Amato Giaccia

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. doi request reprint Role of carcinoma-associated fibroblasts and hypoxia in tumor progression
    Amato J Giaccia
    Department of Radiation Oncology, Division of Cancer and Radiation Biology, Stanford University School of Medicine, Stanford, CA 94305 5152, USA
    Curr Top Microbiol Immunol 345:31-45. 2010
  2. pmc PHD2 in tumour angiogenesis
    D A Chan
    Department of Radiation Oncology, University of California, 2340 Sutter Street, S 332, Box 1331, San Francisco, CA 94143 1331, USA
    Br J Cancer 103:1-5. 2010
  3. pmc Blood and bones: Osteoblastic HIF signaling regulates erythropoiesis
    Colleen Wu
    Division of Radiation and Cancer Biology Department of Radiation Oncology Center for Clinical Sciences Research Stanford University Stanford, CA USA
    Cell Cycle 11:2221-2. 2012
  4. pmc Hif-1alpha regulates differentiation of limb bud mesenchyme and joint development
    Sylvain Provot
    Endocrine Unit, Department of Medicine, Massachusetts General Hospital Harvard Medical School, Boston, MA 02114, USA
    J Cell Biol 177:451-64. 2007
  5. pmc Regulation of the histone demethylase JMJD1A by hypoxia-inducible factor 1 alpha enhances hypoxic gene expression and tumor growth
    Adam J Krieg
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Center for Clinical Sciences Research, Stanford University, Stanford, CA 94303 5152, USA
    Mol Cell Biol 30:344-53. 2010
  6. pmc The biology of hypoxia: the role of oxygen sensing in development, normal function, and disease
    Amato J Giaccia
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305, USA
    Genes Dev 18:2183-94. 2004
  7. ncbi request reprint Anoxia is necessary for tumor cell toxicity caused by a low-oxygen environment
    Ioanna Papandreou
    Department of Radiation Oncology, Division of Radiation and Cancer Biology, Stanford University School of Medicine, Stanford, California, USA
    Cancer Res 65:3171-8. 2005
  8. ncbi request reprint An evaluation of tumor oxygenation and gene expression in patients with early stage non-small cell lung cancers
    Quynh Thu Le
    Department of Radiation Oncology, Stanford University Medical Center, Stanford, California 94305 5847, USA
    Clin Cancer Res 12:1507-14. 2006
  9. ncbi request reprint A noninvasive approach for assessing tumor hypoxia in xenografts: developing a urinary marker for hypoxia
    Daniel W Nelson
    Department of Radiation Oncology, Stanford University, Stanford, California 94305 5847, USA
    Cancer Res 65:6151-8. 2005
  10. ncbi request reprint Lysyl oxidase is essential for hypoxia-induced metastasis
    Janine T Erler
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305, USA
    Nature 440:1222-6. 2006

Research Grants

  1. CTGF in Pancreatic Tumor Growth
    Amato J Giaccia; Fiscal Year: 2010
  2. HYPOXIA AND GENE REPRESSION
    Amato Giaccia; Fiscal Year: 2006
  3. HYPOXIA AND GENE REPRESSION
    Amato Giaccia; Fiscal Year: 2007
  4. HYPOXIA AND GENE REPRESSION
    Amato Giaccia; Fiscal Year: 2009
  5. CTGF in Pancreatic Tumor Growth
    Amato Giaccia; Fiscal Year: 2009
  6. CTGF in Pancreatic Tumor Growth
    Amato Giaccia; Fiscal Year: 2007
  7. HYPOXIA AND GENE REPRESSION
    Amato Giaccia; Fiscal Year: 2005
  8. Tumor Hypoxia: Molecular Studies & Clinical Exploitation
    Amato Giaccia; Fiscal Year: 2007
  9. CTGF in Pancreatic Tumor Growth
    Amato Giaccia; Fiscal Year: 2006
  10. Postdoctoral Training in the Radiation Sciences
    Amato Giaccia; Fiscal Year: 2007

Detail Information

Publications88

  1. doi request reprint Role of carcinoma-associated fibroblasts and hypoxia in tumor progression
    Amato J Giaccia
    Department of Radiation Oncology, Division of Cancer and Radiation Biology, Stanford University School of Medicine, Stanford, CA 94305 5152, USA
    Curr Top Microbiol Immunol 345:31-45. 2010
    ..The potential role of hypoxia in modulating the differentiation and activity of CAFs, and the therapeutical implications of targeting CAFs for anticancer therapy are discussed...
  2. pmc PHD2 in tumour angiogenesis
    D A Chan
    Department of Radiation Oncology, University of California, 2340 Sutter Street, S 332, Box 1331, San Francisco, CA 94143 1331, USA
    Br J Cancer 103:1-5. 2010
    ..This review summarises our current understanding of PHD2 and tumour angiogenesis, focusing on the influences of PHD2 on vascular normalisation and neovascularisation...
  3. pmc Blood and bones: Osteoblastic HIF signaling regulates erythropoiesis
    Colleen Wu
    Division of Radiation and Cancer Biology Department of Radiation Oncology Center for Clinical Sciences Research Stanford University Stanford, CA USA
    Cell Cycle 11:2221-2. 2012
    ..Comment on: Rankin EB, et al. Cell 2012; 149:63-74...
