Opinion - (2025) Volume 11, Issue 1
Received: 01-Feb-2025, Manuscript No. jotr-25-168442;
Editor assigned: 03-Feb-2025, Pre QC No. P-168442;
Reviewed: 15-Feb-2025, QC No. Q-168442;
Revised: 20-Feb-2025, Manuscript No. R-168442;
Published:
27-Feb-2025
, DOI: 10.37421/2476-2261.2025.11.294
Citation: Fearnhead, Sasako. "Personalized Chemotherapy Regimens: Role of Pharmacogenomics and Tumor Profilin." J Oncol Transl Res 11 (2025): 294.
Copyright: © 2025 Fearnhead S. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Cancer treatment has undergone significant transformation over the past few decades, shifting from a one-size-fits-all approach to a more nuanced and individualized strategy. At the forefront of this transformation is personalized chemotherapy, which tailors treatment regimens based on the unique molecular and genetic characteristics of both the patient and their tumor. Two central pillars that support this approach are pharmacogenomics-the study of how a patientâ??s genetic makeup affects their response to drugs-and tumor profiling, which involves molecular characterization of cancer cells to guide therapeutic decisions [1].
Chemotherapy remains a cornerstone in the treatment of many cancers. However, traditional chemotherapy regimens often produce variable outcomes due to differences in drug metabolism, tumor heterogeneity, and patient susceptibility to adverse effects. By incorporating pharmacogenomic data and tumor-specific molecular signatures, clinicians can now design personalized chemotherapy plans that optimize efficacy, minimize toxicity, and improve overall outcomes [2].
Genetic polymorphisms in drug-metabolizing enzymes significantly influence chemotherapy efficacy and toxicity. Patients with TPMT deficiency are at risk of severe myelosuppression when treated with thiopurine drugs (e.g., mercaptopurine, azathioprine). Genotyping TPMT prior to chemotherapy helps identify individuals requiring dose adjustments. DPD is critical for the metabolism of 5-fluorouracil (5-FU). Deficiency in DPD due to DPYD gene mutations can result in life-threatening toxicity. Pre-treatment screening can prevent adverse reactions by guiding dose modification or selecting alternative agents [3].
Tumor profiling involves analyzing the genetic, transcriptomic, and proteomic characteristics of cancer cells. Unlike pharmacogenomics, which examines the patient's germline DNA, tumor profiling focuses on somatic mutations acquired during tumorigenesis. These molecular alterations serve as targets for chemotherapy selection, combination strategies, and resistance prediction. Genomic analysis identifies mutations, gene amplifications, deletions, and chromosomal rearrangements relevant to chemotherapy responsiveness. KRAS/NRAS mutations predict resistance to anti-EGFR therapy (cetuximab, panitumumab) in colorectal cancer. BRAF V600E mutation is associated with poor prognosis and guides targeted therapy combinations in melanoma and colorectal cancer. HER2-positive breast and gastric cancers benefit from HER2-targeted therapies (trastuzumab, lapatinib). HER2 status also influences sensitivity to certain chemotherapeutic agents. These gene fusions in lung cancer dictate response to ALK inhibitors and influence chemotherapy resistance patterns [4].
Combining genomics, transcriptomics, proteomics, metabolomics, and epigenomics will offer a more comprehensive understanding of tumor biology and therapy response. AI algorithms can process large datasets to predict drug response patterns and personalize chemotherapy regimens in real time. These technologies provide insights into cellular heterogeneity and microenvironmental interactions, allowing for highly precise treatment planning. Functional assays using patient-derived cells can test chemotherapy sensitivity ex vivo, complementing molecular data. Development of clinical guidelines by consortia like CPIC (Clinical Pharmacogenetics Implementation Consortium) and PharmGKB will facilitate standardization and implementation in practice [5].
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Journal of Oncology Translational Research received 93 citations as per Google Scholar report