Julio A Aguirre-Ghiso

Summary

Affiliation: University at Albany
Country: USA

Publications

  1. pmc PERK integrates autophagy and oxidative stress responses to promote survival during extracellular matrix detachment
    Alvaro Avivar-Valderas
    Department of Medicine, Tisch Cancer Institute, Black Family Stem Cell Institute, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    Mol Cell Biol 31:3616-29. 2011
  2. pmc Inhibition of proliferation by PERK regulates mammary acinar morphogenesis and tumor formation
    Sharon J Sequeira
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, University at Albany, State University of New York, Rensselaer, New York, United States of America
    PLoS ONE 2:e615. 2007
  3. pmc The problem of cancer dormancy: understanding the basic mechanisms and identifying therapeutic opportunities
    Julio A Aguirre-Ghiso
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, University at Albany, NY, USA
    Cell Cycle 5:1740-3. 2006
  4. pmc Models, mechanisms and clinical evidence for cancer dormancy
    Julio A Aguirre-Ghiso
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, University at Albany, State University of New York, One Discovery Drive, Rensselaer, New York 12144 3456, USA
    Nat Rev Cancer 7:834-46. 2007
  5. ncbi request reprint Green fluorescent protein tagging of extracellular signal-regulated kinase and p38 pathways reveals novel dynamics of pathway activation during primary and metastatic growth
    Julio A Aguirre-Ghiso
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, State University of New York at Albany, Albany, New York, USA
    Cancer Res 64:7336-45. 2004
  6. pmc Dual function of pancreatic endoplasmic reticulum kinase in tumor cell growth arrest and survival
    Aparna C Ranganathan
    Department of Biomedical Sciences, School of Public Health, Center for Excellence in Cancer Genomics, University at Albany, State University of New York, Rensselaer, New York, USA
    Cancer Res 68:3260-8. 2008
  7. pmc Opposing roles of mitogenic and stress signaling pathways in the induction of cancer dormancy
    Aparna C Ranganathan
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, University at Albany, New York, USA
    Cell Cycle 5:1799-807. 2006
  8. pmc Computational identification of a p38SAPK-regulated transcription factor network required for tumor cell quiescence
    Alejandro P Adam
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, SUNY Albany, Rensselaer, New York, USA
    Cancer Res 69:5664-72. 2009
  9. pmc Tumor cell dormancy induced by p38SAPK and ER-stress signaling: an adaptive advantage for metastatic cells?
    Aparna C Ranganathan
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, University at Albany, State University of New York, Rensselaer, NY 12144 3456, USA
    Cancer Biol Ther 5:729-35. 2006
  10. pmc Functional coupling of p38-induced up-regulation of BiP and activation of RNA-dependent protein kinase-like endoplasmic reticulum kinase to drug resistance of dormant carcinoma cells
    Aparna C Ranganathan
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, University at Albany, State University of New York, Rensselaer, NY 12144, USA
    Cancer Res 66:1702-11. 2006

