M M Gottesman

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint Identification of cytoskeletal [14C]carboplatin-binding proteins reveals reduced expression and disorganization of actin and filamin in cisplatin-resistant cell lines
    Ding Wu Shen
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 1A09, Bethesda, MD 20892 4254, USA
    Mol Pharmacol 66:789-93. 2004
  2. pmc SIRT1 contributes in part to cisplatin resistance in cancer cells by altering mitochondrial metabolism
    Xing Jie Liang
    Laboratory of Cell Biology, National Cancer Institute, NIH, Bethesda, MD 20892, USA
    Mol Cancer Res 6:1499-506. 2008
  3. pmc Reduced expression of small GTPases and hypermethylation of the folate binding protein gene in cisplatin-resistant cells
    D W Shen
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, MD 20892 4254, USA
    Br J Cancer 91:270-6. 2004
  4. pmc Reduced endocytosis and altered lysosome function in cisplatin-resistant cell lines
    S S Chauhan
    Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20842 4254, USA
    Br J Cancer 88:1327-34. 2003
  5. pmc The clinical relevance of cancer cell lines
    Jean Pierre Gillet
    Laboratory of Cell Biology, National Cancer Institute, 37 Convent Dr, Rm 2108, Bethesda, MD 20892, USA
    J Natl Cancer Inst 105:452-8. 2013
  6. pmc Cisplatin resistance: a cellular self-defense mechanism resulting from multiple epigenetic and genetic changes
    Ding Wu Shen
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, 37 Convent Dr, Rm 2108, Bethesda, MD 20892, USA
    Pharmacol Rev 64:706-21. 2012
  7. ncbi request reprint Cancer gene therapy: an awkward adolescence
    Michael M Gottesman
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA
    Cancer Gene Ther 10:501-8. 2003
  8. ncbi request reprint Overview: ABC transporters and human disease
    M M Gottesman
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 4255, USA
    J Bioenerg Biomembr 33:453-8. 2001
  9. ncbi request reprint 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
  10. ncbi request reprint 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

Publications93

  1. ncbi request reprint Identification of cytoskeletal [14C]carboplatin-binding proteins reveals reduced expression and disorganization of actin and filamin in cisplatin-resistant cell lines
    Ding Wu Shen
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 1A09, Bethesda, MD 20892 4254, USA
    Mol Pharmacol 66:789-93. 2004
    ....
  2. pmc SIRT1 contributes in part to cisplatin resistance in cancer cells by altering mitochondrial metabolism
    Xing Jie Liang
    Laboratory of Cell Biology, National Cancer Institute, NIH, Bethesda, MD 20892, USA
    Mol Cancer Res 6:1499-506. 2008
    ..Our findings therefore suggest that reduced glucose use and altered mitochondrial metabolism mediated by SIRT1 is one of several alterations that contribute to cellular resistance to cisplatin...
  3. pmc Reduced expression of small GTPases and hypermethylation of the folate binding protein gene in cisplatin-resistant cells
    D W Shen
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, MD 20892 4254, USA
    Br J Cancer 91:270-6. 2004
    ..Both a defective endocytic pathway and DNA hypermethylation resulting in the downregulation of small regulatory GTPases and cell surface receptors contribute to the reduced accumulation of a broad range of compounds in CP-r cells...
  4. pmc Reduced endocytosis and altered lysosome function in cisplatin-resistant cell lines
    S S Chauhan
    Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20842 4254, USA
    Br J Cancer 88:1327-34. 2003
    ....
  5. pmc The clinical relevance of cancer cell lines
    Jean Pierre Gillet
    Laboratory of Cell Biology, National Cancer Institute, 37 Convent Dr, Rm 2108, Bethesda, MD 20892, USA
    J Natl Cancer Inst 105:452-8. 2013
    ..However, the success stories should not obscure the growing body of data that motivates us to develop new in vitro preclinical models that would substantially increase the success rate of new in vitro-assessed cancer treatments...
  6. pmc Cisplatin resistance: a cellular self-defense mechanism resulting from multiple epigenetic and genetic changes
    Ding Wu Shen
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, 37 Convent Dr, Rm 2108, Bethesda, MD 20892, USA
    Pharmacol Rev 64:706-21. 2012
    ..This seems to be a consequence of numerous epigenetic and genetic changes leading to the loss of cell-surface binding sites and/or transporters for cisplatin, and decreased fluid phase endocytosis...
