S W Lowe

Summary

Affiliation: Cold Spring Harbor Laboratory
Country: USA

Publications

  1. pmc Mouse genomic representational oligonucleotide microarray analysis: detection of copy number variations in normal and tumor specimens
    B Lakshmi
    Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA
    Proc Natl Acad Sci U S A 103:11234-9. 2006
  2. ncbi request reprint Tumor suppression by Ink4a-Arf: progress and puzzles
    Scott W Lowe
    Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
    Curr Opin Genet Dev 13:77-83. 2003
  3. ncbi request reprint Apoptosis in cancer
    S W Lowe
    Cold Spring Harbor Laboratory, 1 Bungtown Road, PO Box 100, Cold Spring Harbor, New York, NY 11724, USA
    Carcinogenesis 21:485-95. 2000
  4. ncbi request reprint DNA damage responses and chemosensitivity in the E mu-myc mouse lymphoma model
    C A Schmitt
    Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
    Cold Spring Harb Symp Quant Biol 65:499-510. 2000
  5. pmc Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling
    A W Lin
    Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
    Genes Dev 12:3008-19. 1998
  6. pmc Implications of cellular senescence in tissue damage response, tumor suppression, and stem cell biology
    V Krizhanovsky
    Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
    Cold Spring Harb Symp Quant Biol 73:513-22. 2008
  7. ncbi request reprint Bcl-2 mediates chemoresistance in matched pairs of primary E(mu)-myc lymphomas in vivo
    C A Schmitt
    Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
    Blood Cells Mol Dis 27:206-16. 2001
  8. pmc INK4a/ARF mutations accelerate lymphomagenesis and promote chemoresistance by disabling p53
    C A Schmitt
    Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
    Genes Dev 13:2670-7. 1999
  9. pmc Selective induction of p53 and chemosensitivity in RB-deficient cells by E1A mutants unable to bind the RB-related proteins
    A V Samuelson
    Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA
    Proc Natl Acad Sci U S A 94:12094-9. 1997
  10. ncbi request reprint Generation and analysis of genetically defined liver carcinomas derived from bipotential liver progenitors
    L Zender
    Cold Spring Harbor Laboratory, New York 11724, USA
    Cold Spring Harb Symp Quant Biol 70:251-61. 2005

Collaborators

  • Charles J Sherr
  • W Xue
  • Zhao Yue Wang
  • H O Fearnhead
  • E Hernando
  • J Mora
  • K Zhang
  • M Esteller
  • M Serrano
  • G Ferbeyre
  • Julie Teruya-Feldstein
  • Erik S Knudsen
  • Wayne Tam
  • R M Hoffman
  • R W Johnstone
  • Clemens A Schmitt
  • Michael H Wigler
  • Hans Guido Wendel
  • Lars Zender
  • Masashi Narita
  • Gregory J Hannon
  • Michael T Hemann
  • Jerry Pelletier
  • Carlos Cordon-Cardo
  • Elisa de Stanchina
  • John R Mills
  • L Zender
  • J Shi
  • Masako Narita
  • Jack T Zilfou
  • Jordan S Fridman
  • A W Lin
  • Konstantinos J Mavrakis
  • Francis Robert
  • Darren J Burgess
  • V Krizhanovsky
  • Marie Eve Bordeleau
  • Samuel M H Chen
  • Lin He
  • Clare L Scott
  • Scott C Kogan
  • Rotem Karni
  • David Mu
  • Rocio Sotillo
  • Emily E Bosco
  • Abba Malina
  • B Lakshmi
  • M T Hemann
  • Andrew V Samuelson
  • Ross A Dickins
  • Andreas Herbst
  • Mila E McCurrach
  • Zaher Nahle
  • C R Vakoc
  • E Wang
  • J Zuber
  • C Johns
  • A Rappaport
  • M Taylor
  • A V Samuelson
  • M S Soengas
  • Brigitte Brem
  • Hong Zhu
  • Lisa Lindqvist
  • Chen Ju Lin
  • Jason Doles
  • Ulrike Trojahn
  • Ricardo L A Silva
  • M Yon
  • Beicong Ma
  • Baudouin Gerard
  • David E Housman
  • Al Charest
  • John A Porco
  • Yoshitaka Hippo
  • Roderick T Bronson
  • W Richard McCombie
  • Robert Nadon
  • Harald Greger
  • Karen E Knudsen
  • Gordon Peters
  • Huan Xu
  • Elena Diaz-Rodriguez
  • Xingyue He
  • Dolores Martinez
  • David Beach
  • Johannes Zuber
  • Adrian R Krainer
  • Robert Benezra
  • Bruce J Aronow

