Pier P Pandolfi

Summary

Affiliation: Memorial Sloan-Kettering Cancer Center
Country: USA

Publications

  1. ncbi request reprint Breast cancer--loss of PTEN predicts resistance to treatment
    Pier Paolo Pandolfi
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, USA
    N Engl J Med 351:2337-8. 2004
  2. ncbi request reprint APL as a paradigm in biomedical research: a journey toward the cure
    P P Pandolfi
    Cancer Biology and Genetics Program, Department of Pathology, Memorial Sloan Kettering Cancer Center, Sloan Kettering Institute, 1275 York Avenue, New York, NY 10021, USA
    Curr Top Microbiol Immunol 313:1-2. 2007
  3. pmc Pten dose dictates cancer progression in the prostate
    Lloyd C Trotman
    Molecular Biology Program, Memorial Sloan Kettering Cancer Center, Sloan Kettering Institute, New York, New York, USA
    PLoS Biol 1:E59. 2003
  4. pmc p62(dok), a negative regulator of Ras and mitogen-activated protein kinase (MAPK) activity, opposes leukemogenesis by p210(bcr-abl)
    A Di Cristofano
    Department of Human Genetics, Molecular Biology Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    J Exp Med 194:275-84. 2001
  5. pmc Role of promyelocytic leukemia (PML) protein in tumor suppression
    E M Rego
    Department of Human Genetics and Molecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    J Exp Med 193:521-29. 2001
  6. pmc Promyelocytic leukemia protein (PML) and Daxx participate in a novel nuclear pathway for apoptosis
    S Zhong
    Department of Human Genetics and the Molecular Biology Program, Memorial Sloan Kettering Cancer Center, Sloan Kettering Division, Graduate School of Medical Sciences, Cornell University, New York, New York 10021, USA
    J Exp Med 191:631-40. 2000
  7. ncbi request reprint PML, PLZF and NPM genes in the molecular pathogenesis of acute promyelocytic leukemia
    P P Pandolfi
    Department of Human Genetics, Memorial Sloan Kettering Cancer Center and Molecular Biology Program, Sloan Kettering Institute, New York, New York 10021, USA
    Haematologica 81:472-82. 1996
  8. ncbi request reprint In vivo analysis of the molecular genetics of acute promyelocytic leukemia
    P P Pandolfi
    Molecular Biology Program, Department of Pathology, Memorial Sloan Kettering Cancer Center, Sloan Kettering Division, Graduate School of Medical Sciences, Cornell University, 1275 York Avenue, New York, NY 10021, USA
    Oncogene 20:5726-35. 2001
  9. ncbi request reprint Histone deacetylases and transcriptional therapy with their inhibitors
    P P Pandolfi
    Department of Human Genetics, Memorial Sloan Kettering Cancer Center, Graduate School of Medical Sciences, Cornell University, New York, NY 10021, USA
    Cancer Chemother Pharmacol 48:S17-9. 2001
  10. ncbi request reprint Oncogenes and tumor suppressors in the molecular pathogenesis of acute promyelocytic leukemia
    P P Pandolfi
    Department of Human Genetics and Molecular Biology Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    Hum Mol Genet 10:769-75. 2001

Collaborators

Detail Information

Publications62

  1. ncbi request reprint Breast cancer--loss of PTEN predicts resistance to treatment
    Pier Paolo Pandolfi
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, USA
    N Engl J Med 351:2337-8. 2004
  2. ncbi request reprint APL as a paradigm in biomedical research: a journey toward the cure
    P P Pandolfi
    Cancer Biology and Genetics Program, Department of Pathology, Memorial Sloan Kettering Cancer Center, Sloan Kettering Institute, 1275 York Avenue, New York, NY 10021, USA
    Curr Top Microbiol Immunol 313:1-2. 2007
  3. pmc Pten dose dictates cancer progression in the prostate
    Lloyd C Trotman
    Molecular Biology Program, Memorial Sloan Kettering Cancer Center, Sloan Kettering Institute, New York, New York, USA
    PLoS Biol 1:E59. 2003
    ..Our results provide conclusive genetic support for the notion that PTEN is haploinsufficient in tumor suppression and that its dose is a key determinant in cancer progression...
