Douglas Ball

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. pmc Medullary thyroid cancer: monitoring and therapy
    Douglas W Ball
    Johns Hopkins University School of Medicine, Suite 333, 1830 East Monument Street, Baltimore, MD 21287, USA
    Endocrinol Metab Clin North Am 36:823-37, viii. 2007
  2. ncbi request reprint Management of medullary thyroid cancer
    D W Ball
    Department of Medicine and Oncology, Johns Hopkins University School of Medicine, Baltimore, MA 21287, USA
    Minerva Endocrinol 36:87-98. 2011
  3. ncbi request reprint Selective growth inhibition in BRAF mutant thyroid cancer by the mitogen-activated protein kinase kinase 1/2 inhibitor AZD6244
    Douglas W Ball
    Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins University School of Medicine, 1650 Orleans Street, Room 553, Baltimore, Maryland 21231 1000, USA
    J Clin Endocrinol Metab 92:4712-8. 2007
  4. ncbi request reprint Medullary thyroid cancer: therapeutic targets and molecular markers
    Douglas W Ball
    Division of Endocrinology and Metabolism, Johns Hopkins University School of Medicine, Suite 333, 1830 E Monument Street, Baltimore, MD 21287, USA
    Curr Opin Oncol 19:18-23. 2007
  5. ncbi request reprint Achaete-scute homolog-1 and Notch in lung neuroendocrine development and cancer
    Douglas W Ball
    Department of Medicine, The Sidney Kimmel Comprehensive Cancer Center, Bunting Blaustein Cancer Research Building, John s Hopkins Medical Institutions, Room 553, 1620 Orleans Street, Baltimore, MD 21231 1000, USA
    Cancer Lett 204:159-69. 2004
  6. pmc The Ras/Raf/MEK/extracellular signal-regulated kinase pathway induces autocrine-paracrine growth inhibition via the leukemia inhibitory factor/JAK/STAT pathway
    Jong In Park
    The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Mol Cell Biol 23:543-54. 2003
  7. ncbi request reprint Activity of irinotecan and the tyrosine kinase inhibitor CEP-751 in medullary thyroid cancer
    Christopher J Strock
    Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland 21231, USA
    J Clin Endocrinol Metab 91:79-84. 2006
  8. pmc Notch signaling induces rapid degradation of achaete-scute homolog 1
    Virote Sriuranpong
    Program in Cellular and Molecular Medicine, Oncology Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Mol Cell Biol 22:3129-39. 2002
  9. ncbi request reprint CEP-701 and CEP-751 inhibit constitutively activated RET tyrosine kinase activity and block medullary thyroid carcinoma cell growth
    Christopher J Strock
    The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Cancer Res 63:5559-63. 2003
  10. pmc Achaete-scute complex homologue 1 regulates tumor-initiating capacity in human small cell lung cancer
    Tianyun Jiang
    Departments of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Cancer Res 69:845-54. 2009

