Targeted therapy in T-cell malignancies: dysregulation of the cellular signaling pathways.

Abstract

T-cell malignancies, mainly known as T-cell acute lymphoblastic leukemia (T-ALL) and T-cell non-Hodgkin's lymphoma (T-NHL), are aggressive tumors. Although the clinical outcome of the patients has improved dramatically with combination chemotherapy, significant challenges remain, including understanding of the factors that contribute to the malignant behavior of these tumor cells and developing subsequently optimal targeted therapy. Aberrant cell signal transduction is generally involved in tumor progression and drug resistance. This review describes the pathogenetic role of multiple cellular signaling pathways in T-cell malignancies and the potential therapeutic strategies based on the modulation of these key signaling networks.

• Authors: W-L Zhao
• Journal: Leukemia (Leukemia) Vol. 24 Issue 1 Pg. 13-21 (Jan 2010) ISSN: 1476-5551 [Electronic] England
• PMID: 19865108 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• NF-kappa B
• NFATC Transcription Factors
• NOTCH1 protein, human
• NOTCH3 protein, human
• Phosphoinositide-3 Kinase Inhibitors
• Receptor, Notch1
• Receptor, Notch3
• Receptors, Notch
• STAT5 Transcription Factor
• Protein Kinases
• MTOR protein, human
• Janus Kinase 2
• Proto-Oncogene Proteins c-akt
• TOR Serine-Threonine Kinases

Topics

• Animals
• Humans
• Janus Kinase 2 (physiology)
• Lymphoma, T-Cell (drug therapy)
• MAP Kinase Signaling System
• NF-kappa B (physiology)
• NFATC Transcription Factors (physiology)
• Phosphatidylinositol 3-Kinases (physiology)
• Phosphoinositide-3 Kinase Inhibitors
• Precursor T-Cell Lymphoblastic Leukemia-Lymphoma (drug therapy, physiopathology)
• Protein Kinases
• Proto-Oncogene Proteins c-akt (antagonists & inhibitors, physiology)
• Receptor, Notch1 (physiology)
• Receptor, Notch3
• Receptors, Notch (physiology)
• STAT5 Transcription Factor (physiology)
• Signal Transduction (physiology)
• TOR Serine-Threonine Kinases