  7. ncbi request reprint Cancer gene therapy: an awkward adolescence
    Michael M Gottesman
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA
    Cancer Gene Ther 10:501-8. 2003
    ....
  8. ncbi request reprint Overview: ABC transporters and human disease
    M M Gottesman
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 4255, USA
    J Bioenerg Biomembr 33:453-8. 2001
    ..At least 8 members of this family are involved in the transport of a variety of amphipathic compounds, including anticancer drugs, and some appear to contribute to the resistance of cancer cells to chemotherapy...
  9. ncbi request reprint 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
    ....
  10. ncbi request reprint 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. doi request reprint Commentary: A delicate balance: weighing the effects of conflict-of-interest rules on intramural research at the National Institutes of Health
    Michael M Gottesman
    National Institutes of Health, Bethesda, Maryland 20852, USA
    Acad Med 85:1660-2. 2010
    ....
  12. ncbi request reprint 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...
  13. ncbi request reprint Expression of a human complementary DNA for the multidrug resistance gene in murine hematopoietic precursor cells with the use of retroviral gene transfer
    J R McLachlin
    Laboratory of Molecular Hematology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892
    J Natl Cancer Inst 82:1260-3. 1990
    ..These results may serve as a model for the generation and selection of bone marrow cells resistant to the toxic effects of chemotherapeutic agents in vivo...
  14. ncbi request reprint Efficient expression of functional human MDR1 gene in murine bone marrow after retroviral transduction of purified hematopoietic stem cells
    T Licht
    Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 4255, USA
    Blood 86:111-21. 1995
    ..Transduction of P-glycoprotein may be useful for gene therapy in two ways: to protect bone marrow from myelosuppression after chemotherapy and as a selectable marker in vivo for the introduction of otherwise nonselectable genes...
  15. pmc A retrovirus carrying an MDR1 cDNA confers multidrug resistance and polarized expression of P-glycoprotein in MDCK cells
    I Pastan
    Laboratory of Molecular Biology, National Cancer Institute, Bethesda, MD 20892
    Proc Natl Acad Sci U S A 85:4486-90. 1988
    ..The MDR1 virus should be useful for introducing this drug resistance gene into a variety of cell types for biological experiments in vitro and in vivo...
  16. ncbi request reprint Retroviral transfer of a chimeric multidrug resistance-adenosine deaminase gene
    U A Germann
    Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892
    FASEB J 4:1501-7. 1990
    ..The replication-defective, recombinant MDR-ADA retrovirus should be useful to stably introduce the chimeric MDR-ADA gene into a variety of cell types for biological experiments in vitro and in vivo...
  17. ncbi request reprint Expression of a multidrug resistance-adenosine deaminase fusion gene
    U A Germann
    National Institutes of Health, Bethesda, Maryland 20892
    J Biol Chem 264:7418-24. 1989
    ..The data indicate that the human multidrug resistance gene may be used as a dominant selectable marker to introduce other genes in the form of gene fusions into cultured cells...
  18. pmc Characterisation of high-level cisplatin-resistant cell lines established from a human hepatoma cell line and human KB adenocarcinoma cells: cross-resistance and protein changes
    D W Shen
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Br J Cancer 71:676-83. 1995
    ..These results suggest that alterations of certain proteins occur commonly in cisplatin-resistant cells, particularly proteins of molecular weight 52 and 50 kDa...
  19. ncbi request reprint Expression of the human multidrug resistance and glucocerebrosidase cDNAs from adeno-associated vectors: efficient promoter activity of AAV sequences and in vivo delivery via liposomes
    M Baudard
    Laboratory of Cell Biology, National Cancer Institute, NIH, Bethesda, MD 20892 4255, USA
    Hum Gene Ther 7:1309-22. 1996
    ....
  20. ncbi request reprint In vitro and in vivo liposome-mediated gene transfer leads to human MDR1 expression in mouse bone marrow progenitor cells
    I Aksentijevich
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 4255, USA
    Hum Gene Ther 7:1111-22. 1996
    ..Colony-forming units (CFU-Mix) were obtained after exposure of BMC to lethal doses of vincristine, demonstrating functional expression of the MDR1 gene in hematopoietic progenitor cells for up to 1 month...