Collaborators

Detail Information

Publications29

  1. pmc PERK integrates autophagy and oxidative stress responses to promote survival during extracellular matrix detachment
    Alvaro Avivar-Valderas
    Department of Medicine, Tisch Cancer Institute, Black Family Stem Cell Institute, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    Mol Cell Biol 31:3616-29. 2011
    ..We propose that the normal proautophagic and antioxidant PERK functions may be hijacked to promote the survival of ECM-detached tumor cells in DCIS lesions...
  2. pmc Inhibition of proliferation by PERK regulates mammary acinar morphogenesis and tumor formation
    Sharon J Sequeira
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, University at Albany, State University of New York, Rensselaer, New York, United States of America
    PLoS ONE 2:e615. 2007
    ..The possibility that deficiencies in PERK signaling could lead to hyperproliferation of the mammary epithelium and increase the likelihood of tumor formation, is of significance to the understanding of breast cancer...
  3. pmc The problem of cancer dormancy: understanding the basic mechanisms and identifying therapeutic opportunities
    Julio A Aguirre-Ghiso
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, University at Albany, NY, USA
    Cell Cycle 5:1740-3. 2006
    ..We anticipate that this will initiate a forum of discussion on the problem of cancer dormancy and stimulate investigators to study this rather unexplored but undeniably relevant clinical stage of cancer progression...
  4. pmc Models, mechanisms and clinical evidence for cancer dormancy
    Julio A Aguirre-Ghiso
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, University at Albany, State University of New York, One Discovery Drive, Rensselaer, New York 12144 3456, USA
    Nat Rev Cancer 7:834-46. 2007
    ..The advances in this field provide an emerging picture of how cancer dormancy can ensue and how it could be therapeutically targeted...
  5. ncbi request reprint Green fluorescent protein tagging of extracellular signal-regulated kinase and p38 pathways reveals novel dynamics of pathway activation during primary and metastatic growth
    Julio A Aguirre-Ghiso
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, State University of New York at Albany, Albany, New York, USA
    Cancer Res 64:7336-45. 2004
    ..This approach allows isolation and further characterization of metastatic cells with specific signaling signatures indicative of their phenotypes...
  6. pmc Dual function of pancreatic endoplasmic reticulum kinase in tumor cell growth arrest and survival
    Aparna C Ranganathan
    Department of Biomedical Sciences, School of Public Health, Center for Excellence in Cancer Genomics, University at Albany, State University of New York, Rensselaer, New York, USA
    Cancer Res 68:3260-8. 2008
    ..This is an important consideration in the development of PERK-based therapies, as its inhibition may facilitate the proliferation of slow-cycling or dormant tumor cells...
  7. pmc Opposing roles of mitogenic and stress signaling pathways in the induction of cancer dormancy
    Aparna C Ranganathan
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, University at Albany, New York, USA
    Cell Cycle 5:1799-807. 2006
    ....
  8. pmc Computational identification of a p38SAPK-regulated transcription factor network required for tumor cell quiescence
    Alejandro P Adam
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, SUNY Albany, Rensselaer, New York, USA
    Cancer Res 69:5664-72. 2009
    ..Our results identify components of the regulatory mechanisms driving p38-induced cancer cell quiescence. These may regulate dormancy of residual disease that usually precedes the onset of metastasis in many cancers...
  9. pmc Tumor cell dormancy induced by p38SAPK and ER-stress signaling: an adaptive advantage for metastatic cells?
    Aparna C Ranganathan
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, University at Albany, State University of New York, Rensselaer, NY 12144 3456, USA
    Cancer Biol Ther 5:729-35. 2006
    ..Finally, we propose that this response may recapitulate an evolutionarily conserved program of life-span extension through adaptation and tolerance to stress...
  10. pmc Functional coupling of p38-induced up-regulation of BiP and activation of RNA-dependent protein kinase-like endoplasmic reticulum kinase to drug resistance of dormant carcinoma cells
    Aparna C Ranganathan
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, University at Albany, State University of New York, Rensselaer, NY 12144, USA