  4. pmc p62(dok), a negative regulator of Ras and mitogen-activated protein kinase (MAPK) activity, opposes leukemogenesis by p210(bcr-abl)
    A Di Cristofano
    Department of Human Genetics, Molecular Biology Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    J Exp Med 194:275-84. 2001
    ..These data indicate that p62(dok) acts as a negative regulator of growth factor-induced cell proliferation, at least in part through downregulating Ras/MAPK signaling pathway, and that p62(dok) can oppose leukemogenesis by p210(bcr-abl)...
  5. pmc Role of promyelocytic leukemia (PML) protein in tumor suppression
    E M Rego
    Department of Human Genetics and Molecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    J Exp Med 193:521-29. 2001
    ....
  6. pmc Promyelocytic leukemia protein (PML) and Daxx participate in a novel nuclear pathway for apoptosis
    S Zhong
    Department of Human Genetics and the Molecular Biology Program, Memorial Sloan Kettering Cancer Center, Sloan Kettering Division, Graduate School of Medical Sciences, Cornell University, New York, New York 10021, USA
    J Exp Med 191:631-40. 2000
    ..These results indicate that PML and Daxx cooperate in a novel NB-dependent pathway for apoptosis and shed new light in the role of PML in tumor suppression...
  7. ncbi request reprint PML, PLZF and NPM genes in the molecular pathogenesis of acute promyelocytic leukemia
    P P Pandolfi
    Department of Human Genetics, Memorial Sloan Kettering Cancer Center and Molecular Biology Program, Sloan Kettering Institute, New York, New York 10021, USA
    Haematologica 81:472-82. 1996
    ....
  8. ncbi request reprint In vivo analysis of the molecular genetics of acute promyelocytic leukemia
    P P Pandolfi
    Molecular Biology Program, Department of Pathology, Memorial Sloan Kettering Cancer Center, Sloan Kettering Division, Graduate School of Medical Sciences, Cornell University, 1275 York Avenue, New York, NY 10021, USA
    Oncogene 20:5726-35. 2001
    ..Here we will review the important conclusions, the novel questions and paradoxes that stem from this analysis...
  9. ncbi request reprint Histone deacetylases and transcriptional therapy with their inhibitors
    P P Pandolfi
    Department of Human Genetics, Memorial Sloan Kettering Cancer Center, Graduate School of Medical Sciences, Cornell University, New York, NY 10021, USA
    Cancer Chemother Pharmacol 48:S17-9. 2001
    ....
  10. ncbi request reprint Oncogenes and tumor suppressors in the molecular pathogenesis of acute promyelocytic leukemia
    P P Pandolfi
    Department of Human Genetics and Molecular Biology Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    Hum Mol Genet 10:769-75. 2001
    ....
  11. ncbi request reprint Aberrant mRNA translation in cancer pathogenesis: an old concept revisited comes finally of age
    Pier Paolo Pandolfi
    Molecular Biology Program, Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Oncogene 23:3134-7. 2004
    ..A number of fundamental questions remain to be addressed and a number of novel ones emerge as this exciting field evolves...
  12. ncbi request reprint Mouse modeling in oncologic preclinical and translational research
    Brett S Carver
    Cancer Biology and Genetics Program and Department of Urology, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Clin Cancer Res 12:5305-11. 2006
    ..Ultimately this will translate from preclinical mouse model trials to the development of clinical trials and protocols for cancer patients. Here we review the usefulness of mouse modeling in oncologic translational research...
