Marcus W Bosenberg

Summary

Affiliation: University of Vermont
Country: USA

Publications

  1. pmc Role of epidermal growth factor receptor signaling in RAS-driven melanoma
    Nabeel Bardeesy
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Mol Cell Biol 25:4176-88. 2005
  2. ncbi request reprint Characterization of melanocyte-specific inducible Cre recombinase transgenic mice
    Marcus Bosenberg
    Department of Pathology, University of Vermont, Burlington, Vermont 05405, USA
    Genesis 44:262-7. 2006
  3. doi request reprint A new mechanism of release from senescence: suppression of p16INK4a by beta-catenin
    David P Curley
    Pigment Cell Melanoma Res 21:5-6. 2008
  4. pmc The broad-spectrum receptor tyrosine kinase inhibitor dovitinib suppresses growth of BRAF-mutant melanoma cells in combination with other signaling pathway inhibitors
    Casey G Langdon
    Department of Pathology, Yale University School of Medicine, New Haven, CT, USA
    Pigment Cell Melanoma Res 28:417-30. 2015
  5. pmc Activated cAMP response element binding protein is overexpressed in human mesotheliomas and inhibits apoptosis
    Arti Shukla
    Department of Pathology, University of Vermont College of Medicine, Burlington, VT 05405 0068, USA
    Am J Pathol 175:2197-206. 2009
  6. ncbi request reprint Amplification of CDK4 and MDM2 in malignant melanoma
    Viswanathan Muthusamy
    Department of Pathology, University of Vermont, Burlington, Vermont 05495, USA
    Genes Chromosomes Cancer 45:447-54. 2006
  7. pmc Characterization of melanoma cells capable of propagating tumors from a single cell
    Matthew A Held
    Department of Pathology, University of Vermont College of Medicine, Burlington, Vermont, USA
    Cancer Res 70:388-97. 2010
  8. pmc Genotype-selective combination therapies for melanoma identified by high-throughput drug screening
    Matthew A Held
    Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Cancer Discov 3:52-67. 2013
  9. doi request reprint The YUMM lines: a series of congenic mouse melanoma cell lines with defined genetic alterations
    Katrina Meeth
    Department of Pathology, Yale University School of Medicine, New Haven, CT, USA
    Pigment Cell Melanoma Res 29:590-7. 2016
  10. pmc LKB1 deficiency sensitizes mice to carcinogen-induced tumorigenesis
    Sushma Gurumurthy
    Massachusetts General Hospital, Massachusetts General Hospital Cancer Center, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02114, USA
    Cancer Res 68:55-63. 2008