  4. pmc Hif-1alpha regulates differentiation of limb bud mesenchyme and joint development
    Sylvain Provot
    Endocrine Unit, Department of Medicine, Massachusetts General Hospital Harvard Medical School, Boston, MA 02114, USA
    J Cell Biol 177:451-64. 2007
    ..In addition, mutant mice show a striking impairment of joint development. Our study demonstrates a crucial, and previously unrecognized, role of Hif-1alpha in early chondrogenesis and joint formation...
  5. pmc Regulation of the histone demethylase JMJD1A by hypoxia-inducible factor 1 alpha enhances hypoxic gene expression and tumor growth
    Adam J Krieg
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Center for Clinical Sciences Research, Stanford University, Stanford, CA 94303 5152, USA
    Mol Cell Biol 30:344-53. 2010
    ..Thus, hypoxic regulation of JMJD1A acts as a signal amplifier to facilitate hypoxic gene expression, ultimately enhancing tumor growth...
  6. pmc The biology of hypoxia: the role of oxygen sensing in development, normal function, and disease
    Amato J Giaccia
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305, USA
    Genes Dev 18:2183-94. 2004
    ..It will also comment on future directions for this exciting field...
  7. ncbi request reprint Anoxia is necessary for tumor cell toxicity caused by a low-oxygen environment
    Ioanna Papandreou
    Department of Radiation Oncology, Division of Radiation and Cancer Biology, Stanford University School of Medicine, Stanford, California, USA
    Cancer Res 65:3171-8. 2005
    ..Taken together, these findings indicate that additional molecular events are triggered by anoxia in a HIF-1-independent manner, and these changes are necessary for cell death observed in low-oxygen environments...
  8. ncbi request reprint An evaluation of tumor oxygenation and gene expression in patients with early stage non-small cell lung cancers
    Quynh Thu Le
    Department of Radiation Oncology, Stanford University Medical Center, Stanford, California 94305 5847, USA
    Clin Cancer Res 12:1507-14. 2006
    ..To directly assess tumor oxygenation in resectable non-small cell lung cancers (NSCLC) and to correlate tumor pO2 and the selected gene and protein expression to treatment outcomes...
  9. ncbi request reprint A noninvasive approach for assessing tumor hypoxia in xenografts: developing a urinary marker for hypoxia
    Daniel W Nelson
    Department of Radiation Oncology, Stanford University, Stanford, California 94305 5847, USA
    Cancer Res 65:6151-8. 2005
    ..The 5HRE beta-hCG reporter system described here enables serial, noninvasive monitoring of tumor hypoxia in a mouse model by measuring a urinary reporter protein...
  10. ncbi request reprint Lysyl oxidase is essential for hypoxia-induced metastasis
    Janine T Erler
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305, USA
    Nature 440:1222-6. 2006
    ..Furthermore, LOX may be required to create a niche permissive for metastatic growth. Our findings indicate that LOX is essential for hypoxia-induced metastasis and is a good therapeutic target for preventing and treating metastases...
  11. ncbi request reprint Dead cells don't form tumors: HIF-dependent cytotoxins
    Patrick D Sutphin
    Program in Cancer Biology, Department of Radiation Oncology, Stanford University, Stanford, California 94305 5787, USA
    Cell Cycle 3:160-3. 2004
    ..Specific elimination of HIF-activated cells represents a potential mechanism for inhibiting tumor growth, with the potential advantage of sparing the patient of the normal tissue toxicity associated with current treatment options...
  12. pmc Adaptive myogenesis under hypoxia
    Zhong Yun
    Department of Radiation Oncology, Stanford University School of Medicine, 269 Campus Dr, CCSR 1250, Stanford, CA 94305, USA
    Mol Cell Biol 25:3040-55. 2005
    ..Our studies indicate that the ischemic muscle can be repaired via the adaptive differentiation of myogenic precursors, which depends on the levels of oxygen and glucose in the ischemic microenvironment...
  13. pmc Hypoxia-inducible mir-210 regulates normoxic gene expression involved in tumor initiation
    Xin Huang
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94025, USA
    Mol Cell 35:856-67. 2009
    ..Taken together, these data implicate an important role for mir-210 in regulating the hypoxic response of tumor cells and tumor growth...
  14. ncbi request reprint ATR/ATM targets are phosphorylated by ATR in response to hypoxia and ATM in response to reoxygenation
    Ester M Hammond
    Center for Clinical Sciences Research, Department of Radiation Oncology, Stanford University, Stanford, California 94303 5152, USA
    J Biol Chem 278:12207-13. 2003
    ..Taken together these data implicate both ATR and ATM as critical roles in the response of hypoxia and reperfusion in solid tumors...
  15. ncbi request reprint Comparison of hypoxia-induced replication arrest with hydroxyurea and aphidicolin-induced arrest
    Ester M Hammond
    Center for Clinical Sciences Research, Department of Radiation Oncology, Stanford University, Stanford, CA 94303 5152, USA
    Mutat Res 532:205-13. 2003
    ..In contrast replication arrest induced by severe hypoxia is sensed exclusively through ATR, with ATM only having a role to play after re-oxygenation...