  13. ncbi request reprint Identification of S664 TSC2 phosphorylation as a marker for extracellular signal-regulated kinase mediated mTOR activation in tuberous sclerosis and human cancer
    Li Ma
    Cancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Cancer Res 67:7106-12. 2007
    ..Importantly, our results indicate that Erk-mediated phosphorylation and inactivation of TSC2 can be critical in development of hamartomatous lesions in TSC and cancer pathogenesis...
  14. ncbi request reprint Inositol pentakisphosphate promotes apoptosis through the PI 3-K/Akt pathway
    Enza Piccolo
    Department of Medicine, The Sackler Institute, University College London, 5, University Street, London WC1E 6JJ, UK
    Oncogene 23:1754-65. 2004
    ..These results support a role for Ins(1,3,4,5,6)P5 as a specific inhibitor of the PI 3-K/Akt signalling pathway, that may sensitize cancer cells to the action of commonly used anticancer drugs...
  15. ncbi request reprint Signaling control of mRNA translation in cancer pathogenesis
    Eric C Holland
    Department of Surgery, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    Oncogene 23:3138-44. 2004
    ..Although many studies have correlated deregulation of protein biosynthesis with cancer, it remains to be established whether this process is necessary and/or sufficient for neoplastic transformation and metastasis...
  16. ncbi request reprint PML inhibits HIF-1alpha translation and neoangiogenesis through repression of mTOR
    Rosa Bernardi
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, Sloan Kettering Institute, 1275 York Avenue, New York, New York 10021, USA
    Nature 442:779-85. 2006
    ..Thus, our findings identify PML as a novel suppressor of mTOR and neoangiogenesis...
  17. ncbi request reprint Phosphorylation and functional inactivation of TSC2 by Erk implications for tuberous sclerosis and cancer pathogenesis
    Li Ma
    Cancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cell 121:179-93. 2005
    ..Our findings position the Ras/MAPK pathway upstream of the TSC complex and suggest that Erk may modulate mTOR signaling and contribute to disease progression through phosphorylation and inactivation of TSC2...
  18. ncbi request reprint Does the ribosome translate cancer?
    Davide Ruggero
    Molecular Biology Program, Department of Pathology, Memorial Sloan Kettering Cancer Center, Sloan Kettering Institute, 1275 York Avenue, New York, New York 10021, USA
    Nat Rev Cancer 3:179-92. 2003
    ..Although many studies have correlated deregulation of protein biosynthesis with cancer, it remains to be established whether this translates directly into an increase in cancer susceptibility, and under what circumstances...
  19. ncbi request reprint Dyskeratosis congenita and cancer in mice deficient in ribosomal RNA modification
    Davide Ruggero
    Molecular Biology Program, Department of Pathology, Memorial Sloan Kettering Cancer Center, Sloan Kettering Institute, 1275 York Avenue, New York, NY 10021, USA
    Science 299:259-62. 2003
    ..These results suggest that deregulated ribosome function is important in the initiation of DC, whereas telomere shortening may modify and/or exacerbate DC...
  20. doi request reprint Tolerability, pharmacodynamics, and pharmacokinetics studies of depsipeptide (romidepsin) in patients with acute myelogenous leukemia or advanced myelodysplastic syndromes
    Virginia M Klimek
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Clin Cancer Res 14:826-32. 2008
    ....
  21. pmc NGF-promoted axon growth and target innervation requires GITRL-GITR signaling
    Gerard W O'Keeffe
    School of Biosciences, Biomedical Building, Museum Avenue, Cardiff, CF10 3US, UK
    Nat Neurosci 11:135-42. 2008
    ..Our results reveal a previously unknown signaling loop in developing sympathetic neurons that is crucial for NGF-dependent axon growth and target innervation...
  22. ncbi request reprint ATR, PML, and CHK2 play a role in arsenic trioxide-induced apoptosis
    Yeonsoo Joe
    Laboratory of Biochemical Genetics, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 281:28764-71. 2006
    ....
