perturbation...
- Oncogenic EWS-Fli1 interacts with hsRPB7, a subunit of human RNA polymerase IIR Petermann
Children s Cancer Research Institute, St Anna Kinderspital, Vienna, Austria
Oncogene 17:603-10. 1998....
- MOZ-TIF2, but not BCR-ABL, confers properties of leukemic stem cells to committed murine hematopoietic progenitorsBrian J P Huntly
Division of Hematology, Department of Medicine, Brigham and Women s Hospital, Boston, MA 02115, USA
Cancer Cell 6:587-96. 2004..These data demonstrate that some, but not all, leukemia oncogenes can confer properties of leukemic stem cells to hematopoietic progenitors destined to undergo apoptotic cell death...
- Ewing sarcomas with p53 mutation or p16/p14ARF homozygous deletion: a highly lethal subset associated with poor chemoresponseHsuan Ying Huang
Department of Pathology, Memorial Sloan Kettering Cancer Center, 1275 York Ave, New York, NY 10021, USA
J Clin Oncol 23:548-58. 2005..We provide the first combined prognostic analysis of these three molecular parameters in ES...
- EWS-FLI1 fusion protein up-regulates critical genes in neural crest development and is responsible for the observed phenotype of Ewing's family of tumorsSiwen Hu-Lieskovan
Department of Pathology and Laboratory Medicine, Children s Hospital Los Angeles, Keck School of Medicine, University of Southern California, Los Angeles, California 90027, USA
Cancer Res 65:4633-44. 2005..Such tumors have a limited neural phenotype regardless of tissue of origin. These findings challenge traditional views of histogenesis and tumor origin...
- TMPRSS2:ERG fusion transcripts in urine from prostate cancer patients correlate with a less favorable prognosisKari Rostad
The Gade Institute, University of Bergen, Bergen, Norway
APMIS 117:575-82. 2009..Our findings contribute to the increasing elucidation of the role of TMPRSS2:ERG in the development of prostate cancer...
- EWS and ATF-1 gene fusion induced by t(12;22) translocation in malignant melanoma of soft partsJ Zucman
Laboratory de Tumour Genetics, INSERM CJF 9201, Institut Curie, Paris, France
Nat Genet 4:341-5. 1993..Thus the oncogenic conversion of EWS follows a common scheme of activation, exchanging its putative RNA binding domain with different DNA binding domains that appear to be tumour-specific...
- Analysis of the role of AML1-ETO in leukemogenesis, using an inducible transgenic mouse modelK L Rhoades
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA
Blood 96:2108-15. 2000..Either the introduction of additional genetic changes or the expression of AML1-ETO at a particular stage of hematopoietic cell differentiation will be necessary to develop a model for studying the pathogenesis of t(8;21)...
- AML1-ETO expression is directly involved in the development of acute myeloid leukemia in the presence of additional mutationsY Yuan
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA
Proc Natl Acad Sci U S A 98:10398-403. 2001..The hMRP8-AML1-ETO-transgenic mice provide an excellent model that can be used to isolate additional genetic events and to further understand the molecular pathogenesis of AML1-ETO-related leukemia...
- Site-specific translocation and evidence of postnatal origin of the t(1;19) E2A-PBX1 fusion in childhood acute lymphoblastic leukemiaJoseph L Wiemels
Department of Epidemiology and Biostatistics, University of California, San Francisco 94143, USA
Proc Natl Acad Sci U S A 99:15101-6. 2002....
- The tetramer structure of the Nervy homology two domain, NHR2, is critical for AML1/ETO's activityYizhou Liu
Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, Virginia 22908, USA
Cancer Cell 9:249-60. 2006..Oligomerization is also required for AML1/ETO's interactions with ETO, MTGR1, and MTG16, but not with other corepressor molecules...
- Molecular markers of prostate cancerTimothy J Bradford
Department of Urology, University of Michigan Medical School, Ann Arbor, MI 48109, USA
Urol Oncol 24:538-51. 2006....
- Gene expression profiling of pediatric acute myelogenous leukemiaMary E Ross
Department of Hematology Oncology, Hartwell Center for Bioinformatics and Biotechnology, St Jude Children s Research Hospital, 332 N Lauderdale, Memphis, TN 38105, USA
Blood 104:3679-87. 2004..Surprisingly, AMLs containing partial tandem duplications of MLL failed to cluster with MLL chimeric fusion gene cases, suggesting a significant difference in their underlying mechanism of transformation...
