neoplasm drug resistance

Summary

Summary: Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.

Top Publications

  1. ncbi Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib
    Thomas J Lynch
    Cancer Center, Massachusetts General Hospital and Harvard Medical School, Boston 02129, USA
    N Engl J Med 350:2129-39. 2004
  2. ncbi Tumour stem cells and drug resistance
    Michael Dean
    Laboratory of Genomic Diversity, National Cancer Institute Frederick, Frederick, Maryland 21702, USA
    Nat Rev Cancer 5:275-84. 2005
  3. ncbi Multidrug resistance in cancer: role of ATP-dependent transporters
    Michael M Gottesman
    Laboratory of Cell Biology and Cancer Therapeutics Branch, The Center for Cancer Research, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nat Rev Cancer 2:48-58. 2002
  4. ncbi Cisplatin: mode of cytotoxic action and molecular basis of resistance
    Zahid H Siddik
    Department of Experimental Therapeutics, Unit 104, The University of Texas M D Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030 4009, USA
    Oncogene 22:7265-79. 2003
  5. pmc Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain
    William Pao
    Program in Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    PLoS Med 2:e73. 2005
  6. pmc Molecular mechanisms of resistance and toxicity associated with platinating agents
    Cara A Rabik
    Department of Medicine, Committee on Clinical Pharmacology and Pharmacogenomics, University of Chicago, 5841 S Maryland Avenue, Box MC2115, Section of Hem Onc, Chicago, IL 60637, United States
    Cancer Treat Rev 33:9-23. 2007
  7. pmc Analysis of gene expression and chemoresistance of CD133+ cancer stem cells in glioblastoma
    Gentao Liu
    Maxine Dunitz Neurosurgical Institute, Cedars Sinai Medical Center, Los Angeles, CA, 90048, USA
    Mol Cancer 5:67. 2006
  8. ncbi Molecular determinants of resistance to antiandrogen therapy
    Charlie D Chen
    Department of Medicine, University of California at Los Angeles, Los Angeles, California 90095, USA
    Nat Med 10:33-9. 2004
  9. ncbi Wild-type KRAS is required for panitumumab efficacy in patients with metastatic colorectal cancer
    Rafael G Amado
    Amgen, Inc, One Amgen Center Dr, MS 38 2 B, Thousand Oaks, CA 91320 1799, USA
    J Clin Oncol 26:1626-34. 2008
  10. ncbi Mechanisms of cancer drug resistance
    Michael M Gottesman
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, Maryland 20892 4255, USA
    Annu Rev Med 53:615-27. 2002

Detail Information

Publications314 found, 100 shown here

  1. ncbi Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib
    Thomas J Lynch
    Cancer Center, Massachusetts General Hospital and Harvard Medical School, Boston 02129, USA
    N Engl J Med 350:2129-39. 2004
    ..However, about 10 percent of patients have a rapid and often dramatic clinical response. The molecular mechanisms underlying sensitivity to gefitinib are unknown...
  2. ncbi Tumour stem cells and drug resistance
    Michael Dean
    Laboratory of Genomic Diversity, National Cancer Institute Frederick, Frederick, Maryland 21702, USA
    Nat Rev Cancer 5:275-84. 2005
    ..Gaining a better insight into the mechanisms of stem-cell resistance to chemotherapy might therefore lead to new therapeutic targets and better anticancer strategies...
  3. ncbi Multidrug resistance in cancer: role of ATP-dependent transporters
    Michael M Gottesman
    Laboratory of Cell Biology and Cancer Therapeutics Branch, The Center for Cancer Research, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nat Rev Cancer 2:48-58. 2002
    ..Therefore, the ability to predict and circumvent drug resistance is likely to improve chemotherapy...
  4. ncbi Cisplatin: mode of cytotoxic action and molecular basis of resistance
    Zahid H Siddik
    Department of Experimental Therapeutics, Unit 104, The University of Texas M D Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030 4009, USA
    Oncogene 22:7265-79. 2003
    ..The molecular signature defining the resistant phenotype varies between tumors, and the number of resistance mechanisms activated in response to selection pressures dictates the overall extent of cisplatin resistance...
  5. pmc Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain
    William Pao
    Program in Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York, USA
    PLoS Med 2:e73. 2005
    ..Despite initial responses, patients eventually progress by unknown mechanisms of "acquired" resistance...
  6. pmc Molecular mechanisms of resistance and toxicity associated with platinating agents
    Cara A Rabik
    Department of Medicine, Committee on Clinical Pharmacology and Pharmacogenomics, University of Chicago, 5841 S Maryland Avenue, Box MC2115, Section of Hem Onc, Chicago, IL 60637, United States
    Cancer Treat Rev 33:9-23. 2007
    ..Although the purpose of this review is to provide an overview of cisplatin, carboplatin, and oxaliplatin, we have focused primarily on preclinical data that has clinical relevance generated over the past five years...
  7. pmc Analysis of gene expression and chemoresistance of CD133+ cancer stem cells in glioblastoma
    Gentao Liu
    Maxine Dunitz Neurosurgical Institute, Cedars Sinai Medical Center, Los Angeles, CA, 90048, USA
    Mol Cancer 5:67. 2006
    ..The gene expression and the drug resistance property of CD133 positive cancer stem cells, however, are still unknown...
  8. ncbi Molecular determinants of resistance to antiandrogen therapy
    Charlie D Chen
    Department of Medicine, University of California at Los Angeles, Los Angeles, California 90095, USA
    Nat Med 10:33-9. 2004
    ..These findings provide insight toward the design of new antiandrogens...
  9. ncbi Wild-type KRAS is required for panitumumab efficacy in patients with metastatic colorectal cancer
    Rafael G Amado
    Amgen, Inc, One Amgen Center Dr, MS 38 2 B, Thousand Oaks, CA 91320 1799, USA
    J Clin Oncol 26:1626-34. 2008
    ..Although activating mutations in KRAS, a small G-protein downstream of EGFR, correlate with poor response to anti-EGFR antibodies in mCRC, their role as a selection marker has not been established in randomized trials...
  10. ncbi Mechanisms of cancer drug resistance
    Michael M Gottesman
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, Maryland 20892 4255, USA
    Annu Rev Med 53:615-27. 2002
    ..Studies on mechanisms of cancer drug resistance have yielded important information about how to circumvent this resistance to improve cancer chemotherapy and have implications for pharmacokinetics of many commonly used drugs...
  11. ncbi The resurgence of platinum-based cancer chemotherapy
    Lloyd Kelland
    Cancer Research Technology Development Laboratories, Wolfson Institute for Biomedical Research, University College London, Gower Street, London, WC1E 6BT, UK
    Nat Rev Cancer 7:573-84. 2007
    ....
  12. pmc A distinct "side population" of cells with high drug efflux capacity in human tumor cells
    C Hirschmann-Jax
    Center for Cell and Gene Therapy, Baylor College of Medicine, Methodist Hospital and Texas Children s Hospital, and DeBakey Department of Surgery, One Baylor Plaza, Houston, TX 77030, USA
    Proc Natl Acad Sci U S A 101:14228-33. 2004
    ....
  13. ncbi Molecular mechanisms of drug resistance
    D B Longley
    Drug Resistance Laboratory, Centre for Cancer Research and Cell Biology, Queen s University Belfast, Belfast, N Ireland, UK
    J Pathol 205:275-92. 2005
    ..The ability to predict response to chemotherapy and to modulate this response with targeted therapies will permit selection of the best treatment for individual patients...
  14. ncbi Targeting multidrug resistance in cancer
    Gergely Szakacs
    Institute of Enzymology, Biological Research Center, Hungarian Academy of Sciences, Budapest Karolina út 29 H 1518 Hungary
    Nat Rev Drug Discov 5:219-34. 2006
    ..We describe various approaches to combating multidrug-resistant cancer, including the development of drugs that engage, evade or exploit efflux by ABC transporters...