    Cancer Res 66:1702-11. 2006
    ..We propose that stress-dependent activation of p38 via BiP up-regulation and PERK activation protects dormant tumor cells from stress insults, such as chemotherapy...
  11. pmc Dormancy signatures and metastasis in estrogen receptor positive and negative breast cancer
    Ryung S Kim
    Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York, United States of America
    PLoS ONE 7:e35569. 2012
    ..Furthermore, genes identified with this approach might provide insight into the mechanisms of dormancy onset and maintenance as well as dormancy models using human breast cancer cell lines...
  12. pmc A human tRNA methyltransferase 9-like protein prevents tumour growth by regulating LIN9 and HIF1-α
    Ulrike Begley
    College of Nanoscale Science and Engineering, University at Albany, State University of New York, Albany, NY, USA
    EMBO Mol Med 5:366-83. 2013
    ..Our study links hTRM9L and tRNA modifications to inhibition of tumour growth via LIN9 and HIF1-α-dependent mechanisms. It also suggests that aminoglycoside antibiotics may be useful to treat hTRM9L-deficient tumours...
  13. pmc Regulation of tumor cell dormancy by tissue microenvironments and autophagy
    Maria Soledad Sosa
    Department of Medicine and Otolaryngology, Mount Sinai School of Medicine, New York, NY, USA
    Adv Exp Med Biol 734:73-89. 2013
    ..We also explore how therapy may cause the onset of dormancy in the surviving fraction of cells after treatment and how autophagy may be a mechanism that maintains the residual cells that are viable for prolonged periods...
  14. pmc Analysis of marker-defined HNSCC subpopulations reveals a dynamic regulation of tumor initiating properties
    Paloma Bragado
    Division of Hematology and Oncology, Department of Medicine, Mount Sinai School of Medicine, New York, New York, United States of America
    PLoS ONE 7:e29974. 2012
    ..This allows multiple tumor cell subpopulations to drive tumor growth suggesting that their dynamic nature renders them a "moving target" and their eradication might require more persistent strategies...
  15. pmc ERK1/2 and p38α/β signaling in tumor cell quiescence: opportunities to control dormant residual disease
    Maria Soledad Sosa
    Department of Medicine, Division of Hematology and Oncology, Tisch Cancer Institute at Mount Sinai, New York, New York, USA
    Clin Cancer Res 17:5850-7. 2011
    ..Finally, we draw caution on the use of p38 inhibitors currently in clinical trials for different diseases as these may accelerate metastasis development...
  16. pmc ATF6alpha-Rheb-mTOR signaling promotes survival of dormant tumor cells in vivo
    Denis M Schewe
    Department of Biomedical Sciences, School of Public Health and Center for Excellence in Cancer Genomics, University at Albany, State University of New York, One Discovery Drive, Rensselaer, NY 12144, USA
    Proc Natl Acad Sci U S A 105:10519-24. 2008
    ..Targeting survival signaling by the ATF6alpha-Rheb-mTOR pathway in dormant tumor cells may favor the eradication of residual disease during dormancy periods...
  17. pmc Ribonomic and short hairpin RNA gene silencing methods to explore functional gene programs associated with tumor growth arrest
    Timothy E Baroni
    Gen NY Sis Center for Excellence in Cancer Genomics, Department of Biomedical Sciences, School of Public Health, University of Albany, SUNY, Rensselaer, NY, USA
    Methods Mol Biol 383:227-44. 2007
    ..Finally, this library of gene candidates is evaluated in vivo to address their functional role in the induction or maintenance of dormancy...
  18. pmc Dormancy of metastatic melanoma
    Liliana Ossowski
    Division of Hematology and Oncology, Department of Medicine, Mount Sinai School of Medicine, New York, NY, USA
    Pigment Cell Melanoma Res 23:41-56. 2010
    ..Ultimately, understanding the biology of dormancy and the mechanisms of dormant cell survival, might allow for their specific targeting and elimination...
  19. pmc p38α Signaling Induces Anoikis and Lumen Formation During Mammary Morphogenesis
    Huei Chi Wen
    Department of Medicine, Tisch Cancer Institute at Mount Sinai, Mount Sinai School of Medicine, New York, USA
    Sci Signal 4:ra34. 2011
    ..We conclude that p38α is crucial for the development of hollow ducts during mammary gland development, a function that may be crucial to its ability to suppress breast cancer...
