The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis.

The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis. Abstract Text:

Daniel R Carrasco,Kumar Sukhdeo,Marina Protopopova,Raktim Sinha,Miriam Enos,Daniel E Carrasco,Mei Zheng,Mala Mani,Joel Henderson,Geraldine S Pinkus,Nikhil Munshi,James Horner,Elena V Ivanova,Alexei Protopopov,Kenneth C Anderson,Giovanni Tonon,Ronald A DePinho,

Multiple myeloma (MM) evolves from a highly prevalent premalignant condition termed MGUS. The factors underlying the malignant transformation of MGUS are unknown. We report a MGUS/MM phenotype in transgenic mice with Emu-directed expression of the XBP-1 spliced isoform (XBP-1s), a factor governing unfolded protein/ER stress response and plasma-cell development. Emu-XBP-1s elicited elevated serum Ig and skin alterations. With age, Emu-xbp-1s transgenics develop features diagnostic of human MM, including bone lytic lesions and subendothelial Ig deposition. Furthermore, transcriptional profiles of Emu-xbp-1s lymphoid and MM cells show aberrant expression of known human MM dysregulated genes. 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.

The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis. Publishing Authors By Initials

DR Carrasco,K Sukhdeo,M Protopopova,R Sinha,M Enos,DE Carrasco,M Zheng,M Mani,J Henderson,GS Pinkus,N Munshi,J Horner,EV Ivanova,A Protopopov,KC Anderson,G Tonon,RA DePinho,

For similar genetic processes: gene expression: transcription, genetic research abstracts see: genetic processes: gene expression: transcription, genetic research

PUBMED ID PMID:

MEDLINE DATE:

The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Cancer cell

VOLUME: 11

Page Numbers: 349-60

Journal Abbreviation:

ISSN: 1535-6108

DAY: 3

MONTH: Apr

YEAR: 2007

The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 101130617

The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis. Keywords Mesh Terms:

KEYWORDS: Transcription, Genetic

MESH TERMS: pathology

Chemical & Substance for Abstract: The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis. Information

Substance Name: TRE-binding protein

Registry Number: 0

Grant and Affiliation Information for The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis.

AFFILIATION: 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. ruben_carrasco@dfci.harvard.edu

Country: United States

AGENCY: United States NCI

GRANT: U01 CA84313

ACRONYM: CA

MEDLINETA: Cancer Cell

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis Related Publications

• Bcl2L12-mediated inhibition of effector caspase-3 and caspase-7 via distinct mechanisms in glioblastoma.
• Coactivation of receptor tyrosine kinases affects the response of tumor cells to targeted therapies.
• Common and distinct genomic events in sporadic colorectal cancer and diverse cancer types.
• DNA-dependent protein kinase catalytic subunit is not required for dysfunctional telomere fusion and checkpoint response in the telomerase-deficient mouse.
• Diminished lifespan and acute stress-induced death in DNA-PKcs-deficient mice with limiting telomeres.
• Haploinsufficiency of the mSds3 chromatin regulator promotes chromosomal instability and cancer only upon complete neutralization of p53.
• Ink4a/Arf tumor suppressor does not modulate the degenerative conditions or tumor spectrum of the telomerase-deficient mouse.
• Marked genomic differences characterize primary and secondary glioblastoma subtypes and identify two distinct molecular and clinical secondary glioblastoma entities.
• Pancreatic lkb1 deletion leads to acinar polarity defects and cystic neoplasms.
• Smad4 is dispensable for normal pancreas development yet critical in progression and tumor biology of pancreas cancer.
• Specific requirement of the chromatin modifier mSin3B in cell cycle exit and cellular differentiation.
• Stromal biology of pancreatic cancer.
• Suppression of ovarian follicle activation in mice by the transcription factor Foxo3a.
• The differentiation and stress response factor XBP-1 drives multiple myeloma pathogenesis.
• What drives intense apoptosis resistance and propensity for necrosis in glioblastoma?: A role for Bcl2L12 as a multifunctional cell death regulator.