  15. ncbi Ovarian cancer: strategies for overcoming resistance to chemotherapy
    Roshan Agarwal
    Section of Medicine, Institute for Cancer Research, Sutton, Surrey SM2 5NG, UK
    Nat Rev Cancer 3:502-16. 2003
    ..A better understanding of the mechanisms that underlie this drug resistance should allow treatment to be optimized, so that substantial improvements in the outlook for women with this disease can be achieved...
  16. ncbi ERBB receptors and cancer: the complexity of targeted inhibitors
    Nancy E Hynes
    Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, CH 4058 Basel, Switzerland
    Nat Rev Cancer 5:341-54. 2005
    ..We will discuss the significance of these receptors as clinical targets, in particular the molecular mechanisms underlying response...
  17. ncbi Apoptosis: a link between cancer genetics and chemotherapy
    Ricky W Johnstone
    Cancer Immunology Division, The Peter MacCallum Cancer Institute, Trescowthick Research Laboratories, Smorgon Family Building, St Andrews Place, East Melbourne, 3002 Victoria, Australia
    Cell 108:153-64. 2002
    ....
  18. ncbi Epithelial versus mesenchymal phenotype determines in vitro sensitivity and predicts clinical activity of erlotinib in lung cancer patients
    Robert L Yauch
    Department of Molecular Diagnostics, Genentech, Inc, South San Francisco, California 94080, USA
    Clin Cancer Res 11:8686-98. 2005
    ..These data support a potential role for EMT as a determinant of EGFR activity in NSCLC tumor cells and E-cadherin expression as a novel biomarker predicting clinical activity of the EGFR inhibitor erlotinib in NSCLC patients...
  19. ncbi Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification
    M E Gorre
    Department of Medicine, Molecular Biology Institute, University of California, Los Angeles, CA 90095, USA
    Science 293:876-80. 2001
    ..These studies provide evidence that genetically complex cancers retain dependence on an initial oncogenic event and suggest a strategy for identifying inhibitors of STI-571 resistance...
  20. ncbi Mechanisms of tamoxifen resistance: increased estrogen receptor-HER2/neu cross-talk in ER/HER2-positive breast cancer
    Jiang Shou
    The Breast Center, Baylor College of Medicine, Houston, TX 77030, USA
    J Natl Cancer Inst 96:926-35. 2004
    ..We used a breast cancer model system with high expression of AIB1 and HER2 to investigate the possible mechanisms underlying this resistance...
  21. ncbi Dynamics of chronic myeloid leukaemia
    Franziska Michor
    Program for Evolutionary Dynamics, Department of Organismic and Evolutionary Biology, Department of Mathematics, Harvard University, Cambridge, Massachusetts 02138, USA
    Nature 435:1267-70. 2005
    ..We calculate the probability of developing imatinib resistance mutations and estimate the time until detection of resistance. Our model provides the first quantitative insights into the in vivo kinetics of a human cancer...
  22. ncbi Mechanisms of disease: understanding resistance to HER2-targeted therapy in human breast cancer
    Rita Nahta
    Department of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston 77030 4009, USA
    Nat Clin Pract Oncol 3:269-80. 2006
    ..Novel therapies targeted against these aberrant molecular pathways offer hope that the effectiveness and duration of response to trastuzumab can be greatly improved...
  23. ncbi Nuclear factor-kappaB inhibitors as sensitizers to anticancer drugs
    Chikashi Nakanishi
    Tokyo Metropolitan Cancer and Infectious Disease Center, Komagome Hospital, 3 18 22, Honkomagome, Bunkyoku, Tokyo 113 8677, Japan
    Nat Rev Cancer 5:297-309. 2005
    ..What evidence is there that inhibitors of NF-kappaB might promote apoptosis in cancer cells and can NF-kappaB inhibitors be used to overcome resistance to chemotherapeutic agents?..
  24. ncbi A functional genetic approach identifies the PI3K pathway as a major determinant of trastuzumab resistance in breast cancer
    Katrien Berns
    Division of Molecular Carcinogenesis and Center for Biomedical Genetics, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands
    Cancer Cell 12:395-402. 2007
    ..Thus, assessment of PI3K pathway activation may provide a biomarker to identify patients unlikely to respond to trastuzumab-based therapy...
  25. ncbi PTEN expression and KRAS mutations on primary tumors and metastases in the prediction of benefit from cetuximab plus irinotecan for patients with metastatic colorectal cancer
    Fotios Loupakis
    Department of Oncology, Azienda USL 6, Istituto Toscano Tumori, Livorno, Italy
    J Clin Oncol 27:2622-9. 2009
    ..This retrospective study investigated the role of PTEN loss, AKT phosphorylation, and KRAS mutations on the activity of cetuximab plus irinotecan in patients with metastatic colorectal cancer (mCRC)...
  26. ncbi Phosphatidylinositol 3-kinase/AKT-mediated activation of estrogen receptor alpha: a new model for anti-estrogen resistance
    R A Campbell
    Department of Surgery, Indiana University School of Medicine, Indianapolis 46202, USA
    J Biol Chem 276:9817-24. 2001
    ..Taken together, these results define a molecular link between activation of the PI 3-kinase/AKT survival pathways, hormone-independent activation of ERalpha, and inhibition of tamoxifen-induced apoptotic regression...
  27. ncbi Chemotherapy with mitoxantrone plus prednisone or prednisone alone for symptomatic hormone-resistant prostate cancer: a Canadian randomized trial with palliative end points
    I F Tannock
    Department of Medicine, Princess Margaret Hospital, Toronto, Canada
    J Clin Oncol 14:1756-64. 1996
    ..To investigate the benefit of chemotherapy in patients with symptomatic hormone-resistant prostate cancer using relevant end points of palliation in a randomized controlled trial...
  28. ncbi A family of drug transporters: the multidrug resistance-associated proteins
    P Borst
    Division of Molecular Biology and Center of Biomedical Genetics, The Netherlands Cancer Institute, Amsterdam
    J Natl Cancer Inst 92:1295-302. 2000
    ..The physiologic functions of the other MRPs are not known. Whether long-term inhibition of MRPs in humans can be tolerated (assuming that suitable inhibitors will be found) remains to be determined...
  29. ncbi Chronic oxaliplatin resistance induces epithelial-to-mesenchymal transition in colorectal cancer cell lines
    Anthony D Yang
    Department of Surgical Oncology, The University of Texas M D Anderson Cancer Center, Houston, Texas 77230 1402, USA
    Clin Cancer Res 12:4147-53. 2006
    ..In preliminary studies, we observed that oxaliplatin-resistant (OxR) colorectal cancer (CRC) cells underwent morphologic changes suggestive of a migratory phenotype, leading us to hypothesize that OxR CRC cells undergo EMT...
  30. ncbi Insulin-like growth factor-I receptor signaling and resistance to trastuzumab (Herceptin)
    Y Lu
    Department of Oncology, Jewish General Hospital, and McGill University, Montreal, PQ, Canada
    J Natl Cancer Inst 93:1852-7. 2001
    ..Thus, strategies that target IGF-IR signaling may prevent or delay development of resistance to trastuzumab...
  31. ncbi PTEN activation contributes to tumor inhibition by trastuzumab, and loss of PTEN predicts trastuzumab resistance in patients
    Yoichi Nagata
    Department of Surgical Oncology, The University of Texas M D Anderson Cancer Center, Houston, TX 77030, USA
    Cancer Cell 6:117-27. 2004
    ..Thus, PTEN deficiency is a powerful predictor for trastuzumab resistance. Additionally, PI3K inhibitors rescued PTEN loss-induced trastuzumab resistance, suggesting that PI3K-targeting therapies could overcome this resistance...