  23. ncbi request reprint A CK2-dependent mechanism for degradation of the PML tumor suppressor
    Pier Paolo Scaglioni
    Cancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Cell 126:269-83. 2006
    ..These data identify a key posttranslational mechanism that controls PML protein levels and provide therapeutic means toward PML restoration through CK2 inhibition...
  24. ncbi request reprint Promyelocytic leukemia activates Chk2 by mediating Chk2 autophosphorylation
    Shutong Yang
    Laboratory of Biochemical Genetics, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 281:26645-54. 2006
    ..Thus, by fusing PML with RARalpha, the APL cells appear to have achieved functional suppression of Chk2 compromising the Chk2-p53 apoptotic pathway...
  25. ncbi request reprint Nucleophosmin and cancer
    Silvia Grisendi
    Cancer Biology and Genetics Program, Department of Pathology, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Nat Rev Cancer 6:493-505. 2006
    ..The aim of this review is to analyse the role of NPM in cancer, and examine how deregulated NPM activity (either gain or loss of function) can contribute to tumorigenesis...
  26. pmc The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice
    Mei Ling Chen
    Department of Biochemistry and Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois 60607, USA
    Genes Dev 20:1569-74. 2006
    ..Even haplodeficiency of Akt1 was sufficient to markedly attenuate the development of high-grade prostate intraepithelial neoplasia (PIN) and endometrial carcinoma. These results have significant implications for cancer therapy...
  27. ncbi request reprint Atheroma development in apolipoprotein E-null mice is not affected by partial inactivation of PTEN
    Vicente Andres
    Department of Molecular and Cellular Pathology and Therapy, Instituto de Biomedicina de Valencia IBV CSIC, 46010 Valencia, Spain
    Front Biosci 11:2739-45. 2006
    ....
  28. pmc Inhibition of mTORC1 leads to MAPK pathway activation through a PI3K-dependent feedback loop in human cancer
    Arkaitz Carracedo
    Cancer Genetics Program, Beth Israel Deaconess Cancer Center, Harvard Medical School, Boston, Massachusetts, USA
    J Clin Invest 118:3065-74. 2008
    ....
  29. pmc Acetylation of PML is involved in histone deacetylase inhibitor-mediated apoptosis
    Fumihiko Hayakawa
    Department of Hematology and Oncology, Nagoya University, Graduate School of Medicine, Nagoya 466 8550, Japan
    J Biol Chem 283:24420-5. 2008
    ..Our work provides new insights into PML regulation by post-translational modification and new information about the therapeutic mechanism of HDAC inhibitors...
  30. ncbi request reprint A novel signal transduction cascade involving direct physical interaction of the renin/prorenin receptor with the transcription factor promyelocytic zinc finger protein
    Jan H Schefe
    Center for Cardiovascular Research Institute of Pharmacology, Charite Universitatsmedizin Berlin, Hessische Strasse 3 4, 10115 Berlin, Germany
    Circ Res 99:1355-66. 2006
    ..Our data demonstrate the existence of a novel signal transduction pathway involving the ligand renin, RER, and the transcription factor PLZF, which is of physiological and putative pathophysiological relevance...
  31. doi request reprint SnapShot: PTEN signaling pathways
    Arkaitz Carracedo
    Cell 133:550.e1. 2008
  32. doi request reprint Tenets of PTEN tumor suppression
    Leonardo Salmena
    Cancer Genetics Program, Beth Israel Deaconess Cancer Center, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, New Research Building, 330 Brookline Avenue, Boston, MA 02115, USA
    Cell 133:403-14. 2008
    ..This review discusses emerging modes of PTEN function and regulation, and speculates about how manipulation of PTEN function could be used for cancer therapy...
  33. pmc PI3K pathway regulates survival of cancer stem cells residing in the perivascular niche following radiation in medulloblastoma in vivo
    Dolores Hambardzumyan
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Genes Dev 22:436-48. 2008
    ..These cellular characteristics are similar to human medulloblastomas. Finally, inhibition of Akt signaling sensitizes cells in the perivascular region to radiation-induced apoptosis...