  21. ncbi request reprint Characterization of an MDR1 retroviral bicistronic vector for correction of X-linked severe combined immunodeficiency
    S E Kleiman
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 4255, USA
    Gene Ther 5:671-6. 1998
    ..This construct might be particularly useful if high expression of gamma c is required, as might be achievable through in vivo selection for drug resistance of recipient lymphocytes...
  22. ncbi request reprint Cloning, genomic organization, and chromosomal localization of human cathepsin L
    S S Chauhan
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892
    J Biol Chem 268:1039-45. 1993
    ....
  23. ncbi request reprint 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...
  24. ncbi request reprint Paclitaxel chemotherapy after autologous stem-cell transplantation and engraftment of hematopoietic cells transduced with a retrovirus containing the multidrug resistance complementary DNA (MDR1) in metastatic breast cancer patients
    K H Cowan
    National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Clin Cancer Res 5:1619-28. 1999
    ....
  25. pmc Prolonged drug selection of breast cancer cells and enrichment of cancer stem cell characteristics
    Anna Maria Calcagno
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    J Natl Cancer Inst 102:1637-52. 2010
    ..We investigated whether prolonged continuous selection of cells for drug resistance enriches cultures for cancer stem-like cells...
  26. pmc Exposure to HIV-protease inhibitors selects for increased expression of P-glycoprotein (ABCB1) in Kaposi's sarcoma cells
    M B Lucia
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, 37 Convent Drive, Room 2108, Bethesda, MD 20892, USA
    Br J Cancer 105:513-22. 2011
    ....
  27. ncbi request reprint Targeted disruption of the mouse mdr1b gene reveals that steroid hormones enhance mdr gene expression
    S Altuvia
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892
    J Biol Chem 268:27127-32. 1993
    ....
  28. pmc Topical colchicine selection of keratinocytes transduced with the multidrug resistance gene (MDR1) can sustain and enhance transgene expression in vivo
    W Pfutzner
    Dermatology Branch, Building 10 Room 12N260, National Cancer Institute, National Institutes of Health, 10 Center Drive, MSC 1908, Bethesda, MD 20892 1908, USA
    Proc Natl Acad Sci U S A 99:13096-101. 2002
    ..For clinical skin gene therapy applications, this in vivo selection approach promises to enhance both the duration and expression level of a desired therapeutic gene in KC, by linking its expression to the MDR1 selectable marker gene...
  29. ncbi request reprint P-glycoprotein and multidrug resistance
    M M Gottesman
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Curr Opin Genet Dev 6:610-7. 1996
    ....
  30. pmc Selective toxicity of NSC73306 in MDR1-positive cells as a new strategy to circumvent multidrug resistance in cancer
    Joseph A Ludwig
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
    Cancer Res 66:4808-15. 2006
    ..This article shows that NSC73306 kills cells with intrinsic or acquired P-gp-induced MDR and indirectly acts to eliminate resistance to MDR1 substrates...
  31. pmc Is resistance useless? Multidrug resistance and collateral sensitivity
    Matthew D Hall
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA
    Trends Pharmacol Sci 30:546-56. 2009
    ..g. generation of reactive oxygen species) to account for the underlying generality of this phenomenon, and proposes exploitation of CS as a strategy to improve response to chemotherapy...
  32. pmc Principal expression of two mRNA isoforms (ABCB 5alpha and ABCB 5beta ) of the ATP-binding cassette transporter gene ABCB 5 in melanoma cells and melanocytes
    Kevin G Chen
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
    Pigment Cell Res 18:102-12. 2005
    ..Our findings indicate that expression of ABCB 5alpha/beta might possibly provide two novel molecular markers for differential diagnosis of melanomas and constitute potential molecular targets for therapy of melanomas...
  33. ncbi request reprint P-glycoprotein, expressed in multidrug resistant cells, is not responsible for alterations in membrane fluidity or membrane potential
    Claudina Alemán
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 4254, USA
    Cancer Res 63:3084-91. 2003
    ..The changes in these parameters observed in drug-selected cells must reflect other host adaptations to drug selection...
  34. doi request reprint Mechanisms of multidrug resistance in cancer
    Jean Pierre Gillet
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
    Methods Mol Biol 596:47-76. 2010
    ..The pleotropic response of cancer cells to chemotherapy is summarized in a concluding diagram...