  16. pmc Hypoxia-induced lysyl oxidase is a critical mediator of bone marrow cell recruitment to form the premetastatic niche
    Janine T Erler
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Cancer Cell 15:35-44. 2009
    ..CD11b+ cells and LOX also colocalize in biopsies of human metastases. Our findings demonstrate a critical role for LOX in premetastatic niche formation and support targeting LOX for the treatment and prevention of metastatic disease...
  17. ncbi request reprint Inhibition of PPAR gamma 2 gene expression by the HIF-1-regulated gene DEC1/Stra13: a mechanism for regulation of adipogenesis by hypoxia
    Zhong Yun
    Department of Radiation Oncology, Stanford University, Stanford, CA 94305, USA
    Dev Cell 2:331-41. 2002
    ..These data indicate that an O(2)-sensitive signaling mechanism regulates adipogenesis. Thus, agents that regulate HIF-1 activity or O(2) sensing may be used to inhibit adipogenesis and control obesity...
  18. ncbi request reprint Transient changes in oxygen tension inhibit osteogenic differentiation and Runx2 expression in osteoblasts
    Ali Salim
    Department of Surgery, Stanford University School of Medicine, Stanford, California 94305 5148, USA
    J Biol Chem 279:40007-16. 2004
    ....
  19. ncbi request reprint Plasma osteopontin is an independent prognostic marker for head and neck cancers
    David Petrik
    Department of Radiation Oncology, Stanford University, Stanford, CA, USA
    J Clin Oncol 24:5291-7. 2006
    ..To confirm the relationship between plasma osteopontin (OPN) levels and treatment outcomes in head and neck squamous cell carcinoma (HNSCC) patients in an expanded study...
  20. ncbi request reprint Hypoxia upregulates osteopontin expression in NIH-3T3 cells via a Ras-activated enhancer
    Yonghua Zhu
    Department of Radiation Oncology, 875 Blake Wilbur Dr, R CC G228, Stanford University, Stanford, CA 94305, USA
    Oncogene 24:6555-63. 2005
    ..Taken together, these results have identified a new hypoxia responsive transcriptional enhancer that is regulated by Akt signaling...
  21. ncbi request reprint Identification of hypoxia-regulated proteins in head and neck cancer by proteomic and tissue array profiling
    Yijun Chen
    Department of Radiation Oncology, Center for Clinical Sciences Research, Department of Surgery, Palo Alto VA Health Care System, Palo Alto, CA, USA
    Cancer Res 64:7302-10. 2004
    ..These data suggest that IKKbeta is a novel endogenous marker of tumor hypoxia and may represent a new target for anticancer therapy...
  22. pmc DNA damage during reoxygenation elicits a Chk2-dependent checkpoint response
    Rachel A Freiberg
    CCSR South, Room 1255, Department of Radiation Oncology, Stanford University, Stanford, CA 94305 5152, USA
    Mol Cell Biol 26:1598-609. 2006
    ....
  23. pmc Validation of lysyl oxidase as a prognostic marker for metastasis and survival in head and neck squamous cell carcinoma: Radiation Therapy Oncology Group trial 90-03
    Quynh Thu Le
    Department of Radiation Oncology, Stanford University, Stanford, CA 94305 5847, USA
    J Clin Oncol 27:4281-6. 2009
    ..To validate lysyl oxidase (LOX), a hypoxia-related protein, as a marker for metastasis in an independent head and neck cancer (HNC) patient group enrolled onto a prospective trial...
  24. ncbi request reprint Galectin-1: a link between tumor hypoxia and tumor immune privilege
    Quynh Thu Le
    Department of Radiation Oncology, Stanford University Medical Center, 875 Blake Wilbur Drive, Stanford, CA 94305 5847, USA
    J Clin Oncol 23:8932-41. 2005
    ..To identify a 15-KDa novel hypoxia-induced secreted protein in head and neck squamous cell carcinomas (HNSCC) and to determine its role in malignant progression...
  25. ncbi request reprint Imaging tumoral hypoxia: oxygen concentrations and beyond
    Edward E Graves
    Radiation Oncology Radiation Biology, Department of Radiation Oncology, Stanford University, School of Medicine, Stanford, California 94305 5847, USA
    Oncology (Williston Park) 21:368-76; discussion 377-8, 384. 2007
    ..Finally, we will evaluate the clinical potential of oxygen- and molecular-specific techniques for imaging hypoxia, and discuss how these methods will individually and collectively advance oncology...
  26. ncbi request reprint Mutations in the PI3K/PTEN/TSC2 pathway contribute to mammalian target of rapamycin activity and increased translation under hypoxic conditions
    Fiona Kaper
    Department of Radiation Oncology, Stanford University, Stanford, CA 94305 5152, USA
    Cancer Res 66:1561-9. 2006
    ..Therefore, failure to inhibit mTOR under oxygen-limiting conditions can be affected by upstream activating mutations and increases the survival and growth of hypoxic tumor cells...
  27. ncbi request reprint Expression and prognostic significance of a panel of tissue hypoxia markers in head-and-neck squamous cell carcinomas
    Quynh Thu Le
    Department of Radiation Oncology, Stanford University, Stanford, CA 94305 5847, USA
    Int J Radiat Oncol Biol Phys 69:167-75. 2007
    ..To investigate the expression pattern of hypoxia-induced proteins identified as being involved in malignant progression of head-and-neck squamous cell carcinoma (HNSCC) and to determine their relationship to tumor pO(2) and prognosis...
