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Targeted Cancer Therapies

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...

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Updated: Dec 6, 2025

Retroviral Overexpression of CXCR4 on Murine B-1a Cells and Adoptive Transfer for Targeted B-1a Cell Migration to the Bone Marrow and IgM Production

Retroviral Overexpression of CXCR4 on Murine B-1a Cells and Adoptive Transfer for Targeted B-1a Cell Migration to the Bone Marrow and IgM Production

Published on: May 31, 2020

Targeting CXCR4 in AML and ALL.

Daniel Cancilla¹, Michael P Rettig¹, John F DiPersio¹

¹Division of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO, United States.

Frontiers in Oncology

|October 5, 2020

Summary

Targeting the CXCR4 receptor on acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) blasts can improve treatment outcomes. This review explores strategies for targeting CXCR4 to enhance cancer cell killing and overcome chemotherapy resistance.

Keywords:

ALL AML CXCL12 CXCR4 chemosensitization

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Published on: February 20, 2018

Area of Science:

Hematology
Oncology
Molecular Biology

Background:

The bone marrow microenvironment influences leukemia cell survival and drug resistance.
CXC receptor 4 (CXCR4) and its ligand CXCL12 are crucial for leukemia stem cell homing and survival.
High CXCR4 expression on acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) blasts correlates with poor prognosis.

Purpose of the Study:

To review recent findings and therapeutic strategies targeting the CXCR4 pathway in AML and ALL.
To discuss the role of CXCR4 in regulating leukemia cell behavior and treatment resistance.
To explore the clinical potential of CXCR4-targeting agents.

Main Methods:

Review of preclinical and clinical studies on CXCR4-targeting agents.
Analysis of data on CXCR4 expression in AML and ALL patient samples.
Discussion of various therapeutic modalities including small molecules, peptides, and antibodies.

Main Results:

CXCR4 signaling is implicated in leukemia cell self-renewal, growth, and chemoresistance.
Targeting CXCR4 has shown promise in preclinical models for reducing leukemia burden.
Clinical development of CXCR4 inhibitors, antibodies, and antibody-drug conjugates is ongoing for AML and ALL.

Conclusions:

Targeting CXCR4 represents a promising therapeutic strategy for AML and ALL.
Further research and clinical trials are needed to optimize CXCR4-directed therapies.
Combination strategies involving CXCR4 inhibitors may enhance treatment efficacy and overcome resistance.