  35. pmc Evaluation of current methods used to analyze the expression profiles of ATP-binding cassette transporters yields an improved drug-discovery database
    Josiah N Orina
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892 4256, USA
    Mol Cancer Ther 8:2057-66. 2009
    ..This study also led to an improved database by revealing previously unidentified substrates for ABCB1, ABCC1, and ABCG2, transporters that contribute to MDR...
  36. pmc Imaging the function of P-glycoprotein with radiotracers: pharmacokinetics and in vivo applications
    P Kannan
    Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA
    Clin Pharmacol Ther 86:368-77. 2009
    ..By meeting these criteria, imaging can elucidate the function of P-gp in various disorders and improve the efficacy of treatments...
  37. ncbi request reprint Efficient long-term coexpression of a hammerhead ribozyme targeted to the U5 region of HIV-1 LTR by linkage to the multidrug-resistance gene
    C G Lee
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20895, USA
    Antisense Nucleic Acid Drug Dev 7:511-22. 1997
    ....
  38. ncbi request reprint Comparing solid tumors with cell lines: implications for identifying drug resistance genes in cancer
    Gergely Szakacs
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA
    Mol Interv 4:323-5. 2004
    ..Because anti-tumor compounds are largely evaluated in cell culture assays, these compounds' therapeutic utility must be judged in light of genes described by Stein et al. that better predict tractability...
  39. ncbi request reprint Comparison of drug transporter levels in normal colon, colon cancer, and Caco-2 cells: impact on drug disposition and discovery
    Anna Maria Calcagno
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Mol Pharm 3:87-93. 2006
    ..However, the molecular "fingerprint" of Caco-2 was distinctly different from tumor samples, indicating that the Caco-2 model would unlikely predict accurate drug absorption for colon cancer sites...
  40. pmc Profiling SLCO and SLC22 genes in the NCI-60 cancer cell lines to identify drug uptake transporters
    Mitsunori Okabe
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA
    Mol Cancer Ther 7:3081-91. 2008
    ..Our results indicate that the gene expression database can be used to identify SLCO and SLC22 family members that confer sensitivity to cancer cells...
  41. pmc Involvement of ABC transporters in melanogenesis and the development of multidrug resistance of melanoma
    Kevin G Chen
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
    Pigment Cell Melanoma Res 22:740-9. 2009
    ..The ABC-M model suggests molecular strategies to reverse MDR function in the context of the melanogenic pathway, which could open therapeutic avenues towards the ultimate goal of circumventing clinical MDR in patients with melanoma...
  42. ncbi request reprint Predicting drug sensitivity and resistance: profiling ABC transporter genes in cancer cells
    Gergely Szakacs
    Laboratory of Cell Biology, Center for Cancer Research, NCI, NIH, Bethesda, MD, 20892, USA
    Cancer Cell 6:129-37. 2004
    ..Unexpectedly, we also found and validated compounds whose activity is potentiated, rather than antagonized, by the MDR1 multidrug transporter. Such compounds may serve as leads for development...
  43. pmc A dual-fluorescence high-throughput cell line system for probing multidrug resistance
    Kyle R Brimacombe
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Assay Drug Dev Technol 7:233-49. 2009
    ....
  44. pmc A novel way to spread drug resistance in tumor cells: functional intercellular transfer of P-glycoprotein (ABCB1)
    Suresh V Ambudkar
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 4256, USA
    Trends Pharmacol Sci 26:385-7. 2005
    ..Non-genetic transfer of the multidrug resistance phenotype raises fascinating questions about the mechanism and regulation of cell-surface membrane-protein-mediated spread of traits...
  45. ncbi request reprint P-glycoprotein: from genomics to mechanism
    Suresh V Ambudkar
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute NIH, 37 Convent Drive, Building 37, Room 1A 09, Bethesda, MD 20892 4254, USA
    Oncogene 22:7468-85. 2003
    ..Understanding of the biology, genetics, and biochemistry of P-gp promises to improve the treatment of cancer and explain the pharmacokinetics of many commonly used drugs...
  46. pmc Comparing cDNA and oligonucleotide array data: concordance of gene expression across platforms for the NCI-60 cancer cells
    Jae K Lee
    Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 8322, USA
    Genome Biol 4:R82. 2003
    ..Global concordance is parameterized by a 'correlation of correlations' coefficient...