  32. ncbi Development and characterization of gemcitabine-resistant pancreatic tumor cells
    Ami N Shah
    Department of Surgical Oncology, University of Texas M D Anderson Cancer Center, Houston, Texas, USA
    Ann Surg Oncol 14:3629-37. 2007
    ..To study the mechanisms of chemoresistance in pancreatic cancer we developed two gemcitabine-resistant pancreatic cancer cell lines...
  33. ncbi Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer
    Federica Di Nicolantonio
    Laboratory of Molecular Genetics, The Oncogenomics Center, Institute for Cancer Research and Treatment, University of Torino, Medical School, Candiolo, Torino, Italy
    J Clin Oncol 26:5705-12. 2008
    ..Double-hit therapies aimed at simultaneous inhibition of epidermal growth factor receptor and BRAF warrant exploration in CRC patients carrying the V600E oncogenic mutation...
  34. ncbi Role of NF-kappaB and Akt/PI3K in the resistance of pancreatic carcinoma cell lines against gemcitabine-induced cell death
    Alexander Arlt
    1Laboratory of Molecular Gastroenterology and Hepatology, 1st Department of Medicine, University of Kiel, Germany
    Oncogene 22:3243-51. 2003
    ....
  35. ncbi Mechanisms of resistance to cisplatin
    M Kartalou
    Division of Bioengineering and Environmental Health and Department of Chemistry, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
    Mutat Res 478:23-43. 2001
    ..An improved understanding of the mechanisms of resistance operative in vivo has identified targets for intervention and may increase the utility of cisplatin for the treatment of cancer...
  36. ncbi HER2/PI-3K/Akt activation leads to a multidrug resistance in human breast adenocarcinoma cells
    Christiane Knuefermann
    Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030 USA
    Oncogene 22:3205-12. 2003
    ....
  37. pmc Adaptive therapy
    Robert A Gatenby
    Department of Integrative Mathematical Oncology, Moffitt Cancer Center, Tampa, Florida 33612, USA
    Cancer Res 69:4894-903. 2009
    ..e., when therapy-induced toxicity is absent). In vivo experiments using OVCAR xenografts treated with carboplatin show that adaptive therapy is feasible and, in this system, can produce long-term survival...
  38. ncbi Molecular basis of bortezomib resistance: proteasome subunit beta5 (PSMB5) gene mutation and overexpression of PSMB5 protein
    Ruud Oerlemans
    Department of Rheumatology, VUMC Institute for Cancer and Immunology, VU University Medical Center, Amsterdam, The Netherlands
    Blood 112:2489-99. 2008
    ..Collectively, these findings establish a novel mechanism of bortezomib resistance associated with the selective overexpression of a mutant PSMB5 protein...
  39. ncbi Clinical relevance of MGMT in the treatment of cancer
    Stanton L Gerson
    Division of Hematology Oncology and Comprehensive Cancer Center, University Hospitals of Cleveland, Case Western Reserve University School of Medicine, Cleveland, OH 44106 4937, USA
    J Clin Oncol 20:2388-99. 2002
    ..MGMT remains a paradigm for development of new agents that modulate known mechanisms of drug resistance in cancer cells and raise the spectra of combinatorial therapies that encompass known drug resistance mechanisms...
  40. ncbi Rapamycins: mechanism of action and cellular resistance
    Shile Huang
    Department of Molecular Pharmacology, St Jude Children s Research Hospital, 332 N Lauderdale, Memphis, Tennessee 38105, USA
    Cancer Biol Ther 2:222-32. 2003
    ..Here we review the conserved TOR signaling pathways, conceptual basis for tumor selectivity, and the mechanisms of resistance to this class of antitumor agent...
  41. ncbi Elevated levels of epidermal growth factor receptor/c-erbB2 heterodimers mediate an autocrine growth regulatory pathway in tamoxifen-resistant MCF-7 cells
    Janice M Knowlden
    Tenovus Centre for Cancer Research, Welsh School of Pharmacy, Cardiff University, Cardiff CF10 3XF, United Kingdom
    Endocrinology 144:1032-44. 2003
    ..These results demonstrate that TAM-R MCF-7 cell growth is mediated by the autocrine release and action of an EGFR-specific ligand inducing preferential EGFR/c-erbB2 dimerization and downstream activation of the ERK pathway...
  42. pmc Elevated CRAF as a potential mechanism of acquired resistance to BRAF inhibition in melanoma
    Clara Montagut
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, Massachusetts, USA
    Cancer Res 68:4853-61. 2008
    ..Geldanamycin effectively promotes the degradation of CRAF, thereby revealing a potential therapeutic strategy to overcome resistance to RAF inhibition in a subset of BRAF mutant tumors...
  43. ncbi Apoptosis defects and chemotherapy resistance: molecular interaction maps and networks
    Yves Pommier
    Laboratory of Molecular Pharmacology, Center for Cancer Research, NCI, NIH, DHHS, Bethesda, MD 20892, USA
    Oncogene 23:2934-49. 2004
    ..They complement the p53, Chk2 and c-Abl maps published recently. We will also introduce the 'permissive apoptosis-resistance' model for the selection of multidrug-resistant cells...
  44. ncbi Restoring E-cadherin expression increases sensitivity to epidermal growth factor receptor inhibitors in lung cancer cell lines
    Samir E Witta
    Department of Medicine Medical Oncology, University of Colorado Health Sciences Center and University of Colorado Cancer Center, Campus Box 8117, PO Box 6511, Aurora, CO 80045, USA
    Cancer Res 66:944-50. 2006
    ..Thus, combined HDAC inhibitor and gefitinib treatment represents a novel pharmacologic strategy for overcoming resistance to EGFR inhibitors in patients with lung cancer...
  45. pmc Amplification of MET may identify a subset of cancers with extreme sensitivity to the selective tyrosine kinase inhibitor PHA-665752
    Gromoslaw A Smolen
    Cancer Center and Department of Pathology, Molecular Pathology Research Unit, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 103:2316-21. 2006
    ..MET amplification may thus identify a subset of epithelial cancers that are uniquely sensitive to disruption of this pathway and define a patient group that is appropriate for clinical trials of targeted therapy using MET inhibitors...
  46. ncbi Hypoxia-inducible factor-1 alpha contributes to hypoxia-induced chemoresistance in gastric cancer
    Lili Liu
    State Key Laboratory of Cancer Biology, Institute of Digestive Diseases, Xijing Hospital, Fourth Military Medical University, 15 Changle West Road, Xi an 710032, China
    Cancer Sci 99:121-8. 2008
    ....
  47. ncbi Chemoresistance to paclitaxel induces epithelial-mesenchymal transition and enhances metastatic potential for epithelial ovarian carcinoma cells
    Hiroaki Kajiyama
    Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya 466 8550, Japan
    Int J Oncol 31:277-83. 2007
    ..It is possible that therapeutic benefits such as the restoration of chemosensitivity or suppression of metastasis will be enabled by gaining further insight into the mechanisms underlying chemoresistance and EMT...
  48. ncbi The role of glutathione-S-transferase in anti-cancer drug resistance
    Danyelle M Townsend
    Department of Pharmacology, Fox Chase Cancer Center, 7701 Burholme Avenue, Philadelphia, PA 19111, USA
    Oncogene 22:7369-75. 2003
    ..Some of the therapeutic strategies so far employed are described in this review...
  49. ncbi The molecular basis of multidrug resistance in cancer: the early years of P-glycoprotein research
    Michael M Gottesman
    Laboratory of Cell Biology, The Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    FEBS Lett 580:998-1009. 2006
    ....
  50. ncbi Acquisition of resistance to cisplatin is accompanied by changes in the cellular pharmacology of copper
    Kuniyuki Katano
    Department of Medicine and the Cancer Center, University of California, San Diego, La Jolla, California 92093 0058, USA
    Cancer Res 62:6559-65. 2002
    ..These results are consistent with the concept that DDP enters and exits from the cell via transporters that normally mediate copper homeostasis...