- Microsatellites as EWS/FLI response elements in Ewing's sarcomaKunal Gangwal
Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112, USA
Proc Natl Acad Sci U S A 105:10149-54. 2008..These findings illustrate an unprecedented route to specificity for ETS proteins and use of microsatellites in tumorigenesis...
- Non-muscle myosin heavy chain (MYH9): a new partner fused to ALK in anaplastic large cell lymphomaLaurence Lamant
INSERM U 563, Department of Oncogenesis and Signaling in Hematopoietic Cells, Centre de Physiopathologie de Toulouse Purpan, Toulouse, France
Genes Chromosomes Cancer 37:427-32. 2003..If further investigations confirm this latter result, the in vivo tyrosine phosphorylation of MYH9-ALK protein could involve mechanisms different from those described in the other ALK hybrid proteins...
- Inducible chromosomal translocation of AML1 and ETO genes through Cre/loxP-mediated recombination in the mouseF Buchholz
Hooper Research Foundation, University of California San Francisco, 94143 0552, USA
EMBO Rep 1:133-9. 2000..In both instances, Cre activity mediated interchromosomal translocations that fused the AML1 and ETO genes. Thus, reciprocal chromosomal translocations that closely resemble rearrangements found in human cancers can be achieved in mice...
- Signatures of selection in fusion transcripts resulting from chromosomal translocations in human cancerIñigo Ortiz de Mendíbil
Department of Genetics, University of Navarra, Pamplona, Spain
PLoS ONE 4:e4805. 2009..However, it has also been suggested that functional constraints might contribute to delimit the position of translocation breakpoints within the genes involved, but a quantitative analysis of such contribution has been lacking...
- Role of PML in cell growth and the retinoic acid pathwayZ G Wang
Department of Human Genetics and Molecular Biology Program, Memorial Sloan Kettering Cancer Center, Sloan Kettering Division, Graduate School of Medical Sciences, Cornell University, New York, NY 10021, USA
Science 279:1547-51. 1998..These results indicate that PML is a critical component of the RA pathway and that disruption of its activity by the PML-RARalpha fusion protein may be important in APL pathogenesis...
- Engineering de novo reciprocal chromosomal translocations associated with Mll to replicate primary events of human cancerAlan Forster
MRC Laboratory of Molecular Biology, Cambridge, United Kingdom
Cancer Cell 3:449-58. 2003..This de novo strategy is a direct recapitulation of naturally occurring human cancer-associated translocations...
- Methyltransferase recruitment and DNA hypermethylation of target promoters by an oncogenic transcription factorLuciano Di Croce
Department of Experimental Oncology, European Institute of Oncology, Milan, Italy
Science 295:1079-82. 2002..These results establish a mechanistic link between genetic and epigenetic changes during transformation and suggest that hypermethylation contributes to the early steps of carcinogenesis...
- A new fusion gene TPM3-ALK in anaplastic large cell lymphoma created by a (1;2)(q25;p23) translocationL Lamant
Department of Pathology, Hematology Laboratory, and UPCM ERS 1590 CNRS, CHU Purpan, Toulouse, France
Blood 93:3088-95. 1999..The present cases of ALCL associated with a novel t(1;2)(q25;p23) demonstrate that at least one fusion partner other than NPM can activate the intracytoplasmic domain of the ALK kinase...
- REGULATION OF PAX3/PAX7 EXPRESSION IN RHABDOMYOSARCOMAFREDERIC BARR; Fiscal Year: 2001....
- IRSG STUDIES OF ALVEOLAR RHABDOMYOSARCOMA GENE FUSIONSFREDERIC BARR; Fiscal Year: 2005..These studies will provide a definitive analysis of the occurrence and clinical significance of these genetic alterations in ARMS, and will ultimately impact on the future design of clinical protocols for the treatment of ARMS patients. ..
- FTI Biology & Treatment of Myeloproliferative DisordersJason Gotlib; Fiscal Year: 2005..If clinically efficacious, further studies of R115777 in MPDs will be warranted...
- Studies of the t(2;13) of alveolar rhabdomyosarcomaFREDERIC BARR; Fiscal Year: 2007..abstract_text> ..
- Therapeutic effect of boswellin in prostate cancerYongkui Jing; Fiscal Year: 2005..We hope our proposal will lead to the discovery of a novel complementary agent for prostate cancer treatment. ..
- ASPL TFE3 fusion in human cancersMarc Ladanyi; Fiscal Year: 2006..3->qter; and finally analyze selected candidate genes in the same region for inactivating mutations. ..
- T(15;19) in Aggressive Pediatric CarcinomaChristopher French; Fiscal Year: 2006..These studies will also reveal the range of primary sites from which t(15;19)+ carcinomas arise. ..