Detail Information

Publications44

  1. pmc Mouse genomic representational oligonucleotide microarray analysis: detection of copy number variations in normal and tumor specimens
    B Lakshmi
    Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA
    Proc Natl Acad Sci U S A 103:11234-9. 2006
    ....
  2. ncbi request reprint Tumor suppression by Ink4a-Arf: progress and puzzles
    Scott W Lowe
    Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
    Curr Opin Genet Dev 13:77-83. 2003
    ..Recent evidence emerging from mouse tumor models distinguishes the activities of p16(Ink4a) and p19(Arf) in regulating tumor onset and identifies differences in their responsiveness to drugs...
  3. ncbi request reprint Apoptosis in cancer
    S W Lowe
    Cold Spring Harbor Laboratory, 1 Bungtown Road, PO Box 100, Cold Spring Harbor, New York, NY 11724, USA
    Carcinogenesis 21:485-95. 2000
    ..An intense research effort is uncovering the underlying mechanisms of apoptosis such that, in the next decade, one envisions that this information will produce new strategies to exploit apoptosis for therapeutic benefit...
  4. ncbi request reprint DNA damage responses and chemosensitivity in the E mu-myc mouse lymphoma model
    C A Schmitt
    Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
    Cold Spring Harb Symp Quant Biol 65:499-510. 2000
  5. pmc Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling
    A W Lin
    Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
    Genes Dev 12:3008-19. 1998
    ..Consequently, constitutive MAPK signaling activates p53 and p16 as tumor suppressors...
  6. pmc Implications of cellular senescence in tissue damage response, tumor suppression, and stem cell biology
    V Krizhanovsky
    Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
    Cold Spring Harb Symp Quant Biol 73:513-22. 2008
    ..Understanding extracellular cues that regulate these processes may enable new therapies for these conditions...
  7. ncbi request reprint Bcl-2 mediates chemoresistance in matched pairs of primary E(mu)-myc lymphomas in vivo
    C A Schmitt
    Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
    Blood Cells Mol Dis 27:206-16. 2001
    ..This model, able to test any other candidate gene, will be particularly useful to study the implications of specific mutations for drug action in vivo...
  8. pmc INK4a/ARF mutations accelerate lymphomagenesis and promote chemoresistance by disabling p53
    C A Schmitt
    Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
    Genes Dev 13:2670-7. 1999
    ..Consequently, INK4a/ARF and p53 mutations lead to aggressive tumors by disrupting overlapping tumor suppressor functions. These data have important implications for understanding the clinical behavior of human tumors...
  9. pmc Selective induction of p53 and chemosensitivity in RB-deficient cells by E1A mutants unable to bind the RB-related proteins
    A V Samuelson
    Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA
    Proc Natl Acad Sci U S A 94:12094-9. 1997
    ..Together, these data demonstrate that p53 accumulation and chemosensitivity are linked to E1A's oncogenic potential, and identify a strategy to selectively induce apoptosis in RB-deficient tumor cells...
  10. ncbi request reprint Generation and analysis of genetically defined liver carcinomas derived from bipotential liver progenitors
    L Zender
    Cold Spring Harbor Laboratory, New York 11724, USA
    Cold Spring Harb Symp Quant Biol 70:251-61. 2005
    ..This model provides a powerful platform for applications like cancer gene discovery or high-throughput preclinical drug testing...
  11. pmc E1A signaling to p53 involves the p19(ARF) tumor suppressor
    E de Stanchina
    Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724 USA
    Genes Dev 12:2434-42. 1998
    ..Synergistic effects between the p19(ARF) and DNA damage pathways in inducing p53 may contribute to E1A's ability to enhance radio- and chemosensitivity...
  12. ncbi request reprint Oncogene-dependent apoptosis in extracts from drug-resistant cells
    H O Fearnhead
    Cold Spring Harbor Laboratory, New York 11724, USA
    Genes Dev 11:1266-76. 1997
    ..As this killing relies on an activity generated by an oncogene, the effect of these agents should be selective for transformed cells...
  13. ncbi request reprint Inactivation of the apoptosis effector Apaf-1 in malignant melanoma
    M S Soengas
    Cold Spring Harbor Laboratory, New York 11724, USA
    Nature 409:207-11. 2001
    ..Apaf-1 loss may contribute to the low frequency of p53 mutations observed in this highly chemoresistant tumour type...
  14. pmc Oncogenic ras activates the ARF-p53 pathway to suppress epithelial cell transformation
    A W Lin
    Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA
    Proc Natl Acad Sci U S A 98:5025-30. 2001
    ..Thus, oncogenic ras can activate the ARF-p53 program to suppress epithelial cell transformation. Disruption of this program may be important during skin carcinogenesis and the development of other carcinomas...