  51. ncbi Establishment of a human non-small cell lung cancer cell line resistant to gefitinib
    Fumiaki Koizumi
    Shien Lab, National Cancer Center Hospital, Tokyo, Japan
    Int J Cancer 116:36-44. 2005
    ..These phenotypes including EGFR-SOS complex and heterodimer formation of HER family members are potential biomarkers for predicting resistance to gefitinib...
  52. ncbi NF-kappaB transcription factor induces drug resistance through MDR1 expression in cancer cells
    Mohamed Bentires-Alj
    Center for Cellular and Molecular Therapy, University of Liege, Belgium
    Oncogene 22:90-7. 2003
    ..Moreover, NF-kappaB transactivates an mdr1 promoter luciferase construct. Our data thus demonstrate a role for NF-kappaB in the regulation of the mdr1 gene expression in cancer cells and in drug resistance...
  53. ncbi Activation of the PI3K/Akt pathway and chemotherapeutic resistance
    Kip A West
    Cancer Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Building 8, Room 5101, 8901 Wisconsin Avenue, Bethesda, MD 20889, USA
    Drug Resist Updat 5:234-48. 2002
    ..Specifically inhibiting Akt activity may be a valid approach to treat cancer and increase the efficacy of chemotherapy...
  54. ncbi Multidrug resistance (MDR) in cancer. Mechanisms, reversal using modulators of MDR and the role of MDR modulators in influencing the pharmacokinetics of anticancer drugs
    R Krishna
    Department of Advanced Therapeutics, British Columbia Cancer Agency, BC V5Z 4E6, Vancouver, Canada
    Eur J Pharm Sci 11:265-83. 2000
    ....
  55. ncbi An increase in the expression of ribonucleotide reductase large subunit 1 is associated with gemcitabine resistance in non-small cell lung cancer cell lines
    Jennifer D Davidson
    Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, Indiana, USA
    Cancer Res 64:3761-6. 2004
    ..The results from this study indicate that the level of RRM1 may affect gemcitabine response. Furthermore, RRM1 may serve as a biomarker for gemcitabine response...
  56. ncbi Altered expression of Ape1/ref-1 in germ cell tumors and overexpression in NT2 cells confers resistance to bleomycin and radiation
    K A Robertson
    Herman B. Wells Center for Pediatric Research, Department of Pediatrics, James Whircomb Riley Hospital for Children, Indiana University School of Medicine, Indianapolis 46202, USA
    Cancer Res 61:2220-5. 2001
    ..To our knowledge, this is the first example of overexpressing Ape1/ref-1 in a mammalian system resulting in enhanced protection to DNA-damaging agents...
  57. pmc Mechanisms of Taxol resistance related to microtubules
    George A Orr
    Department of Molecular Pharmacology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    Oncogene 22:7280-95. 2003
    ..A review of tubulin structure, microtubule dynamics, the mechanism of action of Taxol and its binding site on the microtubule are included, so that the reader can evaluate Taxol resistance in context...
  58. ncbi Nucleoside analogues: mechanisms of drug resistance and reversal strategies
    C M Galmarini
    , Laboratoire de Cytologie Analytique, , Lyon, France
    Leukemia 15:875-90. 2001
    ..Strategies aiming to increase the intracellular concentrations of active compounds are presented...
  59. pmc The extracellular matrix protein TGFBI induces microtubule stabilization and sensitizes ovarian cancers to paclitaxel
    Ahmed Ashour Ahmed
    Functional Genomics of Drug Resistance Laboratory, Cancer Research UK Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK
    Cancer Cell 12:514-27. 2007
    ..These data show that ECM can mediate taxane sensitivity by modulating microtubule stability...
  60. ncbi Multicellular resistance: a paradigm for clinical resistance?
    B Desoize
    Laboratoire de Biochimie et de Biologie Moleculaire, Faculte de Pharmacie, IFR 51, EA 2063, Reims, France
    Crit Rev Oncol Hematol 36:193-207. 2000
    ..The explanation given is that it improves drug penetration into spheroids. We now hypothesise that hyaluronidase, in fact, decreases MCR and thus could be the first member of a new therapeutic class...
  61. pmc Inhibition of HIF-1alpha activity by homeodomain-interacting protein kinase-2 correlates with sensitization of chemoresistant cells to undergo apoptosis
    Lavinia Nardinocchi
    Department of Experimental Oncology, Molecular Oncogenesis Laboratory, Regina Elena Cancer Institute, 00158 Rome, Italy
    Mol Cancer 8:1. 2009
    ....
  62. ncbi Chemotherapy resistance in osteosarcoma: current challenges and future directions
    Alexander J Chou
    Department of Pediatrics, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    Expert Rev Anticancer Ther 6:1075-85. 2006
    ..In this review, the focus is on the current understanding of the mechanisms of resistance to the most commonly used agents in the treatment of osteosarcoma and the methods employed to overcome chemotherapy resistance...
  63. ncbi Met receptor contributes to trastuzumab resistance of Her2-overexpressing breast cancer cells
    David L Shattuck
    University of California Davis Cancer Center, Sacramento, CA 95817, USA
    Cancer Res 68:1471-7. 2008
    ..Our study suggests that a subset of Her2 (+) patients may benefit from combined inhibition of Her2 and Met...
  64. ncbi Analysis of epidermal growth factor receptor gene mutation in patients with non-small cell lung cancer and acquired resistance to gefitinib
    Takayuki Kosaka
    Department of Thoracic Surgery, Aichi Cancer Center Hospital, 1 1 Kanokoden, Chikusa ku, Nagoya 464 8681, Japan
    Clin Cancer Res 12:5764-9. 2006
    ..Part of this "acquired resistance" is attributable to a secondary mutation resulting in threonine to methionine at codon 790 (T790M) of EGFR...
  65. ncbi Akt-mediated cisplatin resistance in ovarian cancer: modulation of p53 action on caspase-dependent mitochondrial death pathway
    Xiaokui Yang
    Reproductive Biology Unit and Division of Gynaecology Oncology, Department of Obstetrics and Gynaecology and Cellular and Molecular Medicine, University of Ottawa, Ontario, Canada
    Cancer Res 66:3126-36. 2006
    ..Understanding the precise etiology of chemoresistance may improve treatment for ovarian cancer...
  66. ncbi A new mutation in the KIT ATP pocket causes acquired resistance to imatinib in a gastrointestinal stromal tumor patient
    Elena Tamborini
    Department of Pathology, Istituto Nazionale per lo Studio e al Cura dei Tumori, Milan, Italy
    Gastroenterology 127:294-9. 2004
    ..Molecular mechanisms have been reported in CML and GIST for primary resistance, whereas extensive studies on the mechanisms responsible for secondary resistance have been almost exclusively reported for CML...
  67. ncbi Biochemical, cellular, and pharmacological aspects of the multidrug transporter
    S V Ambudkar
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Annu Rev Pharmacol Toxicol 39:361-98. 1999
    ..This review summarizes current research on the structure-function analysis of P-glycoprotein, its mechanism of action, and facts and speculations about its normal physiological role...
  68. ncbi The proteasome inhibitor PS-341 inhibits growth, induces apoptosis, and overcomes drug resistance in human multiple myeloma cells
    T Hideshima
    Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Res 61:3071-6. 2001
    ..Given the acceptable animal and human toxicity profile of PS-341, these studies provide the framework for clinical evaluation of PS-341 to improve outcome for patients with this universally fatal hematological malignancy...
  69. ncbi Assessment of somatic k-RAS mutations as a mechanism associated with resistance to EGFR-targeted agents: a systematic review and meta-analysis of studies in advanced non-small-cell lung cancer and metastatic colorectal cancer
    Helena Linardou
    1st Department of Medical Oncology, Metropolitan Hospital, Athens, Greece
    Lancet Oncol 9:962-72. 2008
    ..The aim of this systematic review and meta-analysis was to assess if k-RAS mutations represent a candidate predictive biomarker for anti-EGFR-targeted therapeutic strategies in mCRC and NSCLC...