- Cancer Molecular Pathology Training ProgramFREDERIC BARR; Fiscal Year: 2006....
- COG studies of gene amplification in rhabdomyosarcomaFREDERIC BARR; Fiscal Year: 2009..abstract_text> ..
- Cellular and Molecular Studies of Leukemic Stem CellssCraig Jordan; Fiscal Year: 2006..Collectively, these efforts will advance our understanding of basic mechanisms that underlie leukemic transformation and will improve strategies for the preferential ablation of LSCs. ..
- The Role of MLL-AF9 in Acute Myeloid LeukemiaJames C Mulloy; Fiscal Year: 2010..RELEVANCE (See instructions): We have recently shown that human blood stem cells can be induced to make leukemia upon introduction ..
- Role of Wnt signaling in Cervical Cancer PathogenesisAykut Uren; Fiscal Year: 2010..Aykut The name of the principal investigator/program director must be provided at the top of each printed page and each continuation page. RESEARCH GRANT TABLE OF CONTENTS Page Numbers Face Page 1 Description, ..
- Selective in vivo Ablation of Leukemia Stem CellsCraig Jordan; Fiscal Year: 2009..Collectively, the proposed studies will provide a detailed evaluation of how therapeutic agents impact the growth and survival of LSC in vivo. ..
- The Role of CBFb-MYH11 in Acute Myeloid LeukemiaJames C Mulloy; Fiscal Year: 2010..To identify specific signals that will cooperate in the transformation to acute leukemia, defined eenetic elements and saturatine retroviral mutaeenesis will be used. ..
- TLS and TLS Fusion Proteins in LeukemiaLiu Yang; Fiscal Year: 2005..It is envisioned that successful completion of this project will unveil potential therapeutic targets in the treatment of human leukemias characterized by the t(16;21) translocation. ..
- Amnis ImageStream Flow CytometerCraig Jordan; Fiscal Year: 2007..Taken together, the unique capabilities of the ImageStream system will therefore serve to strongly benefit a wide range of research activities. [unreadable] [unreadable] [unreadable]..
- CHONDROGENESIS AND HISTONE MODIFICATION ENZYMESLiu Yang; Fiscal Year: 2007....
- RUNX-fusion Target Genes in Normal and Leukemic HematopoiesisJAMES MULLOY; Fiscal Year: 2007..Understanding the modulation of the self-renewal process by these fusion proteins could give insight into the normal mechanisms of self-renewal employed by the stem cell. [unreadable] [unreadable]..
- Role of AML1/ETO in Hematopoiesis and LeukemogenesisJAMES MULLOY; Fiscal Year: 2005..The establishment of a small animal model of AML will greatly enhance our ability to develop and test treatment strategies and drugs that may be useful in the therapy of AML. ..
- ASSESSMENT OF CLINICAL RETINOID ACTIVITY IN LEUKEMIARobert Gallagher; Fiscal Year: 2009..Accomplishment of these aims may define a novel mechanism of gene-targeted drug resistance and provide greater understanding of clonal evolution in a therapeutic setting leading to relapse. ..
- MOLECULAR ANALYSIS OF TEL AND TEL/AML1 IN PREB LEUKEMIAGiuseppina Nucifora; Fiscal Year: 2001..The experiments outlined in this proposal will allow them to begin to dissect the effects of TEL/AML1 in hematopoiesis and its contribution to leukogenesis. ..
- The function of I(3)mbt in hematopoietic cancersStephen Nimer; Fiscal Year: 2007..The PcG family of proteins is being increasingly implicated in carcinogenesis, and these studies will provide insights into the role that l(3)mbt plays in hematologic malignancies. ..
- TEL, AML1, and TEL/AML1 in HematopoiesisGiuseppina Nucifora; Fiscal Year: 2006....
- The BTB pocket as a novel cancer therapy targetAri Melnick; Fiscal Year: 2003..We expect this research to ultimately lead to the development of a new class of drugs which could provide targeted therapy of non-Hodgkin? s lymphomas as well as retinoid resistant acute promyelocytic leukemia. ..
- Signaling Pathways that Determine Ewings Sarcoma OutcomeJeffrey Toretsky; Fiscal Year: 2008..Clearly, if PTPL1 is validated as a supportive oncoprotein and the pathways modulated by PTPL1 are identified, patients with many other tumors that rely on IGF-IR signaling including breast carcinoma could benefit from our findings. ..
- Ex Vivo Expansion of Cord Blood Progenitor CellsColleen Delaney; Fiscal Year: 2008..abstract_text> ..