  28. ncbi request reprint Oxygen sensitivity of reporter genes: implications for preclinical imaging of tumor hypoxia
    Ivana Cecic
    Department of Radiation Oncology and Molecular Imaging Program, Stanford, Stanford University School of Medicine, Stanford, CA 94305 5847, USA
    Mol Imaging 6:219-28. 2007
    ..These results demonstrate that combining beta-galactosidase with the DDAOG optical probe may be a robust reporter system for the in vivo study of tumor hypoxia...
  29. ncbi request reprint The role of p53 in hypoxia-induced apoptosis
    Ester M Hammond
    Department of Radiation Oncology, Centre for Clinical Sciences Research, Stanford University, Stanford, CA 94303 5152, USA
    Biochem Biophys Res Commun 331:718-25. 2005
    ..In contrast to the response to DNA-damaging agents, hypoxia-induced p53 has little or no transcriptional transactivation capabilities and instead seems to function primarily as a transrepressor in order to induce apoptosis...
  30. ncbi request reprint Checking in on hypoxia/reoxygenation
    Rachel A Freiberg
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Center for Clinical Sciences Research, Stanford University, Stanford, California 94303 5152, USA
    Cell Cycle 5:1304-7. 2006
    ..In contrast, loss of a p53-mediated reoxygenation-induced G1 arrest does not correlate with increased sensitivity to hypoxia/reoxygenation...
  31. pmc Hypoxia links ATR and p53 through replication arrest
    Ester M Hammond
    Center for Clinical Sciences Research, Department of Radiation Oncology, Stanford University, Stanford, CA 94303 5152, USA
    Mol Cell Biol 22:1834-43. 2002
    ....
  32. ncbi request reprint Epigenetic changes in tumor Fas levels determine immune escape and response to therapy
    Heather L Maecker
    Department of Radiation Oncology, Stanford University Medical Center, CCSR South, 269 Campus Drive, Stanford, California 94305, USA
    Cancer Cell 2:139-48. 2002
    ..This work demonstrates the importance of epigenetic modification of Fas in tumor progression and immune evasion, and emphasizes the essential interplay between Fas and innate immunity in the control of chemoresistant tumors...
  33. ncbi request reprint Identification of osteopontin as a prognostic plasma marker for head and neck squamous cell carcinomas
    Quynh Thu Le
    Department of Radiation Oncology, Center for Clinical Science Research South, Stanford, California 94305 5152, USA
    Clin Cancer Res 9:59-67. 2003
    ..Tumor hypoxia modifies treatment efficacy and promotes tumor progression. Here, we investigated the relationship between osteopontin (OPN), tumor pO(2), and prognosis in patients with head and neck squamous cell carcinomas (HNSCC)...
  34. ncbi request reprint Tumor deprivation of oxygen and tumor suppressor gene function
    Zhong Yun
    Department of Radiation Oncology, Stanford University School of Medicine, CA, USA
    Methods Mol Biol 223:485-504. 2003
  35. ncbi request reprint Investigating hypoxic tumor physiology through gene expression patterns
    Nicholas C Denko
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Oncogene 22:5907-14. 2003
    ..Understanding the evolutionary pressure to develop a 'hypoxic response' provides a framework to investigate the biology of the hypoxic tumor microenvironment...
  36. ncbi request reprint Therapeutic exploitation of the physiological and molecular genetic alterations in head and neck cancer
    Quynh Thu Le
    Stanford University School of Medicine, Department of Radiation Oncology, Stanford, California 94305 5032, USA
    Clin Cancer Res 9:4287-95. 2003
    ..This review will summarize these new molecular and physiological based strategies that can be used for both treatment and chemoprevention of head and neck squamous cell carcinoma...
  37. ncbi request reprint Oxygen-dependent regulation of adipogenesis
    Lillian M Swiersz
    Department of Gynecology and Obstetrics, Stanford University, California 94305, USA
    Methods Enzymol 381:387-95. 2004
  38. ncbi request reprint XBP1 is essential for survival under hypoxic conditions and is required for tumor growth
    Lorenzo Romero-Ramirez
    Department of Radiation Oncology, Stanford University, Stanford, California 94305 5152, USA
    Cancer Res 64:5943-7. 2004
    ..Taken together, these studies directly implicate XBP1 as an essential survival factor for hypoxic stress and tumor growth...
  39. pmc Hypoxia in models of lung cancer: implications for targeted therapeutics
    Edward E Graves
    Department of Radiation Oncology, Stanford University, California 94305 5847, USA
    Clin Cancer Res 16:4843-52. 2010
    ....
  40. ncbi request reprint The role of ATM and ATR in the cellular response to hypoxia and re-oxygenation
    Ester M Hammond
    Department of Radiation Oncology, Centre for Clinical Sciences Research, Stanford University, Stanford, CA 94303 5152, USA
    DNA Repair (Amst) 3:1117-22. 2004
    ..Therefore both ATR and ATM have a role to play in hypoxia/re-oxygenation...
  41. pmc A novel aldehyde dehydrogenase-3 activator (Alda-89) protects submandibular gland function from irradiation without accelerating tumor growth
    Nan Xiao
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA, USA
    Clin Cancer Res 19:4455-64. 2013
    ....