  70. pmc Allelic dilution obscures detection of a biologically significant resistance mutation in EGFR-amplified lung cancer
    Jeffrey A Engelman
    Massachusetts General Hospital Cancer Center, Boston, Massachusetts, USA
    J Clin Invest 116:2695-706. 2006
    ....
  71. ncbi Ceramide glycosylation potentiates cellular multidrug resistance
    Y Y Liu
    John Wayne Cancer Institute at Saint John's Health Center, Santa Monica, CA 90404, USA
    FASEB J 15:719-30. 2001
    ..This study reveals that GCS is a novel mechanism of multidrug resistance and positions GCS antisense as an innovative force to overcome multidrug resistance in cancer chemotherapy...
  72. ncbi Interaction between leukemic-cell VLA-4 and stromal fibronectin is a decisive factor for minimal residual disease of acute myelogenous leukemia
    Takuya Matsunaga
    Fourth Department of Internal Medicine, Sapporo Medical University School of Medicine, South 1, West 16, Chuo Ku, Sapporo 060 0061, Japan
    Nat Med 9:1158-65. 2003
    ..4% for 15 VLA-4-positive patients. Thus, the interaction between VLA-4 on leukemic cells and fibronectin on stromal cells may be crucial in bone marrow MRD and AML prognosis...
  73. ncbi Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia
    Neil P Shah
    Department of Medicine, Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
    Cancer Cell 2:117-25. 2002
    ..Multiple independent mutant clones were detected in a subset of relapsed cases. Our data support a clonal selection model of preexisting BCR-ABL mutations that confer imatinib resistance...
  74. ncbi Evidence that resistance to nilotinib may be due to BCR-ABL, Pgp, or Src kinase overexpression
    Francois Xavier Mahon
    Hématopoïèse Leucémique et Cible Thérapeutique, Inserm U876, Universite Victor Segalen, Laboratoire d hématologie CHU de Bordeaux, Bordeaux Cedex, France
    Cancer Res 68:9809-16. 2008
    ..Such mechanisms of resistance are close to those observed in imatinib-resistant cell lines and emphasize the critical role of Lyn in nilotinib resistance...
  75. ncbi Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias
    Moshe Talpaz
    Department of Leukemia, M D Anderson Cancer Center, Houston, USA
    N Engl J Med 354:2531-41. 2006
    ..We evaluated dasatinib, a BCR-ABL inhibitor that targets most imatinib-resistant BCR-ABL mutations, in patients with chronic myelogenous leukemia (CML) or Ph-positive acute lymphoblastic leukemia (ALL)...
  76. ncbi Human breast cancer cells selected for resistance to trastuzumab in vivo overexpress epidermal growth factor receptor and ErbB ligands and remain dependent on the ErbB receptor network
    Christoph A Ritter
    Institute of Pharmacology, University of Greifswald, Greifswald, Germany
    Clin Cancer Res 13:4909-19. 2007
    ..We have investigated mechanisms of acquired resistance to the HER2 antibody trastuzumab in BT-474 human breast cancer cells...
  77. ncbi Docetaxel plus prednisone or mitoxantrone plus prednisone for advanced prostate cancer
    Ian F Tannock
    Department of Medical Oncology and Hematology, Princess Margaret Hospital and University of Toronto, Toronto, ON, Canada
    N Engl J Med 351:1502-12. 2004
    ..We compared such treatment with docetaxel plus prednisone in men with this disease...
  78. ncbi Disruption of the Fanconi anemia-BRCA pathway in cisplatin-sensitive ovarian tumors
    Toshiyasu Taniguchi
    Department of Pediatric Oncology, Dana Farber Cancer Institute, Guy s King s and St Thomas School of Medicine, London, UK
    Nat Med 9:568-74. 2003
    ..We propose a model for ovarian tumor progression in which the initial methylation of FANCF is followed by FANCF demethylation and ultimately results in cisplatin resistance...
  79. ncbi Curcumin down-regulates the multidrug-resistance mdr1b gene by inhibiting the PI3K/Akt/NF kappa B pathway
    Byeong Hyeok Choi
    Department of Biomedical Science and Technology, IBST, Konkuk University, Seoul 143 701, Republic of Korea
    Cancer Lett 259:111-8. 2008
    ..Thus, curcumin can contribute to the reversal of the MDR phenotype, probably due to the suppression of P-gp expression via the inhibition of the PI3K/Akt/NF-kappa B signaling pathway...
  80. ncbi Regulation of MDR1 expression and drug resistance by a positive feedback loop involving hyaluronan, phosphoinositide 3-kinase, and ErbB2
    Suniti Misra
    Department of Cell Biology and Anatomy, Medical University of South Carolina, Charleston, South Carolina 29425, USA
    J Biol Chem 280:20310-5. 2005
    ..This pathway may also be important in progression of other malignant characteristics. These results illustrate the potential importance of hyaluronan as a therapeutic target in multidrug-resistant carcinomas...
  81. ncbi Overriding imatinib resistance with a novel ABL kinase inhibitor
    Neil P Shah
    Division of Hematology and Oncology, Department of Medicine, The David Geffen School of Medicine, University of California, Los Angeles, CA, 90095, USA
    Science 305:399-401. 2004
    ..These data illustrate how molecular insight into kinase inhibitor resistance can guide the design of second-generation targeted therapies...
  82. ncbi Proteasome inhibitors in cancer therapy: lessons from the first decade
    Robert Z Orlowski
    Department of Lymphoma Myeloma, Division of Cancer Medicine, University of Texas M D Anderson Cancer Center, Houston, Texas 77030, USA
    Clin Cancer Res 14:1649-57. 2008
    ..This saga provides a salient example of the promise of translational medicine and a paradigm by which other agents may be successfully brought from the bench to the bedside...
  83. ncbi The activated NF-kappaB-Snail-RKIP circuitry in cancer regulates both the metastatic cascade and resistance to apoptosis by cytotoxic drugs
    Katherine Wu
    Department of Microbiology, Immunology and Molecular Genetics, Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90095 736422, USA
    Crit Rev Immunol 29:241-54. 2009
    ..Thus, pharmacological agents regulating the RKIP-NF-kappaB-Snail loop can be used as both sensitizing agents for apoptosis when combined with cytotoxic therapies as well as inhibitors of metastasis...
  84. ncbi Gefitinib (Iressa) represses FOXM1 expression via FOXO3a in breast cancer
    Ursula B McGovern
    Cancer Research UK Labs, Department of Oncology, Imperial College London, MRC Cyclotron Building, Imperial College School of Medicine at Hammersmith Hospital, Du Cane Road, London W12 0NN, United Kingdom
    Mol Cancer Ther 8:582-91. 2009
    ..In summary, our study defined FOXM1 as a cellular target and marker of gefitinib activity in breast cancer...
  85. ncbi p53 is a determinant of X-linked inhibitor of apoptosis protein/Akt-mediated chemoresistance in human ovarian cancer cells
    Michael Fraser
    Reproductive Biology Unit and Division of Gynaecological Oncology, Department of Obstetrics and Gynaecology, University of Ottawa, Ottawa Health Research Institute, 725 Parkdale Avenue, Ottawa, Ontario KIY 4E9, Canada
    Cancer Res 63:7081-8. 2003
    ..Inhibition of Xiap and/or Akt expression/function may be an effective means of overcoming chemoresistance in ovarian cancer cells expressing either endogenous or reconstituted wild-type p53...
  86. ncbi Tumour hypoxia affects the responsiveness of cancer cells to chemotherapy and promotes cancer progression
    Jean Philippe Cosse
    Laboratory of Biochemistry and Cellular Biology, FUNDP University of Namur, 5000 Namur, Belgium
    Anticancer Agents Med Chem 8:790-7. 2008
    ..The aim of this review is to provide a description of known hypoxia-induced mechanisms of chemoresistance at a cellular level...