  47. pmc alpha-Galactosidase A deficient mice: a model of Fabry disease
    T Ohshima
    Gene Targeting Research and Core Facility, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 94:2540-4. 1997
    ....
  48. ncbi request reprint Different roles for K+ channels in cisplatin-resistant cell lines argue against a critical role for these channels in cisplatin resistance
    Xing Jie Liang
    Laboratory of Cell Biology, National Cancer Institute, NIH, Bethesda 20892 4256, Maryland, USA
    Anticancer Res 25:4113-22. 2005
    ..We conclude that K+ and H+ homeostasis are not critical factors in cisplatin resistance since they affect cisplatin resistance differently in KB and BEL-7404 cells...
  49. pmc Melanosomal sequestration of cytotoxic drugs contributes to the intractability of malignant melanomas
    Kevin G Chen
    Laboratories of Cell Biology and Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 103:9903-7. 2006
    ..Preventing melanosomal sequestration of cytotoxic drugs by inhibiting the functions of melanosomes may have great potential as an approach to improving the chemosensitivity of melanoma cells...
  50. pmc Evidence for dual mode of action of a thiosemicarbazone, NSC73306: a potent substrate of the multidrug resistance linked ABCG2 transporter
    Chung Pu Wu
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892 4256, USA
    Mol Cancer Ther 6:3287-96. 2007
    ....
  51. ncbi request reprint Silent polymorphisms speak: how they affect pharmacogenomics and the treatment of cancer
    Zuben E Sauna
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH and Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA
    Cancer Res 67:9609-12. 2007
    ..We discuss the importance of polymorphisms in drug metabolizing enzymes and transporters in anticancer therapy and suggest that synonymous polymorphisms may play a more significant role than is currently assumed...
  52. pmc N-desmethyl-loperamide is selective for P-glycoprotein among three ATP-binding cassette transporters at the blood-brain barrier
    Pavitra Kannan
    Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, USA
    Drug Metab Dispos 38:917-22. 2010
    ..e., a competitive substrate). Because low concentrations of radiotracer are used for PET imaging, [(11)C]dLop acts selectively and only as a substrate for P-gp...
  53. ncbi request reprint Mislocalization of membrane proteins associated with multidrug resistance in cisplatin-resistant cancer cell lines
    Xing Jie Liang
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 4254, USA
    Cancer Res 63:5909-16. 2003
    ..The reduced accumulation of cytotoxic compounds in the KB-CP cells is presumed to result from the failure of carrier proteins and/or transporters to localize to the plasma membrane...
  54. ncbi request reprint The molecular mysteries underlying P-glycoprotein-mediated multidrug resistance
    Gergely Szakacs
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892 4254, USA
    Cancer Biol Ther 3:382-4. 2004
  55. pmc SV40 Pseudovirion gene delivery of a toxin to treat human adenocarcinomas in mice
    C Kimchi-Sarfaty
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 4256, USA
    Cancer Gene Ther 13:648-57. 2006
    ..These results indicate that SV40 in vitro packaging is an effective system for cancer gene delivery using two different routes of injection and in combination with chemotherapy...
  56. ncbi request reprint DNA-PKcs: a T-cell tumour suppressor encoded at the mouse scid locus
    C Jhappan
    Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 4255, USA
    Nat Genet 17:483-6. 1997
    ..15)...
  57. ncbi request reprint Codominance of cisplatin resistance in somatic cell hybrids
    Yu Lan Mary Ying
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 4254, USA
    J Cell Physiol 196:63-9. 2003
    ..These dominance data suggest that it might be possible to identify one or more genes responsible for cisplatin resistance by gene transfer from a resistant cell line to a sensitive cell line...
  58. ncbi request reprint A "silent" polymorphism in the MDR1 gene changes substrate specificity
    Chava Kimchi-Sarfaty
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
    Science 315:525-8. 2007
    ....
  59. ncbi request reprint Changes in biophysical parameters of plasma membranes influence cisplatin resistance of sensitive and resistant epidermal carcinoma cells
    Xing Jie Liang
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Room 1A 09, 37 Convent Drive, Bethesda, MD 20892 4254, USA
    Exp Cell Res 293:283-91. 2004
    ....