  42. ncbi request reprint HIF-1 as a target for drug development
    Amato Giaccia
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305 5468, USA
    Nat Rev Drug Discov 2:803-11. 2003
    ....
  43. pmc Renal oxygenation suppresses VHL loss-induced senescence that is caused by increased sensitivity to oxidative stress
    Scott M Welford
    Department of Radiation Oncology, Stanford University School of Medicine, 1235 CCSR, 269 Campus Drive, Stanford, CA 93025, USA
    Mol Cell Biol 30:4595-603. 2010
    ..Together, these data demonstrate that in vivo oxygenation promotes tolerance of VHL loss in renal epithelia, which may promote the development of renal carcinoma...
  44. ncbi request reprint Energy regulation: HIF MXIes it up with the C-MYC powerhouse
    Patrick D Sutphin
    Department of Radiation Oncology, Stanford University, Stanford, CA 94305, USA
    Dev Cell 12:845-6. 2007
    ..In the May 2007 issue of Cancer Cell, Zhang and colleagues determine that the hypoxia-inducible factor family of transcriptional factors regulate mitochondrial biogenesis through inhibition of C-MYC...
  45. pmc Functional analysis of p53 binding under differential stresses
    Adam J Krieg
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University, Stanford, CA 94303 5152, USA
    Mol Cell Biol 26:7030-45. 2006
    ..Taken together, these experiments describe the identification of novel p53 target genes and the subsequent discovery of distinctly different expression phenomena for p53 target genes under different stress scenarios...
  46. ncbi request reprint Antiangiogenic therapy and p53
    Ester M Hammond
    Center for Clinical Sciences Research, Department of Radiation Oncology, Stanford University, Stanford, CA 94303 5152, USA
    Science 297:471; discussion 471. 2002
  47. pmc The metastasis-associated gene Prl-3 is a p53 target involved in cell-cycle regulation
    Shashwati Basak
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Mol Cell 30:303-14. 2008
    ..Our findings highlight key dose-dependent functions of Prl-3 in both positive and negative regulation of cell-cycle progression and provide insight into Prl-3's role in cancer progression...
  48. pmc Genome-wide analysis of p53 under hypoxic conditions
    Ester M Hammond
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University, Stanford, CA 94303 5152, USA
    Mol Cell Biol 26:3492-504. 2006
    ..This study defines a new role for residues 53 and 54 of p53 in regulating transrepression and demonstrates that 25-26 and 53-54 work in the same pathway to induce apoptosis through gene repression...
  49. pmc Hypoxia-inducible regulation of a prodrug-activating enzyme for tumor-specific gene therapy
    Toru Shibata
    Department of Radiation Oncology, Stanford University School of Medicine, CA 94305 5152, USA
    Neoplasia 4:40-8. 2002
    ....
  50. ncbi request reprint Inhibition of ATR leads to increased sensitivity to hypoxia/reoxygenation
    Ester M Hammond
    Center for Clinical Sciences Research, Department of Radiation Oncology, Stanford University, Stanford, California 94305, USA
    Cancer Res 64:6556-62. 2004
    ..In conclusion, ATR and Chk1 play critical roles in the cellular response to hypoxia/reoxygenation, and inhibitors of ATR and Chk1 represent new hypoxic cell cytotoxins...
  51. pmc Bringing H2AX into the angiogenesis family
    Erinn B Rankin
    Department of Radiation Oncology, Division of Radiation and Cancer Biology, Center for Clinical Sciences Research, Stanford University, Stanford, CA 94303 5152, USA
    Cancer Cell 15:459-61. 2009
    ..Paradoxically, Economopoulou et al. recently reported that a DNA damage response protein, H2AX, promotes tumor growth and angiogenesis...
  52. ncbi request reprint The roles of Chk 1 and Chk 2 in hypoxia and reoxygenation
    Ester M Hammond
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Center for Clinical Sciences Research, Stanford University, Stanford, California 94303 5152, USA
    Cancer Lett 238:161-7. 2006
    ..Loss or inhibition of either kinase sensitizes cells to hypoxia/reoxygenation indicating that either or both could represent significant therapeutic targets...
  53. pmc The RGD domain of human osteopontin promotes tumor growth and metastasis through activation of survival pathways
    Donald Courter
    Department of Radiation Oncology, Stanford University, Stanford, California, United States of America
    PLoS ONE 5:e9633. 2010
    ..Here, we use genetic approaches to systematically investigate the function of the RGD domain in different OPN isoforms on tumor progression and metastasis for 2 different solid tumor models...
  54. ncbi request reprint Targeting the loss of the von Hippel-Lindau tumor suppressor gene in renal cell carcinoma cells
    Patrick D Sutphin
    Program in Cancer Biology, Department of Radiation Oncology, Stanford University, Stanford, California 94305, USA
    Cancer Res 67:5896-905. 2007
    ....
  55. pmc Tumor vasculature is regulated by PHD2-mediated angiogenesis and bone marrow-derived cell recruitment
    Denise A Chan
    Center for Clinical Sciences Research, Department of Radiation Oncology, Stanford University, Stanford, CA 94305, USA
    Cancer Cell 15:527-38. 2009
    ..PHD2 levels are decreased in human cancers, compared with corresponding normal tissue, and correlate with an increase in mature blood vessels. Thus, PHD2 plays a critical role in regulating tumor angiogenesis...