  87. pmc Bim and Bad mediate imatinib-induced killing of Bcr/Abl+ leukemic cells, and resistance due to their loss is overcome by a BH3 mimetic
    Junya Kuroda
    The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3050, Australia
    Proc Natl Acad Sci U S A 103:14907-12. 2006
    ..These results demonstrate that Bim and Bad account for most, perhaps all, imatinib-induced killing of Bcr/Abl+ leukemic cells and suggest previously undescribed drug combination strategies for cancer therapy...
  88. ncbi Personalized cancer therapy with selective kinase inhibitors: an emerging paradigm in medical oncology
    Ultan McDermott
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center, Charlestown, MA 02129, USA
    J Clin Oncol 27:5650-9. 2009
    ..In this review, we summarize recent developments in this area, and we highlight some of the logistical challenges posed by this emerging paradigm in medical oncology...
  89. pmc Mechanisms of sunitinib resistance in gastrointestinal stromal tumors harboring KITAY502-3ins mutation: an in vitro mutagenesis screen for drug resistance
    Tianhua Guo
    Departments of Pathology, Medicine, and Surgery, Memorial Sloan Kettering Cancer Center, Sloan Kettering Institute, New York, NY 10021, USA
    Clin Cancer Res 15:6862-70. 2009
    ..The clinical benefit of sunitinib is genotype-dependent in regards to both primary and secondary mutations, with GIST patients harboring the KIT(AY502-3ins) exon 9 mutation being the most sensitive...
  90. ncbi Overcoming drug resistance by enhancing apoptosis of tumor cells
    Pepita Gimenez-Bonafe
    Departament de Ciències Fisiològiques II, Campus Ciènces de Salut de Bellvitge, IDIBELL, University of Barcelona, Barcelona, Spain
    Curr Cancer Drug Targets 9:320-40. 2009
    ....
  91. pmc NCX-4016, a nitro-derivative of aspirin, inhibits EGFR and STAT3 signaling and modulates Bcl-2 proteins in cisplatin-resistant human ovarian cancer cells and xenografts
    Karuppaiyah Selvendiran
    Davis Heart and Lung Research Institute and Comprehensive Cancer Center, Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA
    Cell Cycle 7:81-8. 2008
    ..Thus, NCX-4016 appears to be a potential therapeutic agent for treating recurrent human ovarian carcinoma...
  92. ncbi Constitutive and inducible Akt activity promotes resistance to chemotherapy, trastuzumab, or tamoxifen in breast cancer cells
    Amy S Clark
    Cancer Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20889, USA
    Mol Cancer Ther 1:707-17. 2002
    ....
  93. ncbi Key roles of BIM-driven apoptosis in epithelial tumors and rational chemotherapy
    Ting Ting Tan
    Center for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, New Jersey 08854, USA
    Cancer Cell 7:227-38. 2005
    ....
  94. ncbi Drug resistance and the solid tumor microenvironment
    Olivier Tredan
    Division of Applied Molecular Oncology and Department of Medical Oncology and Hematology, Princess Margaret Hospital, 610 University Ave, Toronto, ON M5G 2M9, Canada
    J Natl Cancer Inst 99:1441-54. 2007
    ....
  95. pmc Interleukin-8 mediates resistance to antiangiogenic agent sunitinib in renal cell carcinoma
    Dan Huang
    Laboratory of Cancer Genetics, Laboratory of Computational Biology, Van Andel Research Institute, Grand Rapids, Michigan 49503, USA
    Cancer Res 70:1063-71. 2010
    ..Our results reveal IL-8 as an important contributor to sunitinib resistance in ccRCC and a candidate therapeutic target to reverse acquired or intrinsic resistance to sunitinib in this malignancy...
  96. ncbi Molecular mechanisms of resistance to cetuximab and panitumumab in colorectal cancer
    Alberto Bardelli
    Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment, University of Torino, Medical School, Str Prov 142 Km 3 95, 10060 Candiolo, Italy
    J Clin Oncol 28:1254-61. 2010
    ..Finally, unresolved questions such as understanding the molecular basis of response as well the mechanisms of secondary resistance are presented as the future fundamental goals in this research field...
  97. ncbi Increased cyclooxygenase-2 (COX-2) expression is associated with chemotherapy resistance and outcome in ovarian cancer patients
    G Ferrandina
    Department of Obstetrics and Gynecology, Catholic University of the Sacred Heart, Rome, Italy
    Ann Oncol 13:1205-11. 2002
    ..The aim of this study was to investigate the expression of COX-2 and its association with clinicopathological parameters, response to treatment, and clinical outcome in ovarian cancer patients...
  98. pmc Modes of resistance to anti-angiogenic therapy
    Gabriele Bergers
    University of California, San Francisco, Department of Neurological Surgery, Brain Tumour Research Center, San Francisco, California 94143, USA
    Nat Rev Cancer 8:592-603. 2008
    ....
  99. pmc Selective inhibition of CYP17 with abiraterone acetate is highly active in the treatment of castration-resistant prostate cancer
    Gerhardt Attard
    Royal Marsden National Health Service Foundation Trust, Sutton, Surrey, United Kingdom
    J Clin Oncol 27:3742-8. 2009
    ..Abiraterone acetate is a potent, selective, and orally available inhibitor of CYP17, the key enzyme in androgen and estrogen biosynthesis...
  100. ncbi Crystal structure of the T315I Abl mutant in complex with the aurora kinases inhibitor PHA-739358
    Michele Modugno
    Nerviano Medical Sciences Srl Oncology, Milan, Italy
    Cancer Res 67:7987-90. 2007
    ....
  101. ncbi Signalling via integrins: implications for cell survival and anticancer strategies
    Stephanie Hehlgans
    OncoRay, Center for Radiation Research in Oncology, Medical Faculty Carl Gustav Carus, University of Technology Dresden, Fetscherstrasse 74 PF 86, 01307 Dresden, Germany
    Biochim Biophys Acta 1775:163-80. 2007
    ....

Research Grants73

  1. Monoclonal Antibody Therapy for Follicular Lymphoma
    Jonathan Friedberg; Fiscal Year: 2007
    ..abstract_text> ..
  2. Defibrotide for the treatment of severe hepatic veno-cc*
    Paul Richardson; Fiscal Year: 2007
    ..Abstract Not Provided ..
  3. Inhibition of Tumor Progression by Hyaluronan Oligomers
    Bryan Toole; Fiscal Year: 2008
    ..unreadable] [unreadable]..
  4. TUMOR CELL STROMAL INTERACTIONS IN CANCER
    Bryan Toole; Fiscal Year: 2004
    ..Interference with EMMPRIN action may then be an effective way to inhibit tumor progression patients. ..
  5. PERTURBATION OF HYALURONAN FUNCTION IN CANCER
    Bryan P Toole; Fiscal Year: 2010
    ..Consequently, these approaches will help to guide further development of therapeutic interventions in cancer patients, employing antagonists of deregulated HA interactions. ..
  6. Antioxidant Strategies for Parkinson's Disease
    Nina Schor; Fiscal Year: 2005
    ..abstract_text> ..
  7. TARGETED THERAPY FOR CHEMORESISTANT TUMORS
    Nina Schor; Fiscal Year: 2006
    ..Ultimately, this predictive panel will help to identify those patients whose chemoresistant tumors are likely to be particularly sensitive to enediyne treatment. [unreadable] [unreadable]..
  8. Proapoptotic Therapy for B-cell Non Hodgkin's Lymphoma
    Ajay Gopal; Fiscal Year: 2007
    ..unreadable] [unreadable]..
  9. OPTIMIZING RADIOIMMUNOTHERAPY FOR NON HODGKIN'S LYMPHOMA
    Ajay Gopal; Fiscal Year: 2005
    ..We anticipate that these interventions will ultimately enhance the prognosis for patients with relapsed lymphoma by increasing the response and survival rates, while simultaneously minimizing toxicities. ..