  60. ncbi request reprint Analysis of ATP-binding cassette transporter expression in drug-selected cell lines by a microarray dedicated to multidrug resistance
    Jean Philippe Annereau
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 4256, USA
    Mol Pharmacol 66:1397-405. 2004
    ..The custom-designed ABC-Tox microarray presented here will be helpful to elucidate mechanisms leading to anticancer drug resistance...
  61. ncbi request reprint Down-regulation and altered localization of gamma-catenin in cisplatin-resistant adenocarcinoma cells
    Xing Jie Liang
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 1A09, Bethesda, MD 20892 4254, USA
    Mol Pharmacol 65:1217-24. 2004
    ....
  62. pmc Elevated expression of TMEM205, a hypothetical membrane protein, is associated with cisplatin resistance
    Ding Wu Shen
    Laboratory of Cell Biology, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Cell Physiol 225:822-8. 2010
    ..These results indicate that a novel mechanism for cisplatin resistance is mediated by TMEM205, and also suggest that overexpression of TMEM205 in CP-r cells may be valuable as a biomarker or target in cancer chemotherapy...
  63. ncbi request reprint Isolation and sequence of the promoter region of the human multidrug-resistance (P-glycoprotein) gene
    K Ueda
    Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892
    J Biol Chem 262:17432-6. 1987
    ..This identification and isolation of promoter sequences for the MDR 1 gene will permit studies on how expression of this gene is regulated in normal human tissues and cancers...
  64. pmc Sequence and expression of the cDNA for MEP (major excreted protein), a transformation-regulated secreted cathepsin
    B R Troen
    Laboratory of Molecular Biology, National Cancer Institute, Bethesda, MD 20892
    Biochem J 246:731-5. 1987
    ..We have placed the MEP cDNA in a eukaryotic expression vector and demonstrated the production of the 39 kDa polypeptide form of mouse MEP in monkey CV-1 cells...
  65. pmc A human mitochondrial ATP-dependent protease that is highly homologous to bacterial Lon protease
    N Wang
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892
    Proc Natl Acad Sci U S A 90:11247-51. 1993
    ..coli Lon protease...
  66. ncbi request reprint A pleiotropic defect reducing drug accumulation in cisplatin-resistant cells
    Xing Jie Liang
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 2108, Bethesda, MD 20892 4254, USA
    J Inorg Biochem 98:1599-606. 2004
    ..Multiple mechanisms in CP-r cells keep cytotoxic platinum compounds out of cells through defective expression of cell surface proteins such as transporters and carriers, and decreased expression of proteins involved in endocytosis...
  67. pmc A synonymous polymorphism in a common MDR1 (ABCB1) haplotype shapes protein function
    King Leung Fung
    Laboratory of Cell Biology, Center of Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 2108, Bethesda, MD 20892 4254, USA
    Biochim Biophys Acta 1794:860-71. 2009
    ..A possible molecular mechanism of action by ribosome stalling that can change protein structure and function by altering protein folding is discussed...
  68. doi request reprint Disruption of microfilaments by cytochalasin B decreases accumulation of cisplatin in human epidermal carcinoma and liver carcinoma cell lines
    Xing Jie Liang
    Laboratory of Cell Biology, National Cancer Institute, NIH, Bethesda, MD 20892, USA
    Cancer Chemother Pharmacol 62:977-84. 2008
    ....
  69. ncbi request reprint The development of gene therapy: from monogenic recessive disorders to complex diseases such as cancer
    Jean Pierre Gillet
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
    Methods Mol Biol 542:5-54. 2009
    ..The field of cancer gene therapy experienced an "awkward adolescence." Although this field has certainly not yet reached maturity, it still holds the potential of alleviating the suffering of many individuals with cancer...
  70. ncbi request reprint Trafficking and localization of platinum complexes in cisplatin-resistant cell lines monitored by fluorescence-labeled platinum
    Xing Jie Liang
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892 4256, USA
    J Cell Physiol 202:635-41. 2005
    ....
  71. ncbi request reprint Functional characterization of coding polymorphisms in the human MDR1 gene using a vaccinia virus expression system
    Chava Kimchi-Sarfaty
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 4254, USA
    Mol Pharmacol 62:1-6. 2002
    ..These results demonstrate that the common MDR1 coding polymorphisms result in P-gps with a cell surface distribution and function similar to wild-type P-gp...