Research Grants

Collaborators

Detail Information

Publications24

  1. pmc Medullary thyroid cancer: monitoring and therapy
    Douglas W Ball
    Johns Hopkins University School of Medicine, Suite 333, 1830 East Monument Street, Baltimore, MD 21287, USA
    Endocrinol Metab Clin North Am 36:823-37, viii. 2007
    ..This article highlights early progress in targeted therapy of MTC and significant challenges in disease monitoring to appropriately select and evaluate patients being treated with these therapies...
  2. ncbi request reprint Management of medullary thyroid cancer
    D W Ball
    Department of Medicine and Oncology, Johns Hopkins University School of Medicine, Baltimore, MA 21287, USA
    Minerva Endocrinol 36:87-98. 2011
    ....
  3. ncbi request reprint Selective growth inhibition in BRAF mutant thyroid cancer by the mitogen-activated protein kinase kinase 1/2 inhibitor AZD6244
    Douglas W Ball
    Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins University School of Medicine, 1650 Orleans Street, Room 553, Baltimore, Maryland 21231 1000, USA
    J Clin Endocrinol Metab 92:4712-8. 2007
    ..MAPK kinase (MEK), immediately downstream of BRAF, is a promising target for ras-raf-MEK-ERK pathway inhibition...
  4. ncbi request reprint Medullary thyroid cancer: therapeutic targets and molecular markers
    Douglas W Ball
    Division of Endocrinology and Metabolism, Johns Hopkins University School of Medicine, Suite 333, 1830 E Monument Street, Baltimore, MD 21287, USA
    Curr Opin Oncol 19:18-23. 2007
    ..The present review will provide an update of important studies in medullary thyroid cancer (MTC) with an emphasis on targeted preclinical and translational research studies published over the past 2 years...
  5. ncbi request reprint Achaete-scute homolog-1 and Notch in lung neuroendocrine development and cancer
    Douglas W Ball
    Department of Medicine, The Sidney Kimmel Comprehensive Cancer Center, Bunting Blaustein Cancer Research Building, John s Hopkins Medical Institutions, Room 553, 1620 Orleans Street, Baltimore, MD 21231 1000, USA
    Cancer Lett 204:159-69. 2004
    ..Inhibition of this factor by the Notch pathway is essential in regulating NE commitment in airway epithelial precursor cells, and may play a comparable role in modulating phenotypes of lung cancer and other tumors...
  6. pmc The Ras/Raf/MEK/extracellular signal-regulated kinase pathway induces autocrine-paracrine growth inhibition via the leukemia inhibitory factor/JAK/STAT pathway
    Jong In Park
    The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Mol Cell Biol 23:543-54. 2003
    ..This use of multiple pathways may be important for "fail-safe" induction and maintenance of cell cycle arrest...
  7. ncbi request reprint Activity of irinotecan and the tyrosine kinase inhibitor CEP-751 in medullary thyroid cancer
    Christopher J Strock
    Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland 21231, USA
    J Clin Endocrinol Metab 91:79-84. 2006
    ..Medullary thyroid cancer (MTC) is a cancer of the parafollicular C cells that commonly presents with an inherited or acquired RET gene mutation. There is currently no effective systemic treatment for MTC...
  8. pmc Notch signaling induces rapid degradation of achaete-scute homolog 1
    Virote Sriuranpong
    Program in Cellular and Molecular Medicine, Oncology Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Mol Cell Biol 22:3129-39. 2002
    ..This novel function of activated Notch to rapidly degrade a class II bHLH protein may prove to be important in many contexts in development and in cancer...
  9. ncbi request reprint CEP-701 and CEP-751 inhibit constitutively activated RET tyrosine kinase activity and block medullary thyroid carcinoma cell growth
    Christopher J Strock
    The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Cancer Res 63:5559-63. 2003
    ..CEP-751 and its prodrug, CEP-2563, also inhibited tumor growth in MTC cell xenografts. These results show that inhibiting RET can block the growth of MTC cells and may have a therapeutic benefit in MTC...
  10. pmc Achaete-scute complex homologue 1 regulates tumor-initiating capacity in human small cell lung cancer
    Tianyun Jiang
    Departments of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Cancer Res 69:845-54. 2009
    ..Intrinsic tumor cell heterogeneity, including variation in key regulatory factors such as ASCL1, can modulate tumorigenicity in SCLC...
  11. pmc Dual inhibition of mitogen-activated protein kinase kinase and mammalian target of rapamycin in differentiated and anaplastic thyroid cancer
    Ning Jin
    Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231 1000, USA
    J Clin Endocrinol Metab 94:4107-12. 2009
    ..Differentiated thyroid cancer and anaplastic thyroid cancer tumors frequently have activation of the ras/raf /MAPK kinase (MEK)/ERK and phosphatidylinositol 3-kinase (PI-3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathways...