  10. Changes in Tumor DNA Methylation with Decitabine
    David Stewart; Fiscal Year: 2006
    ..This preliminary look at individual genes may provide a molecular rationale for future decitabine therapeutic studies in specific relevant tumor types. ..
  11. Biology of Imatinib-Resistant Mutants of BCR-ABL
    Michael Deininger; Fiscal Year: 2009
    ..Such crucial proteins may then be exploited as drug targets for the treatment of chronic myeloid leukemia, and further, for other types of cancer. ..
  12. Targeting Akt/NF-kappa beta for Pancreatic Cancer Therapy
    Fazlul Sarkar; Fiscal Year: 2007
    ..These results will provide mechanistic as well as pre-clinical data in support of our hypotheses and may open new and novel avenues for the treatment of human pancreatic cancer. ..
  13. CD44-P185HER2 INTERACTION IN OVARIAN CANCER PROGRESSION
    LILLY BOURGUIGNON; Fiscal Year: 2007
    ..abstract_text> ..
  14. NEUROTROPHIC MECHANISMS IN NEUROBLASTOMA
    Nina Schor; Fiscal Year: 2008
    ..abstract_text> ..
  15. Phase I Clinical Trials of Anti-Cancer Agents
    Francis Giles; Fiscal Year: 2007
    ..abstract_text> ..
  16. Therapeutic Modulation of COX-2-induced Immunosuppression in Metastatic RCC
    Brian Rini; Fiscal Year: 2008
    ..This project will have broad implications for the immunoregulation of cancer and how expression and modulation of COX-2 expression influences the immune response to cancer. [unreadable] [unreadable] [unreadable]..
  17. NEURODEVELOPMENTAL AND NEURODEGERENTATIVE DISEASE
    Nina Schor; Fiscal Year: 2005
    ..Funding of this program will perpetuate this history at an economically and academically critical time. ..
  18. BLys inhibition using TACI-Fc in patients with B-bell non-Hodgkins' Lymphoma
    Stephen Ansell; Fiscal Year: 2008
    ..abstract_text> ..
  19. CD44/VARIANT CYTOSKELETON IN BREAST CANCER PROGRESSION
    LILLY YW BOURGUIGNON; Fiscal Year: 2010
    ....
  20. EPR IMAGING OF TUMOR HETEROGENEITY AND OXYGENATION
    Periannan Kuppusamy; Fiscal Year: 2003
    ..Information obtained from these studies should enable the development and optimization of therapeutic modalities for cancer treatment. ..
  21. MECHANISMS OF TRANSFORMATION OF HEMATOPOIETIC CELLS
    JAMES MC CUBREY; Fiscal Year: 2001
    ..An understanding of how these signal transduction and apoptotic pathways impinge upon one another will further our comprehension of the consequences of abnormal oncogene activation and tumor progression. ..
  22. Antitumor Antimitotics That Reverse Tumor Resistance
    Aleem Gangjee; Fiscal Year: 2010
    ..The study will also further define the mechanism of action of the novel series and could afford agents for clinical use. ..
  23. CANCER AND LEUKEMIA GROUP B
    Martin Edelman; Fiscal Year: 2002
    ..The grant will also allow for continuation of meritorious pilot protocols and will allow GCC to monitor and collect data which will produce mutual benefit to the GCC and CALGB. ..
  24. Epigenetic Chromatin Changes as Melanoma Markers
    Ruth Halaban; Fiscal Year: 2006
    ..Altogether, the results are likely to generate a novel marker(s) that can be used to assess propensity for malignant transformation, tumor progression and/or sensitivity to chemotherapeutic drugs that target chromatin conformation. ..
  25. A Novel Vitamin D Target in Human Prostate Cancer
    TOMASZ BEER; Fiscal Year: 2007
    ..New treatment targets are needed to develop new drugs to treat prostate cancer, the most commonly diagnosed cancer and the second-leading cancer killer in US men. [unreadable] [unreadable]..
  26. ROLE OF THE CELL CYCLE IN HYPERSENSITIVITY TO ESTRADIOL
    Richard Santen; Fiscal Year: 2008
    ..A clinical trial in women, which is designed to specifically demonstrate that high dose estrogen induces tumor regression through the mechanism of apoptosis will be conducted. ..
  27. Perivascular Invasion of GBMs
    Gabriele Bergers; Fiscal Year: 2010
    ..AIM2.1: Identify the exact cell sources of MMP-9 production in GBM. AIM2.2: Reveal function of host cell-produced MMP-9 in angiogenesis and invasion. AIM2.3: Elicit function of tumor cell-produced MMP-9 in angiogenesis and invasion. ..
  28. In Vivo EPR Imaging of Redox Status and Thiols in Tumor
    Periannan Kuppusamy; Fiscal Year: 2007
    ..The results will enable a better understanding of the development of drug resistance in ovarian cancer and offer efficient diagnosis for effective treatment of ovarian cancer patients. ..
  29. THERAPEUTICS STUDIES OF PRIMARY CNS MALIGNANCIES
    Patrick Wen; Fiscal Year: 2008
    ..abstract_text> ..
  30. Role of BMDCs in Solid Tumor Growth and Relapse
    Rakesh K Jain; Fiscal Year: 2010
    ..Furthermore, our results will offer strategies for the inhibition of tumor relapse after radiotherapy by targeting molecular pathways that are critical for both angiogenesis and myeloid BMDC recruitment. ..
  31. Amnis ImageStream Flow Cytometer
    Craig 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]..
  32. Role of Fra-1 in Mesothelioma
    Maria Ramos Nino; Fiscal Year: 2008
    ..The long-term goal of this research plan is to understand the molecular mechanisms governing mesothelial cell tumorigenesis. ..
  33. Integrative Biology of Tumor Metastasis
    Rakesh Jain; Fiscal Year: 2009
    ..Finally, we have the resources and the clinical collaborators in place to initiate a clinical trial based on our findings, as attested by our ongoing trial using a VEGF-specific antibody. ..
  34. Resistance and Response Mechanisms to Prostate Cancer Therapy
    TOMASZ BEER; Fiscal Year: 2009
    ..We will test the effectiveness of novel treatments that exploit newly discovered targets in the laboratory and lay the foundation for human trials to develop effective prostate cancer treatment. ..
  35. TARGET-GUIDED DEVELOPMENT OF SPECIFIC AKT INHIBITORS
    Peter Vogt; Fiscal Year: 2008
    ..4) Investigate the structure-activity relationship through in situ click chemistry and optimize inhibitors for potency, selectivity and cell-based activity ..
  36. Early prediction of response to combined modality therapy by functional imaging
    Jann Sarkaria; Fiscal Year: 2008
    ..If successful, this approach would facilitate the selection of the most efficacious therapies for individual patients. [unreadable] [unreadable] [unreadable]..
  37. Controlling the Max Network
    Peter Vogt; Fiscal Year: 2008
    ..The proposed work on stabilizers in the Myc-Max network could open the door to a new way of influencing and directing cell growth. ..
  38. Targeting HIF-1alpha in renal cell carcinoma: the role of HDAC inhibitors
    Roberto Pili; Fiscal Year: 2010
    ....
  39. DELTAVISION RESTORATION MICROSCOPY SYSTEM MODEL 483
    Conly Rieder; Fiscal Year: 2001
    ..This Core will maintain the instrument and provide technical support to those Principal Investigators/Program Directors who are in need of low-light high- resolution 3-D fluorescent imaging. ..
  40. REGULATION OF MDR GENE EXPRESSION IN LIVER CANCERS
    MACUS KUO; Fiscal Year: 2004
    ..We hope from this research, which includes in vitro cell culture and in vivo animal and tumor models, to gain important molecular insights into the genetic resolution of drug resistance and hepatocarcinogenesis. ..
  41. Oregon Prostate Cancer Conference 2001
    TOMASZ BEER; Fiscal Year: 2003
    ....