  72. ncbi request reprint The role of cellular accumulation in determining sensitivity to platinum-based chemotherapy
    Matthew D Hall
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 4255, USA
    Annu Rev Pharmacol Toxicol 48:495-535. 2008
    ..This review suggests a model that helps reconcile the disparate literature by describing multiple pathways for Pt-containing drugs into and out of the cell...
  73. ncbi request reprint Human ABCB6 localizes to both the outer mitochondrial membrane and the plasma membrane
    Jill K Paterson
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, DHHS, Bethesda, Maryland 20892 4256, USA
    Biochemistry 46:9443-52. 2007
    ..These studies are the first to demonstrate that ABCB6 exists in two molecular weight forms, is localized to both the outer mitochondrial membrane and the plasma membrane, and plays a functional role in the plasma membrane...
  74. pmc Synthesis, activity, and pharmacophore development for isatin-beta-thiosemicarbazones with selective activity toward multidrug-resistant cells
    Matthew D Hall
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Med Chem 52:3191-204. 2009
    ..Together, the models serve as effective approaches for predicting structures with MDR1-selective activity and aid in directing the search for the mechanism of action of 1...
  75. pmc Ethnicity-related polymorphisms and haplotypes in the human ABCB1 gene
    Chava Kimchi-Sarfaty
    National Institutes of Health, Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892 4254, USA
    Pharmacogenomics 8:29-39. 2007
    ..The frequencies with which these polymorphisms exist in a population have also been shown to be ethnically related...
  76. ncbi request reprint SV40 pseudovirions as highly efficient vectors for gene transfer and their potential application in cancer therapy
    Chava Kimchi-Sarfaty
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Curr Pharm Biotechnol 5:451-8. 2004
    ..This review summarizes different strategies in which SV40 vectors are used to deliver genes in vitro, to living mice, and to tumors growing in nude mice...
  77. pmc Influence of melanosome dynamics on melanoma drug sensitivity
    Kevin G Chen
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bldg 37, Rm 2108, Bethesda, MD 20892, USA
    J Natl Cancer Inst 101:1259-71. 2009
    ..Here we propose and test a model that explains drug resistance or sensitivity in terms of melanosome dynamics...
  78. pmc Drug selection with paclitaxel restores expression of linked IL-2 receptor gamma -chain and multidrug resistance (MDR1) transgenes in canine bone marrow
    Thomas Licht
    Laboratories of Molecular Biology and Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 99:3123-8. 2002
    ..In summary, we have shown that with the use of a drug-selectable marker gene, chemotherapy can select for cells that express an otherwise nonselected therapeutic gene in blood and bone marrow...
  79. pmc Identification by functional cloning from a retroviral cDNA library of cDNAs for ribosomal protein L36 and the 10-kDa heat shock protein that confer cisplatin resistance
    Ding Wu Shen
    Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, 37 Convent Dr, Room 2108, Bethesda, MD 20892 4254, USA
    Mol Pharmacol 69:1383-8. 2006
    ..The finding that a ribosomal protein gene, RPL36, contributes to CP-r should stimulate study of the role of ribosomal proteins in multifactorial mechanisms of cisplatin resistance...
  80. pmc P-Glycoprotein is not present in mitochondrial membranes
    Jill K Paterson
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH DHHS, Bethesda, MD 20892 4256, USA
    Exp Cell Res 313:3100-5. 2007
    ..Therefore, contrary to previous speculation, P-glycoprotein does not confer cellular protection by residing in mitochondrial membranes...
  81. pmc Efficient delivery of RNA interference effectors via in vitro-packaged SV40 pseudovirions
    Chava Kimchi-Sarfaty
    Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 4256, USA
    Hum Gene Ther 16:1110-5. 2005
    ..Our findings indicate that SV40 pseudovirions may be a useful addition to the delivery systems currently being used for the transfer of RNAi effector molecules...
  82. ncbi request reprint Useful tool to generate unidirectional deletion vectors by utilizing the star activity of BamHI in an NcoI-BamHI-XhoI cassette
    Kevin G Chen
    Laboratory of Cell Biology, National Cancer Institute, NIH, Bethesda, MD 20892, USA
    Biotechniques 38:198, 200, 202, 204. 2005
  83. pmc Endocytic recycling compartments altered in cisplatin-resistant cancer cells
    Xing Jie Liang
    Laboratory of Cell Biology, National Cancer Institute, NIH, Bethesda, Maryland, USA
    Cancer Res 66:2346-53. 2006
    ....