  12. ncbi request reprint Interleukin-1beta can mediate growth arrest and differentiation via the leukemia inhibitory factor/JAK/STAT pathway in medullary thyroid carcinoma cells
    Jong In Park
    The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins University School of Medicine, CRB572, 1650 Orleans Street, Baltimore, MD 21231, USA
    Cytokine 29:125-34. 2005
    ....
  13. ncbi request reprint GDNF-induced leukemia inhibitory factor can mediate differentiation via the MEK/ERK pathway in pheochromocytoma cells derived from nf1-heterozygous knockout mice
    Jong In Park
    The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Exp Cell Res 303:79-88. 2005
    ..Our findings suggest that LIF may be utilized for signaling mediated by GDNF and may be important in the pathobiology of neuroendocrine tumors...
  14. ncbi request reprint Notch in lung development and lung cancer
    Brendan J Collins
    Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Semin Cancer Biol 14:357-64. 2004
    ..Non-small cell lung cancers, including adenocarcinoma, appear to actively utilize this conserved developmental pathway. Pharmacologic inhibition of the Notch pathway is a potential experimental approach to lung cancer treatment...
  15. ncbi request reprint Notch inhibits Ptf1 function and acinar cell differentiation in developing mouse and zebrafish pancreas
    Farzad Esni
    Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Development 131:4213-24. 2004
    ..These results define a normal inhibitory role for Notch in the regulation of exocrine pancreatic differentiation...
  16. ncbi request reprint Notch mediates TGF alpha-induced changes in epithelial differentiation during pancreatic tumorigenesis
    Yoshiharu Miyamoto
    Departments of Surgery, Oncology, and Pathology, The Sidney Kimmel Cancer Center at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Cancer Cell 3:565-76. 2003
    ..These findings suggest that Notch mediates the tumor-initiating effects of TG alpha by expanding a population of undifferentiated precursor cells...
  17. ncbi request reprint Notch1 and notch2 have opposite effects on embryonal brain tumor growth
    Xing Fan
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Cancer Res 64:7787-93. 2004
    ..Our data indicate that Notch1 and Notch2 can have opposite effects on the growth of a single tumor type, and show that Notch2 can be overexpressed after gene amplification in human tumors...
  18. pmc Inhibiting the cyclin-dependent kinase CDK5 blocks pancreatic cancer formation and progression through the suppression of Ras-Ral signaling
    Georg Feldmann
    Departments of Pathology, Oncology, and Medicine, and The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Cancer Res 70:4460-9. 2010
    ..Conversely, restoring Ral function rescued the effects of CDK5 inhibition in pancreatic cancer cells. Our findings identify CDK5 as a pharmacologically tractable target to degrade Ras signaling in pancreatic cancer...
  19. pmc Clinical review: Incidentally discovered medullary thyroid cancer: diagnostic strategies and treatment
    Shabina R Ahmed
    Division of Endocrinology and Metabolism, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    J Clin Endocrinol Metab 96:1237-45. 2011
    ..Barriers to accurate preoperative diagnosis and management strategies after the discovery of occult MTC are reviewed...
  20. ncbi request reprint Unusual case of metastatic neuroendocrine tumor
    Michele A Manahan
    Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
    Endocr Pract 13:72-6. 2007
    ..To report a rare case of metastatic growth hormone (GH)-secreting pituitary carcinoma causing acromegaly...
  21. ncbi request reprint Regulation of neuroendocrine differentiation in gastrointestinal carcinoid tumor cells by notch signaling
    Eric K Nakakura
    Department of Surgery, University of California, San Francisco, California 94115, USA
    J Clin Endocrinol Metab 90:4350-6. 2005
    ....
  22. ncbi request reprint Notch in malignancy
    Douglas W Ball
    Cancer Treat Res 115:95-121. 2003
  23. ncbi request reprint Thyroid carcinoma
    Steven I Sherman
    The University of Texas M D Anderson Cancer Center, USA
    J Natl Compr Canc Netw 5:568-621. 2007
  24. ncbi request reprint Thyroid carcinoma
    Steven I Sherman
    University of Texas M D Anderson Cancer Center, USA
    J Natl Compr Canc Netw 3:404-57. 2005

Research Grants11

  1. A NEURAL TRANSCRIPTION FACTOR IN LUNG CANCER EVOLUTION
    Douglas Ball; Fiscal Year: 2003
    ..These studies will provide a more comprehensive understanding of hASH1 action in SCLC pathogenesis, potentially leading to exploitation of specific vulnerabilities of SCLC tumors in novel treatment strategies. ..
  2. A NEURAL TRANSCRIPTION FACTOR IN LUNG CANCER EVOLUTION
    Douglas Ball; Fiscal Year: 2006
    ..The proposed studies should provide novel insights in SCLC biology and a firm basis for determining whether hASH1, and hASHl-regulated growth mechanisms, should be intensively pursued as therapeutic targets for SCLC. ..