  56. pmc AXL is an essential factor and therapeutic target for metastatic ovarian cancer
    Erinn B Rankin
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Center for Clinical Sciences Research, Stanford University, Stanford, California 94305 5152, USA
    Cancer Res 70:7570-9. 2010
    ..Furthermore, this study defines the soluble AXL receptor as a therapeutic candidate agent for treatment of metastatic ovarian cancer, for which current therapies are ineffective...
  57. pmc Notch1 is an effector of Akt and hypoxia in melanoma development
    Barbara Bedogni
    Division of Radiation and Cancer Biology, Stanford University, Stanford, California, USA
    J Clin Invest 118:3660-70. 2008
    ..Taken together, these findings demonstrate that Notch1 is a key effector of both Akt and hypoxia in melanoma development and identify the Notch signaling pathway as a potential therapeutic target in melanoma treatment...
  58. ncbi request reprint In vitro expansion of adipose-derived adult stromal cells in hypoxia enhances early chondrogenesis
    Yue Xu
    Department of Surgery, School of Medicine, Stanford University, Stanford, California 94305, USA
    Tissue Eng 13:2981-93. 2007
    ..This study is relevant for the future application of cell-based therapies involving cartilage tissue regeneration...
  59. ncbi request reprint Hypoxia, gene expression, and metastasis
    Denise A Chan
    Department of Radiation Oncology, Division of Cancer and Radiation Biology, Stanford University School of Medicine, Stanford, CA 94305 5152, USA
    Cancer Metastasis Rev 26:333-9. 2007
    ..Particular attention is given to recent studies of specific genes involved in the key steps of metastasis, including extracellular matrix interactions, migration, and proliferation...
  60. ncbi request reprint Role of prolyl hydroxylation in oncogenically stabilized hypoxia-inducible factor-1alpha
    Denise A Chan
    Program in Cancer Biology, Department of Radiation Oncology, Stanford University, Stanford, California 94305, USA
    J Biol Chem 277:40112-7. 2002
    ..Thus, these results indicate distinct pathways for HIF-1alpha stabilization by different oncogenes. More importantly, these findings link oncogenesis with normoxic HIF-1alpha expression through prolyl hydroxylation...
  61. ncbi request reprint Effect of reduced oxygen tension on chondrogenesis and osteogenesis in adipose-derived mesenchymal cells
    Preeti Malladi
    Children s Surgical Research Program, Department of Surgery, Stanford University School of Medicine, 257 Campus Dr, CA 94305, USA
    Am J Physiol Cell Physiol 290:C1139-46. 2006
    ..AMCs differentiated in both 21 and 2% O(2) environments. However, osteogenesis was severely diminished in a low-oxygen environment. These data demonstrated that hypoxia strongly inhibits in vitro chondrogenesis and osteogenesis in AMCs...
  62. ncbi request reprint The hypoxic microenvironment of the skin contributes to Akt-mediated melanocyte transformation
    Barbara Bedogni
    Division of Radiation and Cancer Biology, Stanford University, Stanford, California 94305, USA
    Cancer Cell 8:443-54. 2005
    ..Taken together, these findings demonstrate that Akt hyperactivation and HIF1alpha induction by normally occurring hypoxia in the skin significantly contribute to melanoma development...
  63. pmc HIF1alpha delays premature senescence through the activation of MIF
    Scott M Welford
    Division of Radiation and Cancer Biology, Stanford University, Stanford, California 94305, USA
    Genes Dev 20:3366-71. 2006
    ..Inhibition of MIF phenocopies loss of HIF1alpha. Our findings highlight a novel role for HIF1alpha under aerobic conditions, and identify MIF as a target responsible for this function...
  64. ncbi request reprint Lysyl oxidase mediates hypoxic control of metastasis
    Janine T Erler
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305, USA
    Cancer Res 66:10238-41. 2006
    ..In an orthotopic rodent model of breast cancer, a small-molecule or antibody inhibitor of LOX abolished metastasis, offering preclinical validation of this enzyme as a therapeutic target...
  65. pmc Prognostic and predictive significance of plasma HGF and IL-8 in a phase III trial of chemoradiation with or without tirapazamine in locoregionally advanced head and neck cancer
    Quynh Thu Le
    Radiation Oncology and Pathology, Stanford University, Stanford, CA, USA
    Clin Cancer Res 18:1798-807. 2012
    ..We evaluated the role of circulating HGF and IL-8 as prognostic and predictive factors for efficacy of tirapazamine (TPZ), a hypoxic cell cytotoxin...
  66. ncbi request reprint The p53QS transactivation-deficient mutant shows stress-specific apoptotic activity and induces embryonic lethality
    Thomas M Johnson
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, California 94305, USA
    Nat Genet 37:145-52. 2005
    ..Taken together, these results suggest that p53 has different mechanisms of action depending on specific contextual cues, which may help to clarify the function of p53 in preventing cancer...
  67. pmc Hypoxia, inflammation, and the tumor microenvironment in metastatic disease
    Elizabeth C Finger
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University, Stanford, CA, USA
    Cancer Metastasis Rev 29:285-93. 2010
    ..Central players involved in this process and discussed in this review include integrins, matrix metalloproteinases, and soluble growth factors/matrix proteins, including the connective tissue growth factor and lysyl oxidase...