- FUNCTION OF MEF IN HEMATOPOIETIC CELLSStephen Nimer; Fiscal Year: 2007..abstract_text> ..
- Activation of BCL-2 in Hematologic MalgnanciesLINDA BOXER; Fiscal Year: 2007..These studies will provide new information that can be used to treat the disease in humans. ..
- Inactivating EVI1 for the Treatment of Myelodysplastic *Giuseppina Nucifora; Fiscal Year: 2008..The third aim will be focused on the role of arsenic trioxide in the treatment of EVI1-positive MDS and on the isolation of small molecules that inhibit EVI1. ..
- Developmental Regulation of MacroH2A1 Chromatin AssemblyTheodore Rasmussen; Fiscal Year: 2009..Research proposed here will provide basic insights into differentiation biology and provide a framework for future attempts to achieve rationally-guided ES cell differentiation. ..
- Role of EVI1 Modifications in Cell TransformationGiuseppina Nucifora; Fiscal Year: 2009..2. To identify the components and the functions of the nuclear EVI1 multiprotein complexes. 3. To characterize the sumoylation and acetylation of EVI1 in vivo and to define their role in EVI1- induced transformation. ..
- MECHANISMS OF TRANSCRIPTIONAL REPRESSION BY AML1-ETOBruce Hug; Fiscal Year: 2004..Such an environment maximizes the potential for the principal investigator to establish a scientific niche from which an academic career can be constructed. ..
- Signaling and targeting of FGFR1 fusions in 8p11 myeloproliferative syndromeJing Chen; Fiscal Year: 2010..In summary, this proposal will provide detailed information about signaling and transforming properties of FGFR1 fusions, and explore therapeutic strategies to treat FGFR1-associated malignancies. ..
- Ras Pathway Mutations in Human LeukemiaMignon Loh; Fiscal Year: 2008..unreadable] [unreadable] [unreadable]..
- Meningioma: Risk Factors and Quality of LifeJOSEPH LEO WIEMELS; Fiscal Year: 2010..This study represents the first concentrated effort to examine environmental and genetic risk factors for meningioma. ..
- Minimal Residual Disease in Pediatric ALL in Relation to Other Prognostic FactorsMichael J Borowitz; Fiscal Year: 2010..These studies will give us a better understanding of how to use prognostic information in treating children with ALL, and bring us closer to our goal of curing the maximum number of children with ALL with the least toxic therapy. ..
- FUSION GENES IN LEUKEMIA--DETERMINING SIGNIFICANCEMignon Loh; Fiscal Year: 2003..abstract_text> ..
- Vitamin D3 inducible Genes Mediating DifferentiationStephen Nimer; Fiscal Year: 2004..The functional requirement of the DRIP coactivator complex in mediating VDR and RAR transactivation, in the context of nuclear receptor-dependent myeloid differentiation, will be determined. ..
- PROTO ONCOGENE PBX1 IN NORMAL HEMATOPOIETIC DEVELOPMENTJorge DiMartino; Fiscal Year: 2005..By defining the specific requirements for Pbx1 function in normal hematopoiesis, these experiments will further our understanding of the molecular pathogenesis of leukemia, aplastic anemia and myelodysplasia. ..
- Biacore T100Jeffrey Toretsky; Fiscal Year: 2006..These enhanced capabilities of the T100 will allow projects investigating many types of biologic processes to advance. ..
- Minimal Residual Disease in Childhood ALL in RelapseMichael Borowitz; Fiscal Year: 2006..We will also be able to extend these studies to other situations where we can use MRD as a rapid means to compare therapies. ..
- CONTROL OF C-MYC TRANSCRIPTION IN HIGH GRADE LYMPHOMALINDA BOXER; Fiscal Year: 2005..5.Development of strategies to interfere with c-myc transcription that is driven by the IgH enhancers. We have shown that several NF-kB sites are critical for deregulated c-myc expression, and we will first target the function of NF-kB. ..
- ANALYSIS OF MULTIPLE CHIMERIC TRANSCRIPTS IN THE T(3;21)Giuseppina Nucifora; Fiscal Year: 2004..In addition, our results will provide insight in the study of leukemias in which either AML 1 or MDS1/EVI1 are rearranged. ..
- Quantitative RT-PCR: Prediction Lymphoma TransformationKojo Elenitoba Johnson; Fiscal Year: 2005....
- THYROID/RETINOIC ACID RECEPTOR INTERACTING PROTEINSMukul Mathur; Fiscal Year: 2004..We will also specify the region on the DNA binding domain of these receptors where these three proteins interact. ..
