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TRAIL/TRAIL-R in hematologic malignancies.

¹Department of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Viale Regina Elena 299, Rome 00161, Italy. ugo.testa@iss.it

Journal of Cellular Biochemistry

|March 26, 2010

Summary

This summary is machine-generated.

Defects in apoptosis contribute to cancer. Tumor cells resist Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) therapy, but combinations show promise for hematologic malignancies.

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Area of Science:

Oncology
Cell Biology
Immunology

Background:

Apoptosis, or programmed cell death, is crucial for maintaining homeostasis, especially in the hematopoietic system.
Dysregulation of apoptosis contributes significantly to cancer development and progression.
The TNF-related apoptosis-inducing ligand (TRAIL) pathway offers a promising avenue for cancer therapy due to its selective tumor cell killing ability.

Purpose of the Study:

To review the expression and abnormalities of the TRAIL/TRAIL-Receptor (TRAIL-R) system in hematologic malignancies.
To explore the mechanisms of TRAIL resistance in these cancers.
To discuss strategies for overcoming TRAIL resistance in treating hematologic malignancies.

Main Methods:

Review of scientific literature on TRAIL/TRAIL-R system in hematologic malignancies.
Analysis of mechanisms underlying TRAIL resistance, including anti-apoptotic pathways and decoy receptors.
Examination of combination therapies designed to enhance TRAIL-induced apoptosis.

Main Results:

Most primary hematologic tumors exhibit resistance to TRAIL-mediated apoptosis.
Resistance mechanisms include activation of NF-kappaB, overexpression of anti-apoptotic proteins (FLIP, Bcl-2, XIAP), decoy receptors, and reduced TRAIL-R1/-R2 expression.
Combination strategies involving TRAIL with chemotherapy, radiotherapy, or inhibitors show potential to overcome resistance.

Conclusions:

TRAIL-mediated apoptosis is frequently impaired in hematologic malignancies due to various resistance mechanisms.
Combining TRAIL with other agents can enhance its efficacy by upregulating TRAIL receptors or downregulating anti-apoptotic proteins.
These combinatorial therapies represent a promising future direction for treating hematologic malignancies.