  34. pmc Npm1 is a haploinsufficient suppressor of myeloid and lymphoid malignancies in the mouse
    Paolo Sportoletti
    Cancer Biology and Genetics Program, Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Blood 111:3859-62. 2008
    ..Our results conclusively demonstrate that Npm1 acts as a haploinsufficient tumor suppressor in the hematopoietic compartment...
  35. pmc NEDD4-1 is a proto-oncogenic ubiquitin ligase for PTEN
    Xinjiang Wang
    Cell Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 522, New York, NY 10021, USA
    Cell 128:129-39. 2007
    ..Therefore, NEDD4-1 is a potential proto-oncogene that negatively regulates PTEN via ubiquitination, a paradigm analogous to that of Mdm2 and p53...
  36. ncbi request reprint The AKT-mTOR pathway plays a critical role in the development of leiomyosarcomas
    Eva Hernando
    Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Nat Med 13:748-53. 2007
    ....
  37. ncbi request reprint The effect of deleting p110delta on the phenotype and function of PTEN-deficient B cells
    Michelle L Janas
    Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham, Cambridge, United Kingdom
    J Immunol 180:739-46. 2008
    ..These results demonstrate an epistatic relationship between p110delta and PTEN. In addition, they also suggest that additional PI3K catalytic subunits contribute to B cell development and function...
  38. pmc Identification of a tumour suppressor network opposing nuclear Akt function
    Lloyd C Trotman
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, Sloan Kettering Institute, 1275 York Avenue, New York, New York 10021, USA
    Nature 441:523-7. 2006
    ..Our results demonstrate that Pml orchestrates a nuclear tumour suppressor network for inactivation of nuclear pAkt, and thus highlight the importance of AKT compartmentalization in human cancer pathogenesis and treatment...
  39. ncbi request reprint Breaking the rules of cancer
    David R Shaffer
    Nat Med 12:14-5. 2006
  40. ncbi request reprint Role of nucleophosmin in embryonic development and tumorigenesis
    Silvia Grisendi
    Cancer Biology and Genetics Program, Department of Pathology
    Nature 437:147-53. 2005
    ..Notably, Npm1+/- mice develop a haematological syndrome with features of human MDS. Our findings uncover an essential developmental role for Npm and implicate its functional loss in tumorigenesis and MDS pathogenesis...
  41. ncbi request reprint The promyelocytic leukemia protein protects p53 from Mdm2-mediated inhibition and degradation
    Igal Louria-Hayon
    Lautenberg Center for General and Tumor Immunology, The Hebrew University Hadassah Medical School, Jerusalem 91120, Israel
    J Biol Chem 278:33134-41. 2003
    ..PML recruits Chk2 and p53 into the PML nuclear bodies and enhances p53/Chk2 interaction. Our results provide a novel mechanistic explanation for the cooperation between PML and p53 in response to DNA damage...
  42. ncbi request reprint Promyelocytic leukemia protein sensitizes tumor necrosis factor alpha-induced apoptosis by inhibiting the NF-kappaB survival pathway
    Wen Shu Wu
    Department of Molecular Pathology, The University of Texas M D Anderson Cancer Center, Houston, Texas 77030, USA
    J Biol Chem 278:12294-304. 2003
    ..Furthermore, PML(-/-) mouse embryo fibroblasts are more resistant to TNFalpha-induced apoptosis. Together this study defines a novel mechanism by which PML induces apoptosis through repression of the NF-kappaB survival pathway...
  43. ncbi request reprint The nucleolus: at the stem of immortality
    Rosa Bernardi
    Nat Med 9:24-5. 2003
  44. ncbi request reprint SUMO-1 protease-1 regulates gene transcription through PML
    Jennifer L Best
    Division of Hematology Oncology, Children s Hospital, Department of Medicine, Boston, MA 02115, USA
    Mol Cell 10:843-55. 2002
    ..SuPr-1 action on transcription was enhanced by PML, and SuPr-1 failed to activate transcription in PML-deficient fibroblasts. Our studies establish an important role for SUMO proteases in transcription...