- Examination of FLT3 Mutations in Acute Myeloid LeukemiaDerek Stirewalt; Fiscal Year: 2006..Together, the research proposal and educational program provide Dc Stirewalt with the skills to become an independent clinical investigator. ..
- MOLECULAR CLASSIFICATION OF PROSTATE CANCERWilliam Gerald; Fiscal Year: 2004..abstract_text> ..
- Molecular Studies of Human AllLINDA BOXER; Fiscal Year: 2004..Determination of changes in gene expression in ALL cells, both sensitive and resistant, in response to chemotherapeutic agents. 4. Identification of fusion protein-specific events and studies of important genes and pathways in cell line ..
- INTRACELLULAR AMYLOIDOGENESIS AND APOPTOSIS IN NIDDMNORMAN EBERHARDT; Fiscal Year: 2006..These studies will increase our understanding of the contribution of intracellular amyloid accumulation, induction of apoptosis, and/or interference with ER trafficking to the pathogenesis of NIDDM. ..
- EVI1 Expression is a Prognostic Marker of CMLGiuseppina Nucifora; Fiscal Year: 2004..Real-time RT-PCR analysis and statistical analysis of CML and control samples will be used for this study. ..
- Akt Inhibitors to Treat Ewing's SarcomaJeffrey Toretsky; Fiscal Year: 2005..Our findings from this Phase I Sun will hopefully lead to a key compound that can be further developed in a Phase II STTR ultimately leading to clinical trials in patients with ESFT. ..
- GENES INVOLVED IN AIDS LYMPHOMAGENESISMichael Teitell; Fiscal Year: 2002..Genes with significant involvement in the etiology and/or progression of lymphomagenesis, or those with reproducible in vitro biochemical effects, will be further characterized by molecular methods. ..
- Gefitinib-sensitive EGF receptor mutants in lung cancerJeffrey Settleman; Fiscal Year: 2009....
- Regulation and Functin of the p190 RhoGAPsJeffrey Settleman; Fiscal Year: 2006..This is an important step toward establishing an accurate picture of the regulatory mechanisms for small GTPases in vivo, and the nature of their dysregulation in human cancers. ..
- TUMOR SUPPRESSORS AND DIFFERENTIATED THYROID CANCERNORMAN EBERHARDT; Fiscal Year: 2008..4) The inhibitory effects of PPFP can be modulated by PPARgamma and RXR Iigand binding. (5) PPFP alters multiple PARgamma-regulated transcription pathways, which alter growth control and/or apoptosis. ..
- THE HYPEREOSINOPHILIC SYNDROMES AND MEPOLIZUMABGerald Gleich; Fiscal Year: 2007..unreadable] [unreadable] [unreadable] [unreadable]..
- STRUCTURE/FUNCTION OF GROWTH HORMONE RELATED GENENORMAN EBERHARDT; Fiscal Year: 2002..The chromosomal TEF-P locus will be cloned and characterized, including chromosomal localization and promoter characterization (Aim 3). ..
- TAILORING ANTICANCER THERAPY TO LOSS OF P53David Fisher; Fiscal Year: 2003..abstract_text> ..
- Mitf-Signal Responsive Transcription in OsteoclastsDavid Fisher; Fiscal Year: 2009..The second represents a systematic approach to the identification of transcriptional targets of Mitf/TFE3 using screens which couple their biochemical activities to the signaling pathways in which they reside. ..
- PATHOGENESIS AND THERAPY OF ACUTE PROMYELOCYTIC LEUKEMIAScott Kogan; Fiscal Year: 2003....
- Specific Biochemical Inactivation of Oncogenic RasJeffrey Settleman; Fiscal Year: 2008..Together, the proposed studies are expected to lead to the eventual development of a novel therapeutic approach for achieving specific targeting of human tumors that harbor oncogenic mutant forms of Ras. ..
- The MiT Transcription Factor in Pediatric MalignanciesDavid Fisher; Fiscal Year: 2008..Small molecules inhibitors of c-MET exist and will be examined (together with molecular controls) as potential targeted therapy for these incurable cancers. ..
- FASEB Summer Research Conference on Small G-ProteinsJeffrey Settleman; Fiscal Year: 2004..The conference will cover the biochemical, structural, and functional aspects of the various small GTPases and their regulators and targets. ..
- Eosinophil Granule Proteins and Their FunctionsGerald Gleich; Fiscal Year: 2006..Overall, these studies will expand our knowledge of the molecules composing the eosinophil granule and provide new tools to dissect eosinophil function in disease. ..