  68. ncbi request reprint Hypoxic gene expression and metastasis
    Quynh Thu Le
    Division of Cancer and Radiation Biology, Stanford University School of Medicine, Department of Radiation Oncology, CCSR South, Room 1255, 269 Campus Drive, Stanford, CA 94305 5152
    Cancer Metastasis Rev 23:293-310. 2004
    ..Particular emphasis is given to recent findings that provide insight to the role of hypoxia in the metastatic process...
  69. ncbi request reprint Topical treatment with inhibitors of the phosphatidylinositol 3'-kinase/Akt and Raf/mitogen-activated protein kinase kinase/extracellular signal-regulated kinase pathways reduces melanoma development in severe combined immunodeficient mice
    Barbara Bedogni
    Division of Radiation and Cancer Biology, Stanford University, Stanford, California, USA
    Cancer Res 64:2552-60. 2004
    ..These studies demonstrate that topical treatment targeting Ras effectors is efficacious, without systemic toxicities, and may prove to be useful in treating and preventing the progression of cutaneous melanoma...
  70. ncbi request reprint Molecular imaging of hypoxia-inducible factor 1 alpha and von Hippel-Lindau interaction in mice
    Clara Y H Choi
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305 5152, USA
    Mol Imaging 7:139-46. 2008
    ..This method represents a new approach for studying interaction of proteins involved in the regulation of protein degradation...
  71. ncbi request reprint Deletion of Vhlh in chondrocytes reduces cell proliferation and increases matrix deposition during growth plate development
    David Pfander
    Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA
    Development 131:2497-508. 2004
    ..This is the first study reporting the novel and intriguing findings that pVHL has a crucial role in endochondral bone development and is necessary for normal chondrocyte proliferation in vivo...
  72. ncbi request reprint Proceedings of the Oxygen Homeostasis/Hypoxia Meeting
    Bennett Kaufman
    TRI Inc, Rockville, Maryland, USA
    Cancer Res 64:3350-6. 2004
  73. pmc Distinct aerobic and hypoxic mechanisms of HIF-alpha regulation by CSN5
    Lynne Bemis
    Departments of Medicine and Biochemistry, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA
    Genes Dev 18:739-44. 2004
    ..These results indicate that CSN5 regulates aerobic as well as hypoxic HIF-1 alpha stability by different mechanisms during oncogenesis...
  74. pmc Hypoxia-induced gene expression occurs solely through the action of hypoxia-inducible factor 1alpha (HIF-1alpha): role of cytoplasmic trapping of HIF-2alpha
    Sang Ki Park
    Molecular Biology Section, Division of Biological Sciences, University of California, San Diego, La Jolla, California 92093 0366, USA
    Mol Cell Biol 23:4959-71. 2003
    ....
  75. pmc Regulation of hypoxia-inducible factor 1alpha expression and function by the mammalian target of rapamycin
    Christine C Hudson
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Mol Cell Biol 22:7004-14. 2002
    ..These studies position mTOR as an upstream activator of HIF-1 function in cancer cells and suggest that the antitumor activity of rapamycin is mediated, in part, through the inhibition of cellular responses to hypoxic stress...
  76. ncbi request reprint HIF-alpha, a gender independent transcription factor
    Quynh Thu Le
    Clin Cancer Res 9:2391-3. 2003
  77. ncbi request reprint The hypoxic tumor microenvironment and gene expression
    Cornelia Leo
    Department of Gynecology, University of Leipzig, Germany
    Semin Radiat Oncol 14:207-14. 2004
    ..An understanding of the coordinated functions of hypoxia induced and repressed genes can lead to a better understanding of the clinical significance of the hypoxic tumor phenotype...
  78. ncbi request reprint JunD reduces tumor angiogenesis by protecting cells from oxidative stress
    Damien Gerald
    Unit of Gene Expression and Diseases, CNRS URA 1644, Pasteur Institute, 25 rue du Docteur Roux, 75724 Paris, Cedex 15, France
    Cell 118:781-94. 2004
    ..Furthermore, we provide new insights into the regulation of PHD activity, allowing immediate reactive adaptation to changes in O2 or iron levels in the cell...
  79. ncbi request reprint Developmental response to hypoxia
    S T Joseph Huang
    Department of Obstetrics and Gynecology, Stanford University Medical Center, California 94305 5317, USA
    FASEB J 18:1348-65. 2004
    ..Furthermore, induction of inflammation-related genes in placentas exposed to long-term hypoxia (11 days) suggests a mechanism for placental dysfunction and impaired pregnancy outcome accompanying in utero hypoxia...
  80. ncbi request reprint OS-9 interacts with hypoxia-inducible factor 1alpha and prolyl hydroxylases to promote oxygen-dependent degradation of HIF-1alpha
    Jin Hyen Baek
    Institute for Cell Engineering, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Mol Cell 17:503-12. 2005
    ..These data indicate that OS-9 is an essential component of a multiprotein complex that regulates HIF-1alpha levels in an O2-dependent manner...
  81. ncbi request reprint Hypoxia: importance in tumor biology, noninvasive measurement by imaging, and value of its measurement in the management of cancer therapy
    James L Tatum
    National Cancer Institute, Executive Plaza North, Room 6000, 6130 Executive Boulevard, Rockville, MD 20852 7440, USA
    Int J Radiat Biol 82:699-757. 2006
    ....
