Daniel R Carrasco

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. pmc The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis
    Daniel R Carrasco
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, and Department of Pathology, Brigham and Women s Hospital, Boston, MA 02115, USA
    Cancer Cell 11:349-60. 2007
  2. pmc Biologic sequelae of I{kappa}B kinase (IKK) inhibition in multiple myeloma: therapeutic implications
    Teru Hideshima
    Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Blood 113:5228-36. 2009
  3. pmc A novel Aurora-A kinase inhibitor MLN8237 induces cytotoxicity and cell-cycle arrest in multiple myeloma
    Gullu Gorgun
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Blood 115:5202-13. 2010
  4. doi request reprint BCL9 promotes tumor progression by conferring enhanced proliferative, metastatic, and angiogenic properties to cancer cells
    Mala Mani
    Department of Medical Oncology and Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Cancer Res 69:7577-86. 2009
  5. doi request reprint Milk fat globule EGF-8 promotes melanoma progression through coordinated Akt and twist signaling in the tumor microenvironment
    Masahisa Jinushi
    Department of Medical Oncology and Cancer Vaccine Center, Dana Farber Cancer Institute, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Cancer Res 68:8889-98. 2008
  6. doi request reprint Aurora kinase A is a target of Wnt/beta-catenin involved in multiple myeloma disease progression
    Jui Dutta-Simmons
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Blood 114:2699-708. 2009
  7. pmc Targeting the beta-catenin/TCF transcriptional complex in the treatment of multiple myeloma
    Kumar Sukhdeo
    Department of Medical Oncology, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 104:7516-21. 2007
  8. pmc A proto-oncogene BCL6 is up-regulated in the bone marrow microenvironment in multiple myeloma cells
    Teru Hideshima
    Jerome Lipper Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Blood 115:3772-5. 2010
  9. pmc CS1 promotes multiple myeloma cell adhesion, clonogenic growth, and tumorigenicity via c-maf-mediated interactions with bone marrow stromal cells
    Yu Tzu Tai
    LeBow Institute for Myeloma Therapeutics and Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Blood 113:4309-18. 2009
  10. pmc MFG-E8-mediated uptake of apoptotic cells by APCs links the pro- and antiinflammatory activities of GM-CSF
    Masahisa Jinushi
    Department of Medical Oncology and Cancer Vaccine Center, Dana Farber Cancer Institute, Boston, MA 02115, USA
    J Clin Invest 117:1902-13. 2007