  84. ncbi request reprint An MDR-EGFP gene fusion allows for direct cellular localization, function and stability assessment of P-glycoprotein
    Jordi Petriz
    Servei d Hemateràpia i Hemostàsia, Institut d Investigacions Biomèdiques August Pi i Sunyer DIBAPS, Hospital Clinic, Universitat de Barcelona Villarroel, Barcelona, Spain
    Curr Drug Deliv 1:43-56. 2004
    ..2 days), but revealed that surface-Pgp acquires extra stability as an active pump (t(1/2 surface Pgp-EGFP) = 3.7 days)...
  85. ncbi request reprint Drug-selected co-expression of P-glycoprotein and gp91 in vivo from an MDR1-bicistronic retrovirus vector Ha-MDR-IRES-gp91
    Yoshikazu Sugimoto
    Division of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo 170 8455, Japan
    J Gene Med 5:366-76. 2003
    ..Co-expression of a human multidrug resistance gene (MDR1) with a therapeutic gene affords selectable growth advantage to genetically modified cells...
  86. ncbi request reprint Transmembrane inhibitors of P-glycoprotein, an ABC transporter
    Nadya I Tarasova
    Molecular Aspects of Drug Design Section, Structural Biophysics Laboratory, NCI Frederick, P O Box B, Frederick, Maryland 21702, USA
    J Med Chem 48:3768-75. 2005
    ..The newly synthesized P-gp antagonists appear to be promising nontoxic drug resistance inhibitors that merit further development...
  87. ncbi request reprint Overexpression of glucosylceramide synthase and P-glycoprotein in cancer cells selected for resistance to natural product chemotherapy
    Valerie Gouaze
    John Wayne Cancer Institute at Saint John s Health Center, Santa Monica, California 90404, USA
    Mol Cancer Ther 3:633-9. 2004
    ..A possible connection between glucosylceramide synthase and P-gp in drug resistance biology is suggested...
  88. ncbi request reprint 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...
  89. ncbi request reprint Studies with novel Pdr5p substrates demonstrate a strong size dependence for xenobiotic efflux
    John Golin
    Department of Biology and Chemistry, Catholic University of America, Washington, DC 20064, USA
    J Biol Chem 278:5963-9. 2003
    ..The surprising observation that Pdr5p mediates resistance to tetraalkyltins suggests that one of the sites might use only hydrophobic interactions to bind substrates...
  90. ncbi request reprint Modulation by the ATP/GTP ratio of the phosphorylation level of P-glycoprotein and of various plasma membrane proteins of KB-V1 multidrug resistant cells
    Isabelle H Lelong-Rebel
    UPR 9003 CNRS, IRCAD, Hopitaux Universitaires, BP 426, 67091, Strasbourg, France
    Anticancer Res 23:2363-75. 2003
    ..Mastoparan, a G-protein regulator, increased the phosphorylation of some proteins that were already enhanced by the presence of [ATP + GTP] mixtures, especially proteins migrating in gels at the same position as P-glycoprotein...
  91. ncbi request reprint Low and high concentrations of the topo II inhibitor daunorubicin in NIH3T3 cells: reversible G2/M versus irreversible G1 and S arrest
    Wilfred D Stein
    Biological Chemistry, Institute of Life Sciences, Hebrew University, Jerusalem, Israel
    Cell Cycle 2:134-42. 2003
    ....
  92. ncbi request reprint Mouse mammary tumor virus Env-derived peptide associates with nucleolar targets in lymphoma, mammary carcinoma, and human breast cancer
    Allan Bar-Sinai
    Department of Cell and Animal Biology, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel
    Cancer Res 65:7223-30. 2005
    ..Affinity purification studies define a number of proteins, mostly nucleolar, that bind p14. Taken together, these findings point towards a more general involvement of p14 in lymphomagenesis and mammary carcinogenesis...
  93. doi request reprint Modulation of Na+-Ca2+ exchanger expression by immunosuppressive drugs is isoform-specific
    Benayahu Elbaz
    Department of Biochemistry, Hebrew University Hadassah Medical School, P O Box 12272, Jerusalem 91120, Israel
    Mol Pharmacol 73:1254-63. 2008
    ..Expression of NCX genes is tissue-specific. Hence, our results can potentially provide a tool for choosing the immunosuppressive protocol to be used...