  15. doi request reprint The Polycomb complex PRC2 supports aberrant self-renewal in a mouse model of MLL-AF9;Nras(G12D) acute myeloid leukemia
    J Shi
    Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA
    Oncogene 32:930-8. 2013
    ....
  16. ncbi request reprint The p53-Bcl-2 connection
    M T Hemann
    Cold Spring Harbor Laboratory, Howard Hughes Medical Institute, NY 11724, USA
    Cell Death Differ 13:1256-9. 2006
  17. ncbi request reprint Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
    M Serrano
    Cold Spring Harbor Laboratory, New York 11724, USA
    Cell 88:593-602. 1997
    ..Negation of ras-induced senescence may be relevant during multistep tumorigenesis...
  18. pmc Therapeutic suppression of translation initiation modulates chemosensitivity in a mouse lymphoma model
    Marie Eve Bordeleau
    Department of Biochemistry, McGill University, Montreal, Quebec, Canada
    J Clin Invest 118:2651-60. 2008
    ..These results establish that targeting translation initiation can restore drug sensitivity in vivo and provide an approach to modulating chemosensitivity...
  19. ncbi request reprint Determinants of sensitivity and resistance to rapamycin-chemotherapy drug combinations in vivo
    Hans Guido Wendel
    Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA
    Cancer Res 66:7639-46. 2006
    ..Understanding these genotype-response relationships in human tumors will be important for the effective use of rapamycin or other compounds targeting the PI(3)K pathway in the clinic...
  20. pmc The retinoblastoma tumor suppressor modifies the therapeutic response of breast cancer
    Emily E Bosco
    Department of Cell Biology, The Vontz Center for Molecular Studies, University of Cincinnati, College of Medicine, Cincinnati, Ohio 45267, USA
    J Clin Invest 117:218-28. 2007
    ..Thus, because the RB pathway is a critical determinant of tumorigenic proliferation and differential therapeutic response, it may represent a critical basis for directing therapy in the treatment of breast cancer...
  21. pmc Mad2 overexpression promotes aneuploidy and tumorigenesis in mice
    Rocio Sotillo
    Cancer Biology and Genetics Program, Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Cancer Cell 11:9-23. 2007
    ..These results demonstrate that transient Mad2 overexpression and chromosome instability can be an important stimulus in the initiation and progression of different cancer subtypes...
  22. ncbi request reprint The gene encoding the splicing factor SF2/ASF is a proto-oncogene
    Rotem Karni
    Cold Spring Harbor Laboratory, PO Box 100, Cold Spring Harbor, New York 11724, USA
    Nat Struct Mol Biol 14:185-93. 2007
    ..Knockdown of either SF2/ASF or isoform-2 of S6K1 is sufficient to reverse transformation caused by the overexpression of SF2/ASF in vitro and in vivo. Thus, SF2/ASF can act as an oncoprotein and is a potential target for cancer therapy...
  23. pmc Role of the chromobox protein CBX7 in lymphomagenesis
    Clare L Scott
    Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA
    Proc Natl Acad Sci U S A 104:5389-94. 2007
    ..These data identify CBX7 as a chromobox protein causally linked to cancer development and may help explain the low frequency of INK4a/ARF mutations observed in human follicular lymphoma...
  24. ncbi request reprint Snapshot: genetic mouse models of cancer
    Lars Zender
    Cell 129:838. 2007
  25. pmc Tumorigenic activity and therapeutic inhibition of Rheb GTPase
    Konstantinos J Mavrakis
    Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Genes Dev 22:2178-88. 2008
    ..Of these, only eIF4E was able to enhance lymphomagenesis in vivo. In summary, the Rheb GTPase is an oncogenic activity upstream of mTORC1 and eIF4E and a direct therapeutic target of farnesyltransferase inhibitors in cancer...
  26. pmc mTORC1 promotes survival through translational control of Mcl-1
    John R Mills
    Department of Biochemistry, McGill University, Montreal, QC, Canada H3G 1Y6
    Proc Natl Acad Sci U S A 105:10853-8. 2008
    ..Our results indicate that the extent by which rapamycin can modulate expression of Mcl-1 is an important feature of the rapamycin response...
  27. ncbi request reprint microRNAs join the p53 network--another piece in the tumour-suppression puzzle
    Lin He
    Watson School of Biological Sciences, Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA
    Nat Rev Cancer 7:819-22. 2007
    ..These data reinforce the growing awareness that non-coding RNAs are key players in tumour development by placing miRNAs in a central role in a well-known tumour-suppressor network...
  28. pmc Topoisomerase levels determine chemotherapy response in vitro and in vivo
    Darren J Burgess
    Cold Spring Harbor Laboratory and Howard Hughes Medical Institute, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA
    Proc Natl Acad Sci U S A 105:9053-8. 2008