  20. pmc Inhibition of eIF2alpha dephosphorylation maximizes bortezomib efficiency and eliminates quiescent multiple myeloma cells surviving proteasome inhibitor therapy
    Denis M Schewe
    Department of Medicine, Division of Hematology and Oncology, Mount Sinai School of Medicine, New York, New York, USA
    Cancer Res 69:1545-52. 2009
    ..Thus, strategies that maintain eIF2alpha in a hyperphosphorylated state may be a novel therapeutic approach to maximize bortezomib-induced apoptosis and reduce residual disease and recurrences in this type of cancer...
  21. ncbi request reprint ERK(MAPK) activity as a determinant of tumor growth and dormancy; regulation by p38(SAPK)
    Julio A Aguirre-Ghiso
    Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA
    Cancer Res 63:1684-95. 2003
    ....
  22. ncbi request reprint A region in urokinase plasminogen receptor domain III controlling a functional association with alpha5beta1 integrin and tumor growth
    Pratima Chaurasia
    Department of Medicine, Division of Hematology Oncology, Mount Sinai School of Medicine, 1 Gustave L Levy Place, New York, NY 10029, USA
    J Biol Chem 281:14852-63. 2006
    ..The relevance of this binding site, and of the lateral uPAR-alpha5beta1 integrin interaction, to ERK pathway activation and tumor growth implicates it as a possible specific target for cancer therapy...
  23. pmc On the theory of tumor self-seeding: implications for metastasis progression in humans
    Julio A Aguirre-Ghiso
    Department of Medicine and Department of Otolaryngology, Division of Hematology and Oncology, Tisch Cancer Institute at Mount Sinai, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    Breast Cancer Res 12:304. 2010
    ..A viewpoint presented here addresses the implications of these studies for human cancer metastasis...
  24. pmc Inhibition of eIF2alpha dephosphorylation inhibits ErbB2-induced deregulation of mammary acinar morphogenesis
    Sharon J Sequeira
    Department of Medicine, Division of Hematology and Oncology, Tisch Cancer Institute at Mount Sinai, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    BMC Cell Biol 10:64. 2009
    ..Here we explore whether ErbB2 modulates eIF2alpha phosphorylation and whether forced phosphorylation of the latter can antagonize ErbB2 deregulation of mammary acinar morphogenesis...
  25. pmc Microenvironments dictating tumor cell dormancy
    Paloma Bragado
    Division of Hematology and Oncology, Department of Medicine, Department of Otolaryngology, Mount Sinai School of Medicine, Tisch Cancer Institute, Black Family Stem Cell Institute, New York, NY, USA
    Recent Results Cancer Res 195:25-39. 2012
    ..For these non-mutually exclusive scenarios we review experimental and clinical evidence in their support...
  26. pmc Extracellular signal-regulated kinase 1/2 activity is not required in mammalian cells during late G2 for timely entry into or exit from mitosis
    Mio Shinohara
    Division of Molecular Medicine, Wadsworth Center, New York State Department of Health, Albany, NY 12201, USA
    Mol Biol Cell 17:5227-40. 2006
    ..Together, our data reveal that ERK1/2 activity is required in early G2 for a timely entry into mitosis but that it does not directly regulate cell cycle progression from late G2 through mitosis in normal or transformed mammalian cells...
  27. ncbi request reprint Inhibition of FAK signaling activated by urokinase receptor induces dormancy in human carcinoma cells in vivo
    Julio A Aguirre Ghiso
    Division of Medical Oncology, Department of Medicine, Rochelle Belfer Chemotherapy Foundation Laboratory, Mount Sinai School of Medicine, New York, NY 10029, USA
    Oncogene 21:2513-24. 2002
    ....
  28. ncbi request reprint Immortalized mammary epithelial cells overexpressing protein kinase C gamma acquire a malignant phenotype and become tumorigenic in vivo
    Esteban Mazzoni
    Department of Cell Biology, Research Area, Institute of Oncology Angel H Roffo, University of Buenos Aires, Argentina
    Mol Cancer Res 1:776-87. 2003
    ....
  29. pmc The urokinase receptor (u-PAR)--a link between tumor cell dormancy and minimal residual disease in bone marrow?
    Heike Allgayer
    Department of Experimental Surgery and Molecular Oncology of Solid Tumors, Medical Faculty Mannheim, University of Heidelberg, and DKFZ German Cancer Research Center Heidelberg, Germany
    APMIS 116:602-14. 2008
    ..Finally, we discuss the hypothesis that u-PAR might be an essential molecule in bone marrow disseminated tumor cells for long-term survival during dormancy, and/or reactivation of their proliferation years after primary treatment...