Collaborators

Detail Information

Publications21

  1. pmc The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis
    Daniel R Carrasco
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, and Department of Pathology, Brigham and Women s Hospital, Boston, MA 02115, USA
    Cancer Cell 11:349-60. 2007
    ..The similarities of this model with the human disease, coupled with documented frequent XBP-1s overexpression in human MM, serve to implicate XBP-1s dysregulation in MM pathogenesis...
  2. pmc Biologic sequelae of I{kappa}B kinase (IKK) inhibition in multiple myeloma: therapeutic implications
    Teru Hideshima
    Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Blood 113:5228-36. 2009
    ..Combination therapy targeting these kinases therefore represents a promising treatment strategy in MM...
  3. pmc A novel Aurora-A kinase inhibitor MLN8237 induces cytotoxicity and cell-cycle arrest in multiple myeloma
    Gullu Gorgun
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Blood 115:5202-13. 2010
    ..MLN8237 is currently in phase 1 and phase 2 clinical trials in patients with advanced malignancies, and our preclinical results suggest that MLN8237 may be a promising novel targeted therapy in MM...
  4. doi request reprint BCL9 promotes tumor progression by conferring enhanced proliferative, metastatic, and angiogenic properties to cancer cells
    Mala Mani
    Department of Medical Oncology and Jerome Lipper Multiple Myeloma Center, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Cancer Res 69:7577-86. 2009
    ..The pleiotropic roles of BCL9 reported in this study underscore its value as a drug target for therapeutic intervention in several malignancies associated with aberrant Wnt signaling...
  5. doi request reprint Milk fat globule EGF-8 promotes melanoma progression through coordinated Akt and twist signaling in the tumor microenvironment
    Masahisa Jinushi
    Department of Medical Oncology and Cancer Vaccine Center, Dana Farber Cancer Institute, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Cancer Res 68:8889-98. 2008
    ..Together, these findings delineate pleiotropic roles for MFG-E8 in the tumor microenvironment and raise the possibility that systemic MFG-E8 blockade might prove therapeutic for melanoma patients...
  6. doi request reprint Aurora kinase A is a target of Wnt/beta-catenin involved in multiple myeloma disease progression
    Jui Dutta-Simmons
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Blood 114:2699-708. 2009
    ..Our data provide evidence for a novel functional link between beta-catenin and Aurora kinase A, underscoring a critical role of these pathways in MM disease progression...
  7. pmc Targeting the beta-catenin/TCF transcriptional complex in the treatment of multiple myeloma
    Kumar Sukhdeo
    Department of Medical Oncology, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 104:7516-21. 2007
    ..Taken together, these data demonstrate the efficacy of disrupting the beta-catenin/TCF transcriptional complex to exploit tumor dependence on Wnt signaling as a therapeutic approach in the treatment of MM...
  8. pmc A proto-oncogene BCL6 is up-regulated in the bone marrow microenvironment in multiple myeloma cells
    Teru Hideshima
    Jerome Lipper Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Blood 115:3772-5. 2010
    ....
  9. pmc CS1 promotes multiple myeloma cell adhesion, clonogenic growth, and tumorigenicity via c-maf-mediated interactions with bone marrow stromal cells
    Yu Tzu Tai
    LeBow Institute for Myeloma Therapeutics and Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Blood 113:4309-18. 2009
    ..These studies provide direct evidence of the role of CS1 in myeloma pathogenesis, define molecular mechanisms regulating its effects, and further support novel therapies targeting CS1 in MM...
  10. pmc MFG-E8-mediated uptake of apoptotic cells by APCs links the pro- and antiinflammatory activities of GM-CSF
    Masahisa Jinushi
    Department of Medical Oncology and Cancer Vaccine Center, Dana Farber Cancer Institute, Boston, MA 02115, USA
    J Clin Invest 117:1902-13. 2007
    ..These findings clarify the immunoregulatory effects of apoptotic cells and suggest new therapeutic strategies to modulate CD4(+) T cell subsets in cancer and autoimmunity...
  11. ncbi request reprint Mouse models of human myeloma
    Constantine S Mitsiades
    Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
    Hematol Oncol Clin North Am 21:1051-69, viii. 2007
    ..Here we review the recent developments in the generation of mouse models of MM and their impact as preclinical models for designing and assessing target-based therapeutic approaches...
  12. pmc Ink4a/Arf tumor suppressor does not modulate the degenerative conditions or tumor spectrum of the telomerase-deficient mouse
    Christine M Khoo
    Department of Medical Oncology, Belfer Foundation Institute for Innovative Cancer Science, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 104:3931-6. 2007
    ..These observations highlight the importance of genetic context in dictating whether telomere dysfunction promotes or suppresses age-related degenerative conditions as well as the rate of initiation and type of spontaneous cancers...
  13. pmc TRIM13 (RFP2) downregulation decreases tumour cell growth in multiple myeloma through inhibition of NF Kappa B pathway and proteasome activity
    Moshe E Gatt
    Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
    Br J Haematol 162:210-20. 2013
    ..Although this data does not support a role of TRIM13 as a TSG, it substantiates important roles of TRIM13 in MM tumour survival and proliferation, underscoring its potential role as a novel target for therapeutic intervention. ..
  14. pmc Bruton tyrosine kinase inhibition is a novel therapeutic strategy targeting tumor in the bone marrow microenvironment in multiple myeloma
    Yu Tzu Tai
    LeBow Institute for Myeloma Therapeutics and Jerome Lipper Center for Multiple Myeloma Research, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA
    Blood 120:1877-87. 2012
    ..Together, these results delineate functional sequelae of Btk activation mediating osteolysis and growth of MM cells, supporting evaluation of PCI-32765 as a novel therapeutic in MM...
  15. pmc FoxOs are lineage-restricted redundant tumor suppressors and regulate endothelial cell homeostasis
    Ji Hye Paik
    Department of Medical Oncology, Dana Farber Cancer Institute, Brigham and Women s Hospital, and Harvard Medical School, Boston, MA 02115, USA
    Cell 128:309-23. 2007
    ..Functional studies validated Sprouty2 and PBX1, among others, as FoxO-regulated mediators of endothelial cell morphogenesis and vascular homeostasis...
  16. ncbi request reprint The PTEN and INK4A/ARF tumor suppressors maintain myelolymphoid homeostasis and cooperate to constrain histiocytic sarcoma development in humans
    Daniel R Carrasco
    Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer Cell 9:379-90. 2006
    ..These genetic and translational observations establish a cooperative role of Pten and Ink4a/Arf in the development of HS and provide mechanistic insights into the pathogenesis of human HS...
  17. doi request reprint Pathogenesis of myeloma
    Kenneth C Anderson
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Annu Rev Pathol 6:249-74. 2011
    ....
  18. pmc Constitutive telomerase expression promotes mammary carcinomas in aging mice
    Steven E Artandi
    Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street M413, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 99:8191-6. 2002
    ..These data indicate that enforced mTERT expression can promote the development of spontaneous cancers even in the setting of ample telomere reserve...
  19. ncbi request reprint High-resolution genomic profiles define distinct clinico-pathogenetic subgroups of multiple myeloma patients
    Daniel R Carrasco
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Cancer Cell 9:313-25. 2006
    ....
  20. pmc Bortezomib induces canonical nuclear factor-kappaB activation in multiple myeloma cells
    Teru Hideshima
    Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Blood 114:1046-52. 2009
    ..Moreover, IKKbeta inhibitors enhanced bortezomib-induced cytotoxicity. Our studies therefore suggest that bortezomib-induced cytotoxicity cannot be fully attributed to inhibition of canonical NF-kappaB activity in MM cells...
  21. pmc PD-1 on immature and PD-1 ligands on migratory human Langerhans cells regulate antigen-presenting cell activity
    Victor Pena-Cruz
    Department of Medical Oncology, Dana Farber Cancer Institute and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Invest Dermatol 130:2222-30. 2010
    ..Thus the PD-1 pathway is active in iLCs and inhibits iLC activities, but expression of receptor and ligands reverses upon maturation and PD-L1 and PD-L2 on mLC function to inhibit T-cell responses...

Research Grants2

  1. Novel System to Study Telomere Dynamics in Hemotopoiesis
    Ruben Carrasco; Fiscal Year: 2005
    ..He also holds a Ph.D. in Biochemistry. The research will be carried out in a cancer/aging biology laboratory within the Dana-Farber Cancer Institute, an affiliate of the Harvard Medical School, under the mentorship of Dr. Ron DePinho. ..
  2. Mining B-catenin/BCL9 transcriptional complex for Multiple Myeloma therapeutics
    Ruben D Carrasco; Fiscal Year: 2010
    ..The studies proposed in this RO1 are significant to Public Health in that they may lead to the development of novel pharmacologic strategies to treat MM and other cancers associated with deregulated Wnt signaling. ..