  82. pmc Multiple factors affecting cellular redox status and energy metabolism modulate hypoxia-inducible factor prolyl hydroxylase activity in vivo and in vitro
    Yi Pan
    Howard Hughes Medical Institute, Abramson Family Cancer Research Institute, University of Pennsylvania School of Medicine, 421 Curie Boulevard, Philadelphia, PA 19104, USA
    Mol Cell Biol 27:912-25. 2007
    ..Our results suggest that multiple mitochondrial products, including TCA cycle intermediates and reactive oxygen species, can coordinate PHD activity, HIF stabilization, and cellular responses to O(2) depletion...
  83. ncbi request reprint Oxygen sensing and the DNA-damage response
    Ester M Hammond
    Radiobiology Research Institute, Churchill Hospital, Oxford OX3 7LJ, UK
    Curr Opin Cell Biol 19:680-4. 2007
  84. pmc Coordinate regulation of the oxygen-dependent degradation domains of hypoxia-inducible factor 1 alpha
    Denise A Chan
    Center for Clinical Science Research, Department of Radiation Oncology, Stanford University, Stanford, CA 94305 5152, USA
    Mol Cell Biol 25:6415-26. 2005
    ..Together, these findings demonstrate that each hydroxylated proline of HIF-1alpha has a distinct activity in controlling HIF-1alpha stability in response to different levels of oxygenation...
  85. pmc Short hairpin RNA interference therapy for ischemic heart disease
    Mei Huang
    Stanford University School of Medicine, Edwards Building R354, Stanford, CA 94305 5344, USA
    Circulation 118:S226-33. 2008
    ..Here we hypothesize that short hairpin RNA (shRNA) interference therapy targeting PHD2 can be used for treatment of myocardial ischemia and this process can be followed noninvasively by molecular imaging...
  86. pmc A molecule targeting VHL-deficient renal cell carcinoma that induces autophagy
    Sandra Turcotte
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Cancer Cell 14:90-102. 2008
    ..Thus, we have found a small molecule that selectively induces cell death in VHL-deficient cells, representing a paradigm shift for targeted therapy...

Research Grants23

  1. CTGF in Pancreatic Tumor Growth
    Amato J Giaccia; Fiscal Year: 2010
    ..In summary, the proposed studies are intended to address an important mechanism by which CTGF affects tumor progression in pancreatic cancers and to determine how effective it is in combination therapy to bring it to the clinic. ..
  2. HYPOXIA AND GENE REPRESSION
    Amato Giaccia; Fiscal Year: 2006
    ..We will test these hypotheses through a combination of genetic and biochemical approaches in cell lines and in mice. ..
  3. HYPOXIA AND GENE REPRESSION
    Amato Giaccia; Fiscal Year: 2007
    ..We will test these hypotheses through a combination of genetic and biochemical approaches in cell lines and in mice. ..
  4. HYPOXIA AND GENE REPRESSION
    Amato Giaccia; Fiscal Year: 2009
    ..We will test these hypotheses through a combination of genetic and biochemical approaches in cell lines and in mice. ..
  5. CTGF in Pancreatic Tumor Growth
    Amato Giaccia; Fiscal Year: 2009
    ..In summary, the proposed studies are intended to address an important mechanism by which CTGF affects tumor progression in pancreatic cancers and to determine how effective it is in combination therapy to bring it to the clinic. ..
  6. CTGF in Pancreatic Tumor Growth
    Amato Giaccia; Fiscal Year: 2007
    ..In summary, the proposed studies are intended to address an important mechanism by which CTGF affects tumor progression in pancreatic cancers and to determine how effective it is in combination therapy to bring it to the clinic. ..
  7. HYPOXIA AND GENE REPRESSION
    Amato Giaccia; Fiscal Year: 2005
    ..We will test these hypotheses through a combination of genetic and biochemical approaches in cell lines and in mice. ..
  8. Tumor Hypoxia: Molecular Studies & Clinical Exploitation
    Amato Giaccia; Fiscal Year: 2007
    ..Few groups could be better positioned to use yeast and mammalian genetics to develop novel hypoxia based therapeutics. ..
  9. CTGF in Pancreatic Tumor Growth
    Amato Giaccia; Fiscal Year: 2006
    ..In summary, the proposed studies are intended to address an important mechanism by which CTGF affects tumor progression in pancreatic cancers and to determine how effective it is in combination therapy to bring it to the clinic. ..
  10. Postdoctoral Training in the Radiation Sciences
    Amato Giaccia; Fiscal Year: 2007
    ..It is therefore imperative to develop a well trained cohort of professionals who will be responsible for the next generation of therapeutic advancements. ..
  11. Hypoxia--Molecular Studies and Clinical Exploitation
    Amato Giaccia; Fiscal Year: 2006
    ..abstract_text> ..
  12. CANCER ETIOLOGY, PREVENTION, DETECTION AND DIAGNOSIS
    Amato Giaccia; Fiscal Year: 2007
    ....
  13. CTGF in Pancreatic Tumor Growth
    Amato Giaccia; Fiscal Year: 2009
    ..In summary, the proposed studies are intended to address an important mechanism by which CTGF affects tumor progression in pancreatic cancers and to determine how effective it is in combination therapy to bring it to the clinic. ..