Journal of Leukemia
Open Access

Minimal Residual Disease as a Precision Marker for Individualized Leukemia Therapy

Julia Weber^{* *}Correspondence: Julia Weber, Department of Cancer Biology, Karolinska Institutet, Stockholm, Sweden, Email:

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Description

Personalized medicine in leukemia treatment represents one of the most transformative developments in modern oncology, shifting the focus from a one-size-fits-all approach to a tailored therapeutic strategy based on the unique molecular and genetic characteristics of each patient’s disease. Over the past two decades, remarkable progress in genomics, molecular diagnostics, and bioinformatics has unveiled the heterogeneity of leukemia, demonstrating that even within a single clinical subtype, such as Acute Myeloid Leukemia (AML) or Chronic Lymphocytic Leukemia (CLL), there exists tremendous biological diversity. This realization has fundamentally altered how clinicians diagnose, classify, and treat leukemia, paving the way for precision-based therapies that aim to maximize efficacy while minimizing unnecessary toxicity. The rise of personalized medicine has not only revolutionized treatment outcomes but also reshaped the philosophical understanding of what it means to cure cancer at the individual level.

Traditional response assessment in leukemia was based largely on morphological evaluation, which lacks the sensitivity to detect small numbers of residual leukemic cells that can lead to relapse. With the advent of highly sensitive techniques such as flow cytometry, Quantitative Polymerase Chain Reaction (QPCR), and Next-Generation Sequencing (NGS), clinicians can now detect MRD at levels as low as one leukemic cell among a million normal cells. MRD status has become one of the most powerful prognostic indicators across leukemia subtypes. Patients achieving MRD negativity after therapy exhibit significantly improved relapse-free and overall survival compared to MRD-positive patients. Importantly, MRD monitoring enables dynamic treatment adaptation—patients with persistent MRD may receive additional targeted therapy, stem cell transplantation, or maintenance regimens, while those who achieve deep molecular remission can potentially avoid overtreatment and its associated toxicity. This individualized approach embodies the essence of personalized medicine: continuous refinement of therapy based on the evolving biology of the disease.

The integration of immunotherapy into personalized leukemia treatment further exemplifies the field’s progress. Therapies such as Chimeric Antigen Receptor (CAR) T-cell therapy and bispecific T-cell engagers represent a convergence of molecular precision and immune engineering. In Acute Lymphoblastic Leukemia (ALL), particularly in relapsed or refractory cases, CAR T-cell therapy targeting CD19 has achieved remarkable remission rates. Each patient’s T cells are genetically modified to express a receptor that recognizes a specific antigen on leukemia cells, enabling personalized immune attack. Although not without challenges such as cytokine release syndrome and neurotoxicity, this approach underscores the power of individualized treatment strategies that harness the patient’s own immune system to eradicate malignancy. Bispecific antibodies, which simultaneously bind T cells and leukemia cells, have also demonstrated success, offering off-the-shelf immunotherapeutic options that complement the personalized framework.

Despite its transformative potential, personalized medicine in leukemia faces several challenges that temper its universal implementation. One of the foremost limitations is the intrinsic complexity and heterogeneity of leukemia at both the genetic and epigenetic levels. Many leukemias exhibit multiple concurrent mutations that interact in intricate networks, influencing disease behavior and therapeutic response. Targeting one driver mutation may not be sufficient if compensatory pathways promote resistance or survival. Clonal evolution, wherein new mutations emerge during therapy, remains a major cause of relapse. As a result, combination strategies that simultaneously inhibit multiple pathways are being explored to preempt resistance. Ensuring equitable access to precision diagnostics and therapies is essential to realizing the full promise of personalized medicine.