T
Theresa A. Guise
Researcher at Indiana University
Publications - 133
Citations - 7749
Theresa A. Guise is an academic researcher from Indiana University. The author has contributed to research in topics: Cancer & Bone metastasis. The author has an hindex of 46, co-authored 133 publications receiving 7054 citations. Previous affiliations of Theresa A. Guise include Indiana University – Purdue University Indianapolis & University of Texas Health Science Center at San Antonio.
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MonographDOI
Primer on the metabolic bone diseases and disorders of mineral metabolism
John P. Bilezikian,Roger Bouillon,Thomas L. Clemens,Juliet E. Compston,Douglas C. Bauer,Peter R. Ebeling,Klaus Engelke,David Goltzman,Theresa A. Guise,Suzanne M. Jan de Beur,Harald Jüppner,Karen M. Lyons,Laurie K. McCauley,Michael R. McClung,Paul D. Miller,Socrates E. Papapoulos,G. David Roodman,Clifford J. Rosen,Ego Seeman,Ego Seeman,Rajesh V. Thakker,Michael P. Whyte,Michael P. Whyte,Mone Zaidi +23 more
TL;DR: This Book have some digital formats such us :paperbook, ebook, kindle, epub, fb2 and another formats.
Journal ArticleDOI
Runx2 association with progression of prostate cancer in patients: Mechanisms mediating bone osteolysis and osteoblastic metastatic lesions
Jacqueline Akech,John J. Wixted,Krystin Bedard,M. Van der Deen,Sadiq Hussain,Theresa A. Guise,A. J. Van Wijnen,Janet L. Stein,Lucia R. Languino,Dario C. Altieri,Jitesh Pratap,Evan T. Keller,Gary S. Stein,Jane B. Lian +13 more
TL;DR: Mechanisms of Runx2 function were identified in co-culture studies showing that PC3 cells promote osteoclastogenesis and inhibit osteoblast activity, and indicate that Runx 2 is a key regulator of events associated with prostate cancer metastatic bone disease.
Journal ArticleDOI
Molecular mechanisms of tumor-bone interactions in osteolytic metastases
TL;DR: A vicious cycle model is confirmed at the molecular level driving the formation of osteolytic metastases: tumor cells secrete factors stimulating osteoclasts through adjacent bone marrow stromal cells; osteoclastic resorption in turn releases growth factors from the bone matrix; finally, locally released growth factors activate the tumor cells.
Journal ArticleDOI
Tumor-Derived Interleukin-8 Stimulates Osteolysis Independent of the Receptor Activator of Nuclear Factor-κB Ligand Pathway
Manali S. Bendre,Aaron G. Margulies,Brandon Walser,Nisreen S. Akel,Sudeepa Bhattacharrya,Robert A. Skinner,Frances L. Swain,Vishnu C. Ramani,Khalid S. Mohammad,Lisa L. Wessner,Alfredo Martinez,Theresa A. Guise,John M. Chirgwin,Dana Gaddy,Larry J. Suva +14 more
TL;DR: The data support a model in which tumor cells cause osteolytic bone destruction independently of the RANK ligand (RANKL) pathway, and indicate that tumor cells that support osteoclast formation independent of RANKL secrete other pro-osteoclastogenic factors in addition to IL-8.
Journal ArticleDOI
Enhanced serine production by bone metastatic breast cancer cells stimulates osteoclastogenesis
Sirkku Pollari,Sanna Maria Käkönen,Sanna Maria Käkönen,Henrik Edgren,Maija Wolf,Pekka Kohonen,Henri Sara,Theresa A. Guise,Matthias Nees,Olli Kallioniemi +9 more
TL;DR: In conclusion, high expression of serine biosynthesis genes in metastatic breast cancer cells and the stimulating effect of l-serine on osteoclastogenesis and cancer cell proliferation indicate a functionally critical role for serinesynthesis in bone metastatic Breast cancer and thereby an opportunity for targeted therapeutic interventions.