Browsing by Author "Manvi Bansal"

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Potential therapeutic targets in chronic myeloid leukemia
(Springer, 2025) Manvi Bansal; Malkhey Verma
Chronic myeloid leukemia (CML) is driven by the BCR::ABL fusion oncoprotein, caused by a reciprocal translocation between chromosomes no. 9 and 22, leading to the formation of the Philadelphia chromosome having aberrant tyrosine kinase activity. Tyrosine kinase inhibitors (TKIs) revolutionized the CML treatment and helped patients to achieve a higher survival rate. However, TKI resistance, leukemia stem cell (LSC) persistence, and disease relapse highlight the necessity for alternative treatment strategies. Furthermore, oxidative stress pathways are critical in promoting leukemic development and resistance, offering an emerging avenue for targeted intervention. This review explores several promising therapeutic targets in CML, such as suppressor pathways, autophagy modulation, the BCL-2 family proteins, and microRNAs (miRNAs) modulation. Restoring the function of tumor suppressors, such as PTPRG and p53, may complement current therapies since they are essential in regulating cell proliferation and apoptosis. Tumor suppressors offer the potential to enhance apoptosis, while the precise modulation of autophagy, a complex cellular process with context-dependent roles, can regulate cell survival under therapeutic pressure. The BCL-2 family proteins regulate apoptosis by the mitochondrial intrinsic apoptosis pathway, representing a critical target for overcoming apoptotic resistance in CML cells. Meanwhile, miRNAs emerge as potent modulators of oncogenic and apoptotic pathways by acting as tumor suppressors or oncomiRs, presenting an opportunity for advanced treatment. This review also includes gene editing to target oncogenic drivers or correcting mutations and USP inhibition to overcome resistance. Finally, it concludes by emphasizing the importance of combining these diverse therapeutic approaches with ongoing next-generation TKIs and comprehensive and personalized approaches for CML treatment, offering a path toward deeper remissions and ultimately achieving curative outcomes for CML patients. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2025.
Role of miRNAs to control the progression of Chronic Myeloid Leukemia by their expression levels
(Springer, 2024) Manvi Bansal; Sana Ansari; Malkhey Verma
Chronic Myeloid Leukemia (CML) is a myeloproliferative disorder distinguished by a specific genetic anomaly known as a reciprocal translocation between chromosomes 9 and 22. This translocation causes fusion between the BCR and ABL regions. Consequently, BCR::ABL oncoprotein is formed, which plays a significant role in driving CML progression. Imatinib, a tyrosine kinase inhibitor (TKI), became the first line of drugs against CML. However, with continuous treatment, patients developed resistance against it. Indeed, to address this challenge, microRNA-based therapy emerges as a promising approach. miRNAs are 20–25 nucleotides long and hold great significance in various cellular processes, including cell differentiation, proliferation, migration, and apoptosis. In several malignancies, it has been reported that miRNAs might help to promote or prevent tumourigenesis and abnormal expression because they could act as both oncogenes/tumor suppressors. Recently, because of their vital regulatory function in maintaining cell homeostasis, miRNAs might be used to control CML progression and in developing new therapies for TKI-resistant patients. They might also act as potential prognostic, diagnostic, and therapeutic biomarkers based on their expression profiles. Various annotation tools and microarray-based expression profiles can be used to predict dysregulated miRNAs and their target genes. The main purpose of this review is to provide brief insights into the role of dysregulated miRNAs in CML pathogenesis and to emphasize their clinical relevance, such as their significant potential as therapeutics against CML. Utilizing these miRNAs as a therapeutic approach by inhibition or amplification of their activity could unlock new doors for the therapy of CML. © 2024, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.