  42. Biomodulation of capecitabine by docetaxel in non-small*
    MIGUEL VILLALONA; Fiscal Year: 2005
    ..Confirmation of our working hypothesis may lead to a new treatment paradigm suitable for evaluation in the adjuvant setting. ..
  43. CONFERENCE/WORKSHOP ON EPR SPECTROSCOPY AND IMAGING
    Periannan Kuppusamy; Fiscal Year: 2005
    ..S. members of the International Advisory Committee for this meeting. Particular emphasis will be given to the minority and women scientists, encouraging their active participation. ..
  44. PROLIFERATION & MALIGNANT TRANSFORMATION OF MELANOCYTES
    Ruth Halaban; Fiscal Year: 2004
    ..Our functional studies may provide a basis for the design of new therapeutical agents for the treatment of patients with metastatic melanomas. ..
  45. Interdisciplinary Study of Acid-Meditated Tumor Invasion
    Robert Gatenby; Fiscal Year: 2005
    ..Perturbations that produce slowing or reversal of the traveling wave solution to the state equations (ie tumor growth) will be explored to predict possible new treatment strategies. ..
  46. NEW SYNTHESIS OF BIOCHEMICALS WITH HOMOGENEOUS CATALYSTS
    Iwao Ojima; Fiscal Year: 2003
    ..In this project, we plan to develop new synthetic routes to a variety of enantiopure heterocyclic and carbocyclic compounds of medicinal interest featuring diastereoselective or enantioselective catalytic processes as the key steps. ..
  47. Conference on Angiogenesis in Cancer and Other Diseases
    Rakesh Jain; Fiscal Year: 2002
    ..The meeting's synthesis of available information will be particularly thought-provoking for students and post- doctoral fellows. ..
  48. Anti-Angiogenesis/Drugs in Tumors--Bench /Bedside & Back
    Rakesh Jain; Fiscal Year: 2005
    ..Attendance at this conference will provide an excellent opportunity for young investigators working on cancer to educate and familiarize themselves with the field of angiogenesis and the complexities of the system. ..
  49. Structural biology of kinase signaling in T-cells
    Michael J Eck; Fiscal Year: 2010
    ..Also, they will help us to understand the causes of immune deficiency diseases XLP and SCID at a detailed molecular level. ..
  50. Novel Cationic 99mTc Complexes for Heart Imaging
    Shuang Liu; Fiscal Year: 2006
    ..Successful development of new 99mTc perfusion imaging agents will have a profound impact on diagnostic evaluation, risk stratification, and therapeutic decision-making in patients with CAD. ..
  51. CALCITRIOL & DEXAMETHASONE FOR MYELODYSPLASTIC SYNDROMES
    ROBERT REDNER; Fiscal Year: 2004
    ..Abstract Not Provided ..
  52. REGULATION OF GENES BY T AND DHT IN RAT AND HUMAN PROSTA
    Michael McPhaul; Fiscal Year: 2001
    ..The results of these studies will help define the distinct roles that T and DHT play in androgen physiology and indicate the directions that efforts to selectively interfere with the actions of T and DHT can take. ..
  53. LIPOSOMAL BCL-2 ANTISENSE THERAPY FOR SOLID TUMORS
    Francisco Esteva; Fiscal Year: 2003
    ..Gabriel Lopez-Berestein (Department of Bioimmunotherapy). M. D. Anderson Cancer Center has the patients and resources necessary for Dr. Esteva to successfully complete this research project. ..
  54. Effect of HIV-1 Vpr on Basic Cellular Functions (II)
    Richard Zhao; Fiscal Year: 2007
    ..abstract_text> ..
  55. Alpha Folate Receptor Mediated GARFTase Inhibitors as Selective Antitumor Agents
    Aleem Gangjee; Fiscal Year: 2010
    ....
  56. Single Agents with Designed Combination Chemotherapy Potential
    Aleem Gangjee; Fiscal Year: 2010
    ..abstract_text> ..
  57. FUNCTIONAL ANALYSIS OF THE PTEN TUMOR SUPPRESSOR PROTEIN
    Levi Garraway; Fiscal Year: 2009
    ..Based on this data we propose in specific aims 2 and 3: 2. To generate antibody reagents that selectively recognizes unphosphorylated PTEN. 3. To purify and identify proteins in the PTEN associated complex (PAC). ..
  58. Novel, P. jirovecii Specific Antipneumocystis Agents
    Aleem Gangjee; Fiscal Year: 2009
    ..These agents could be used alone or in combination to treat PCP thus providing novel agents against a new target. ..
  59. NOVEL NONINDUCIBLE THYMIDYLATE SYNTHASE INHIBITORS
    Aleem Gangjee; Fiscal Year: 2004
    ....
  60. AIDS MALIGNANCY CONSORTIUM
    Joseph Sparano; Fiscal Year: 2005
    ..abstract_text> ..
  61. Implications of Retinoid-Induced CD38 Antigen Expression
    Kapil Mehta; Fiscal Year: 2006
    ..unreadable] [unreadable]..
  62. Novel Single, Dual and Multitargeted Inhibitors of RTKs
    Aleem Gangjee; Fiscal Year: 2007
    ..abstract_text> ..
  63. Reversal of 5-FU Resistance by Arsenic Trioxide in Colorectal Carcinoma
    Bach Ardalan; Fiscal Year: 2008
    ..Aim 2: Determine if ATO administration down regulates the expression of thymidylate synthase in tumor and in PBMC in patients receiving ATO + 5-FU. [unreadable] [unreadable] [unreadable]..
  64. Combination Strategies for Angiogenesis Inhibition
    Keith Flaherty; Fiscal Year: 2008
    ..He is a recognized leader in the field of investigational therapies, has a record of mentoring successful clinical researchers, and is committed to Dr. Flaherty's training. ..
  65. Chemical Complementation Assay for MKP-3 (RMI)
    JOHN LAZO; Fiscal Year: 2005
    ..This proposal will provide sufficient reagents, including cells and DMA transfection vectors, to permit the high throughput screening of 100,000 compounds. ..
  66. FUSION GENES IN LEUKEMIA--DETERMINING SIGNIFICANCE
    Mignon Loh; Fiscal Year: 2003
    ..abstract_text> ..
  67. Bleomycin Hydrolase and Alzheimer's Disease
    JOHN LAZO; Fiscal Year: 2004
    ..These studies should provide new mechanistic information concerning the pathogenesis of AD as well as reagents for future therapeutic studies. ..
  68. BIOCHEMICAL REGULATORS OF BLEOMYCIN INDUCED TUMORS
    JOHN LAZO; Fiscal Year: 2001
    ..The Specific Aims are to: 1) develop cells and mice deficient in BH, 2) develop cells and mice that overexpress BH, 3) isolate and characterize potential proteins that interact with BH and, 4) analyze the regulation of BH expression. ..
  69. In Vitro High Throughput Screening Assay for MKP-3(RMI)
    JOHN LAZO; Fiscal Year: 2005
    ..Nonetheless, no potent or selective small molecule inhibitors of this protein phosphatase have been identified. This proposal will provide sufficient reagents to permit a high throughput screening of 100,000 compounds ..
  70. ACOUSTICALLY ACTIVATED MICELLAR DRUG DELIVERY
    Natalya Rapoport; Fiscal Year: 2001
    ....
  71. A Phase 2 Trial of Dasatinib in Patients with NSCLC and Acquired Resistance to Er
    Vincent Miller; Fiscal Year: 2008
    ..The proposed work is a clinical trial to determine whether dasatinib is an effective treatment for patients with NSCLC and acquired resistance to erlotinib or gefitinib. [unreadable] [unreadable] [unreadable]..
  72. Chemical Complementation Assay for MKP-1 (RMI)
    JOHN LAZO; Fiscal Year: 2005
    ..This proposal will provide sufficient reagents, including cells and DMA transfection vectors, to permit the high throughput screening of 100,000 compounds. ..