    ..These results highlight the utility of pooled shRNA screens for identifying genetic determinants of chemotherapy response and suggest strategies for improving the effectiveness of topoisomerase poisons in the clinic...
  29. ncbi request reprint Probing tumor phenotypes using stable and regulated synthetic microRNA precursors
    Ross A Dickins
    Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
    Nat Genet 37:1289-95. 2005
    ..In practice, this primary microRNA-based short hairpin RNA vector system is markedly similar to cDNA overexpression systems and is a powerful tool for studying gene function in cells and animals...
  30. ncbi request reprint 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
    ....
  31. ncbi request reprint Apoptosis and chemoresistance in transgenic cancer models
    Clemens A Schmitt
    Max Delbruck Center for Molecular Medicine, Department of Hematology Oncology, Charité Campus and Virchow Hospital, Humboldt University, Augustenburger Platz 1, 13353 Berlin, Germany
    J Mol Med (Berl) 80:137-46. 2002
    ....
  32. ncbi request reprint Dissecting p53 tumor suppressor functions in vivo
    Clemens A Schmitt
    Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA
    Cancer Cell 1:289-98. 2002
    ..Therefore, apoptosis is the only p53 function selected against during lymphoma development, whereas defective cell-cycle checkpoints and aneuploidy are mere byproducts of p53 loss...
  33. ncbi request reprint Direct coupling of the cell cycle and cell death machinery by E2F
    Zaher Nahle
    Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA
    Nat Cell Biol 4:859-64. 2002
    ..The data also underscore how cell cycle progression can be coupled to the apoptotic machinery...
  34. ncbi request reprint Tumour suppression: something for nothing?
    Elisa de Stanchina
    Nat Cell Biol 4:E275-6. 2002
  35. ncbi request reprint An epi-allelic series of p53 hypomorphs created by stable RNAi produces distinct tumor phenotypes in vivo
    Michael T Hemann
    Cold Spring Harbor Laboratory, Watson School of Biological Sciences, Cold Spring Harbor, New York 11724, USA
    Nat Genet 33:396-400. 2003
    ..In addition, intrinsic differences between individual shRNA expression vectors targeting the same gene can be used to create an 'epi-allelic series' for dissecting gene function in vivo...
  36. ncbi request reprint Rb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence
    Masashi Narita
    Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA
    Cell 113:703-16. 2003
    ..These results provide a molecular explanation for the stability of the senescent state, as well as new insights into the action of Rb as a tumor suppressor...
  37. ncbi request reprint Control of apoptosis by p53
    Jordan S Fridman
    Incyte Corporation, Wilmington, DE 19880, USA
    Oncogene 22:9030-40. 2003
    ..Understanding this network in more detail will provide insights into cancer and other diseases, and will identify strategies to improve their therapeutic treatment...
  38. ncbi request reprint Executing cell senescence
    Masashi Narita
    Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
    Cell Cycle 3:244-6. 2004
    ..Here we show how these changes might contribute to the stability of the senescent state...
  39. ncbi request reprint Reversing drug resistance in vivo
    Hans Guido Wendel
    Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA
    Cell Cycle 3:847-9. 2004
    ..They also illustrate the importance of tailoring cancer therapy based on tumor genotype...
  40. ncbi request reprint Rb inactivation promotes genomic instability by uncoupling cell cycle progression from mitotic control
    Eva Hernando
    Department of Pathology, Memorial Sloan Kettering Cancer Center New York, New York 10021, USA
    Nature 430:797-802. 2004
    ....
  41. ncbi request reprint Intrinsic tumour suppression
    Scott W Lowe
    Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA
    Nature 432:307-15. 2004
    ..Although oncogenic mutations that disable such networks can have profound and varied effects on tumour evolution, they may leave intact latent tumour-suppressive potential that can be harnessed therapeutically...
  42. pmc A conserved element in Myc that negatively regulates its proapoptotic activity
    Andreas Herbst
    Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA
    EMBO Rep 6:177-83. 2005
    ..These findings reveal a role for MbIII in Myc biology, and establish that the oncogenic capacity of Myc is linked directly to its ability to temper the apoptotic response...
  43. ncbi request reprint p400 is required for E1A to promote apoptosis
    Andrew V Samuelson
    Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA
    J Biol Chem 280:21915-23. 2005
    ..These results identify p400 as a regulator of the ARF-p53 pathway and a component of the cellular machinery that couples proliferation to cell death...
  44. ncbi request reprint The price of tumour suppression?
    Gerardo Ferbeyre
    Nature 415:26-7. 2002