Journal of Molecular Oncology Research

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +1 (202) 780-3397

Short Communication - Journal of Molecular Oncology Research (2024) Volume 8, Issue 6

Advancing oncology: Targeted therapy in the treatment of acute lymphoblastic leukemia.

Amini Join *

Department of Oncology, Queens University, Canada

*Corresponding Author:
Amini Join
Department of Oncology, Queens University, Canada
E-mail: amini@join.ca

Received: 01-Nov-2024, Manuscript No. AAMOR -24-155333; Editor assigned: 02-Nov-2024, PreQC No. AAMOR -24-155333(PQ); Reviewed: 18-Nov-2024, QC No. AAMOR -24-155333; Revised: 22-Nov-2024, Manuscript No. AAMOR -24-155333(R); Published: 29-Nov-2024, DOI: 10.35841/ aamor-8.6.265

Citation: : Join A. Advancing oncology: Targeted therapy in the treatment of acute lymphoblastic leukemia. J Mol Oncol Res. 2024;8(6):265.

Visit for more related articles at Journal of Molecular Oncology Research

Introduction

Acute Lymphoblastic Leukemia (ALL), a type of blood cancer that affects both children and adults, has long been a challenge for oncologists worldwide. Despite advancements in traditional chemotherapy and radiation therapy, many patients face relapse or severe side effects. Targeted therapy, a revolutionary approach in oncology, has emerged as a beacon of hope, offering precision treatment while minimizing collateral damage to healthy tissues. This article explores the transformative potential of targeted therapy in managing ALL [1, 2].

ALL is characterized by the rapid proliferation of immature lymphoblasts in the bone marrow and blood. This uncontrolled growth disrupts normal blood cell production, leading to anemia, infection susceptibility, and bleeding disorders. ALL is classified into subtypes based on genetic and molecular abnormalities, which play a crucial role in guiding treatment strategies. Conventional therapies for ALL include a combination of chemotherapy, corticosteroids, and, in some cases, stem cell transplantation. While these methods have improved survival rates, they are associated with significant toxicities and may not address the underlying molecular drivers of the disease, particularly in high-risk or relapsed cases [3, 4].

Targeted therapy is a personalized cancer treatment that focuses on specific molecules and pathways critical for cancer cell survival and growth. Unlike chemotherapy, which indiscriminately attacks rapidly dividing cells, targeted therapy spares healthy cells, reducing adverse effects and improving patient quality of life. In ALL, targeted therapy works by interfering with aberrant signaling pathways, blocking proteins that promote cell division, or inducing apoptosis in cancer cells. These therapies are often developed based on insights from genomic and proteomic studies, ensuring a tailored approach to each patient’s cancer profile. Tyrosine Kinase Inhibitors (TKIs): These drugs, such as imatinib and dasatinib, are used for patients with Philadelphia chromosome-positive ALL. TKIs block the BCR-ABL protein, a driver of cancer cell proliferation, leading to improved remission rates. Monoclonal Antibodies: Agents like blinatumomab target CD19, a protein expressed on B cells, and recruit T-cells to destroy cancer cells. These therapies have shown remarkable efficacy in relapsed and refractory ALL cases. Antibody-Drug Conjugates (ADCs): ADCs combine the specificity of antibodies with the potency of chemotherapy drugs, delivering cytotoxic agents directly to cancer cells [5, 6].

Targeted therapy offers several advantages over traditional treatments. It provides higher specificity, reduces systemic toxicity, and improves treatment outcomes. For patients with ALL, targeted therapy has resulted in longer remission periods, fewer side effects, and a better quality of life compared to standard chemotherapy. Despite its promise, targeted therapy is not without challenges. Resistance to therapy can develop over time due to genetic mutations in cancer cells. Additionally, the high cost of targeted treatments may limit accessibility for many patients, highlighting the need for policy interventions and financial support programs. Ongoing research in molecular oncology continues to uncover new targets and pathways for drug development. Advances in CRISPR technology and next-generation sequencing are accelerating the identification of genetic drivers of ALL, paving the way for even more precise treatments [7, 8].

To overcome resistance and enhance efficacy, researchers are exploring combination therapies that integrate targeted agents with traditional chemotherapy or immunotherapy. This multi-pronged approach aims to deliver a more comprehensive attack on cancer cells while sparing healthy tissues. The success of targeted therapy relies on accurate diagnosis and molecular profiling. Developing robust infrastructure for genetic testing and personalized treatment planning is essential for integrating these therapies into standard care. Targeted therapy represents a paradigm shift in oncology, offering hope to millions of ALL patients worldwide. Efforts to expand access, reduce costs, and improve treatment adherence are critical for maximizing its impact [9, 10].

Conclusion

The advent of targeted therapy has redefined the treatment landscape for Acute Lymphoblastic Leukemia. By addressing the molecular underpinnings of the disease, these therapies have improved outcomes and transformed patient care. As research continues to advance, targeted therapy promises to further enhance the fight against ALL, bringing us closer to the goal of curing this challenging malignancy.

References

  1. Ott PA. Intralesional Cancer Immunotherapies. Hematol Oncol Clin North Am. 2019;33(2):249-260.

    2. Indexed at, Google Scholar, Cross Ref

  2. Janz TA, Neskey DM, Nguyen SA, et al. Is imaging of the brain necessary at diagnosis for cutaneous head and neck melanomas?. Am J Otolaryngol. 2018;39(5):631-635.

    3. Indexed at, Google Scholar, Cross Ref

  3. Barker CA, Salama AK. New NCCN Guidelines for Uveal Melanoma and Treatment of Recurrent or Progressive Distant Metastatic Melanoma. J Natl Compr Canc Netw. 2018;16(5S):646-650.

    4. Indexed at, Google Scholar, Cross Ref

  4. Blakely AM, Comissiong DS, Vezeridis MP, et al. Suboptimal compliance with national comprehensive cancer network melanoma guidelines. Am J Clin Oncol. 2018 Aug;41(8):754-759.

    5. Indexed at, Google Scholar, Cross Ref

  5. Cho SI, Lee J, Jo G, et al. Local recurrence and metastasis in patients with malignant melanomas after surgery: A single-center analysis of 202 patients in South Korea. PLoS One. 2019;14(3):e0213475.

    6. Indexed at, Google Scholar, Cross Ref

  6. Gurney JG, Severson RK, Davis S, et al. Incidence of cancer in children in the United States. Sex?, race?, and 1?year age?specific rates by histologic type.  1995;75(8):2186-95.

    7. Indexed at, Google Scholar, Cross Ref

  7. Jt S. downing Jr, Crist WM. Non-Hodgkin’s lymphoma in childhood. N engl J Med. 1996;334:1238-48.

    8. Indexed at, Google Scholar, Cross Ref

  8. Jaffe ES, Harris NL, Stein H, et al. Classification of lymphoid neoplasms: the microscope as a tool for disease discovery.  2008;112(12):4384-99.

    9. Indexed at, Google Scholar, Cross Ref

  9. Mbulaiteye SM, Biggar RJ, Bhatia K, et al. Sporadic childhood Burkitt lymphoma incidence in the United States during 1992-2005. Pediatr Blood Canc. 2009;53(3):366-70.

    10. Indexed at, Google Scholar, Cross Ref

  10. Klapper W, Szczepanowski M, Burkhardt B, et al. Molecular profiling of pediatric mature B-cell lymphoma treated in population-based prospective clinical trials.  2008;112(4):1374-81.

    11. Indexed at, Google Scholar, Cross Ref

     

Get the App