A jagged road to lymphoma aggressiveness

Vedran Radojcic; Ivan Maillard

doi:10.1016/j.ccr.2014.03.001

A jagged road to lymphoma aggressiveness

Cancer Cell. 2014 Mar 17;25(3):261-3. doi: 10.1016/j.ccr.2014.03.001.

Authors

Vedran Radojcic¹, Ivan Maillard²

Affiliations

¹ Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA; Division of Hematology-Oncology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
² Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA; Division of Hematology-Oncology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA; Department of Cell and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA. Electronic address: [email protected].

Abstract

In this issue of Cancer Cell, Cao and colleagues identify an FGF4/Jagged1-driven crosstalk between tumor cells and their vascular niche that activates Notch signaling, sustaining the aggressiveness of certain mouse and human B cell lymphomas. These findings identify new therapeutic opportunities to target pathogenic angiocrine functions in cancer.

Publication types

Comment

MeSH terms

Animals
Burkitt Lymphoma / metabolism*
Burkitt Lymphoma / pathology*
Calcium-Binding Proteins / metabolism*
Drug Resistance, Neoplasm*
Fibroblast Growth Factor 4 / metabolism*
Humans
Intercellular Signaling Peptides and Proteins / metabolism*
Jagged-1 Protein
Membrane Proteins / metabolism*
Receptor, Fibroblast Growth Factor, Type 1 / metabolism*
Receptor, Notch2 / metabolism*
Serrate-Jagged Proteins

Substances

Calcium-Binding Proteins
Fibroblast Growth Factor 4
Intercellular Signaling Peptides and Proteins
JAG1 protein, human
Jag1 protein, mouse
Jagged-1 Protein
Membrane Proteins
Receptor, Notch2
Serrate-Jagged Proteins
Receptor, Fibroblast Growth Factor, Type 1

Grants and funding

R01 AI091627/AI/NIAID NIH HHS/United States