  45. pmc Activation of Akt/protein kinase B overcomes a G(2)/m cell cycle checkpoint induced by DNA damage
    Eugene S Kandel
    Department of Molecular Genetics, College of Medicine, University of Illinois at Chicago, Chicago, Illinois 60607, USA
    Mol Cell Biol 22:7831-41. 2002
    ..We suggest that this new activity of Akt in conjunction with its antiapoptotic activity may contribute to genetic instability and could explain its frequent activation in human cancers...
  46. ncbi request reprint PTEN and TNF-alpha regulation of the intestinal-specific Cdx-2 homeobox gene through a PI3K, PKB/Akt, and NF-kappaB-dependent pathway
    Sunghoon Kim
    Department of Surgery, The University of Texas Medical Branch, Galveston, Texas 77555, USA
    Gastroenterology 123:1163-78. 2002
    ..However, the regulation of the Cdx-2 gene has not been entirely elucidated. Here, we hypothesize that Cdx-2 may be a target of PTEN signaling in the intestine...
  47. ncbi request reprint Reciprocal products of chromosomal translocations in human cancer pathogenesis: key players or innocent bystanders?
    Eduardo M Rego
    Molecular Biology Program, Dept of Pathology, Memorial Sloan Kettering Cancer Center, Graduate School of Medical Sciences, Cornell University, New York, NY 10021, USA
    Trends Mol Med 8:396-405. 2002
    ..Here, we review the current knowledge on the role of reciprocal products in cancer pathogenesis, and highlight how their expression might impact on the biology of their respective tumour types...
  48. pmc Designed transcription factors as structural, functional and therapeutic probes of chromatin in vivo. Fourth in review series on chromatin dynamics
    Fyodor D Urnov
    Sangamo BioSciences, Pt Richmond Technology Center, CA 94804, USA
    EMBO Rep 3:610-5. 2002
    ..We evaluate the potential applications of these proteins as probes of mammalian chromatin-based regulatory pathways and their potential for the therapy of human disease, highlighting leukemia in particular...
  49. ncbi request reprint Modelling haematopoietic malignancies in the mouse and therapeutical implications
    Rosa Bernardi
    Molecular Biology Program and Department of Pathology, Memorial Sloan Kettering Cancer Center, Sloan Kettering Institute, Graduate School of Medical Sciences, Cornell University, 1275 York Avenue, New York, NY 10021, USA
    Oncogene 21:3445-58. 2002
    ..Finally, we discuss the power of mouse modelling in developing and testing novel therapeutic modalities in pre-clinical studies...
  50. ncbi request reprint Mutations of the PML tumor suppressor gene in acute promyelocytic leukemia
    Carmela Gurrieri
    Molecular Biology Program and Department of Pathology, Memorial Sloan Kettering Cancer Center, Sloan Kettering Division, Graduate School of Medical Sciences, Cornell University, New York, NY 10021, USA
    Blood 103:2358-62. 2004
    ..Complete functional loss of PML is therefore selected by the APL phenotype and associates with poor prognosis and RA unresponsiveness...
  51. ncbi request reprint Role of PML and the PML-nuclear body in the control of programmed cell death
    Rosa Bernardi
    Molecular Biology Program and Department of Pathology, Memorial Sloan Kettering Cancer Center, Sloan Kettering Division, Graduate School of Medical Sciences, Cornell University, 1275 York Avenue, New York, NY 10021, USA
    Oncogene 22:9048-57. 2003
    ..Here, we will discuss the molecular mechanisms by which PML regulates these processes and the implication of these findings for cancer pathogenesis and therapy...