Research Grants

  1. ROLE OF THE PTEN PATHWAY IN MELANOMA
    Marcus Bosenberg; Fiscal Year: 2005

Collaborators

Detail Information

Publications14

  1. pmc Role of epidermal growth factor receptor signaling in RAS-driven melanoma
    Nabeel Bardeesy
    Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA
    Mol Cell Biol 25:4176-88. 2005
    ..Thus, this inducible tumor model system permits the identification and validation of alternative points of therapeutic intervention without neutralization of the primary genetic lesion...
  2. ncbi request reprint Characterization of melanocyte-specific inducible Cre recombinase transgenic mice
    Marcus Bosenberg
    Department of Pathology, University of Vermont, Burlington, Vermont 05405, USA
    Genesis 44:262-7. 2006
    ....
  3. doi request reprint A new mechanism of release from senescence: suppression of p16INK4a by beta-catenin
    David P Curley
    Pigment Cell Melanoma Res 21:5-6. 2008
  4. pmc The broad-spectrum receptor tyrosine kinase inhibitor dovitinib suppresses growth of BRAF-mutant melanoma cells in combination with other signaling pathway inhibitors
    Casey G Langdon
    Department of Pathology, Yale University School of Medicine, New Haven, CT, USA
    Pigment Cell Melanoma Res 28:417-30. 2015
    ..Hence, combinations of dovitinib with second agents are potentially effective therapies for BRAF-mutant melanomas, regardless of their sensitivity to BRAF inhibitors. ..
  5. pmc Activated cAMP response element binding protein is overexpressed in human mesotheliomas and inhibits apoptosis
    Arti Shukla
    Department of Pathology, University of Vermont College of Medicine, Burlington, VT 05405 0068, USA
    Am J Pathol 175:2197-206. 2009
    ..Since activated CREB1 also is increased endogenously in human MM and modifies migration and resistance to Dox-induced apoptosis, inhibition of CREB1 may be a new strategy for MM therapy...
  6. ncbi request reprint Amplification of CDK4 and MDM2 in malignant melanoma
    Viswanathan Muthusamy
    Department of Pathology, University of Vermont, Burlington, Vermont 05495, USA
    Genes Chromosomes Cancer 45:447-54. 2006
    ..These results suggest that coamplification of CDK4 and MDM2 may substitute for loss of P16INK4A and P14ARF function in a subset of melanomas...
  7. pmc Characterization of melanoma cells capable of propagating tumors from a single cell
    Matthew A Held
    Department of Pathology, University of Vermont College of Medicine, Burlington, Vermont, USA
    Cancer Res 70:388-97. 2010
    ..We anticipate that purification of these MPCs may allow a more comprehensive evaluation of the molecular features that define tumor-forming capability and chemotherapeutic resistance in melanoma...
  8. pmc Genotype-selective combination therapies for melanoma identified by high-throughput drug screening
    Matthew A Held
    Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Cancer Discov 3:52-67. 2013
    ..These results show the use of combinatorial drug screening for discovering unique treatment regimens that overcome resistance phenotypes of mutant BRAF- and RAS-driven melanomas...
  9. doi request reprint The YUMM lines: a series of congenic mouse melanoma cell lines with defined genetic alterations
    Katrina Meeth
    Department of Pathology, Yale University School of Medicine, New Haven, CT, USA
    Pigment Cell Melanoma Res 29:590-7. 2016
    ..This will be a useful tool for the study of tumor immunology and genotype-specific cancer biology. ..
  10. pmc LKB1 deficiency sensitizes mice to carcinogen-induced tumorigenesis
    Sushma Gurumurthy
    Massachusetts General Hospital, Massachusetts General Hospital Cancer Center, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02114, USA
    Cancer Res 68:55-63. 2008
    ..Our data indicate that Lkb1 is a potent suppressor of carcinogen-induced skin and lung cancers and that downstream targets beyond the AMPK-mTOR pathway are likely mediators of Lkb1-dependent tumor suppression...
  11. ncbi request reprint Loss of xeroderma pigmentosum C (Xpc) enhances melanoma photocarcinogenesis in Ink4a-Arf-deficient mice
    Guang Yang
    Wellman Center for Photomedicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA
    Cancer Res 67:5649-57. 2007
    ..033). Taken together, results from this novel UV-inducible melanoma model suggest that NER loss, in conjunction with Ink4a-Arf inactivation, can drive melanoma photocarcinogenesis possibly through signature Kras mutagenesis...
  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. ncbi request reprint Precancer in mice: animal models used to understand, prevent, and treat human precancers
    Robert D Cardiff
    The UCD Center for Comparative Medicine, University of California, Davis, Davis, California 95616, USA
    Toxicol Pathol 34:699-707. 2006
    ..These studies suggest that genetically engineered mice are very useful preclinical models for chemoprevention and therapy...
  14. pmc Genetic analysis of Pten and Ink4a/Arf interactions in the suppression of tumorigenesis in mice
    Mingjian James You
    Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 99:1455-60. 2002
    ..This study provides genetic evidence of collaboration between Pten and Ink4a/Arf in constraining the growth and oncogenic transformation of cultured cells and in suppressing a wide spectrum of tumors in vivo...

Research Grants1

  1. ROLE OF THE PTEN PATHWAY IN MELANOMA
    Marcus Bosenberg; Fiscal Year: 2005
    ..He has also completed Ph.D. training in cell biology. The proposed research will be carried out in the laboratory of Dr. Ronald DePinho at the Dana-Farber Cancer Institute, an affiliate of the Harvard Medical School. ..