  52. ncbi request reprint The translation factor eIF-4E promotes tumor formation and cooperates with c-Myc in lymphomagenesis
    Davide Ruggero
    Cancer Biology and Genetics Program, and Department of Pathology, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Nat Med 10:484-6. 2004
    ..Our results implicate activation of eIF-4E as a key event in oncogenic transformation by phosphoinositide-3 kinase and Akt...
  53. pmc mTOR promotes survival and astrocytic characteristics induced by Pten/AKT signaling in glioblastoma
    Xiaoyi Hu
    Department of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Neoplasia 7:356-68. 2005
    ....
  54. ncbi request reprint Somatic induction of Pten loss in a preclinical astrocytoma model reveals major roles in disease progression and avenues for target discovery and validation
    Andrew Xiao
    Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
    Cancer Res 65:5172-80. 2005
    ....
  55. ncbi request reprint Role of the proto-oncogene Pokemon in cellular transformation and ARF repression
    Takahiro Maeda
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, Sloan Kettering Institute, 1275 York Avenue, New York, New York 10021, USA
    Nature 433:278-85. 2005
    ..Pokemon's critical role in cellular transformation makes it an attractive target for therapeutic intervention...
  56. pmc Role of Dok-1 and Dok-2 in leukemia suppression
    Masaru Niki
    Cancer Biology and Genetics Program and Dept of Pathology, Box 110, Memorial Sloan Kettering Cancer Center, 1275 York Ave, New York, NY 10021, USA
    J Exp Med 200:1689-95. 2004
    ..These findings unravel the critical and unexpected role of Dok-1 and Dok-2 in tumor suppression and control of the hematopoietic compartment homeostasis...
  57. ncbi request reprint The role of PML in tumor suppression
    Paolo Salomoni
    Molecular Biology Program and Department of Pathology, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Cell 108:165-70. 2002
    ..PML controls apoptosis, cell proliferation, and senescence. Here, we review the current understanding of its role in tumor suppression...
  58. ncbi request reprint Initiation of mRNA translation in oncogenesis: the role of eIF4E
    Lorenzo Montanaro
    Cancer Biology and Genetics Program, Department of Pathology, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New, York 10021, USA
    Cell Cycle 3:1387-9. 2004
    ....
  59. ncbi request reprint Stromal cell-derived factor-1alpha/CXCL12-induced chemotaxis of T cells involves activation of the RasGAP-associated docking protein p62Dok-1
    Seiichi Okabe
    Department of Microbiology Immunology and the Walther Oncology Center, Indiana University School of Medicine, Indianapolis, IN 46202, USA
    Blood 105:474-80. 2005
    ....
  60. ncbi request reprint PML regulates p53 stability by sequestering Mdm2 to the nucleolus
    Rosa Bernardi
    Cancer Biology and Genetics Program, Department of Pathology and Medicine, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Nat Cell Biol 6:665-72. 2004
    ..These findings demonstrate an unexpected role of PML in the nucleolar network for tumour suppression...
  61. pmc c-Abl phosphorylates Dok1 to promote filopodia during cell spreading
    Pamela J Woodring
    Molecular and Cell Biology Laboratory, The Salk Institute for Biological Sciences, 10010 North Torrey Pines Rd, La Jolla, CA 92037 1099, USA
    J Cell Biol 165:493-503. 2004
    ..Our data suggest a novel pathway by which c-Abl transduces signals to the actin cytoskeleton through phosphorylating Dok1 Y361 and recruiting Nck...
  62. ncbi request reprint Downstream of kinase, p62(dok), is a mediator of Fc gamma IIB inhibition of Fc epsilon RI signaling
    Vanessa L Ott
    Integrated Department of Immunology, National Jewish Medical and Research Center and University of Colorado Health Sciences Center, Denver, CO 80206, USA
    J Immunol 168:4430-9. 2002
    ..Taken together, these data suggest a role for p62(dok) as a mediator of Fc gamma RIIB inhibition of Fc epsilon RI signal transduction in mast cells...