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Machine Learning Approach to Overcome the Challenges in Theranostics
Published in Shampa Sen, Leonid Datta, Sayak Mitra, Machine Learning and IoT, 2018
Bishwambhar Mishra, Sayak Mitra, Karthikeya Srinivasa Varma Gottimukkala, Shampa Sen
Due to the role of CXCR4 in HIV, multiple CXCR4 antagonists—although not sufficient for the treatment of HIV, are currently being evaluated and/or used for stem cell mobilization and as antitumor therapy. Some of the antagonists were also shown in animal models to be of use in evaluating CXCR4 expression in whole tumors noninvasively by molecular imaging. The research on CXCR4 has been ongoing for the last decade and has yielded more than 11,398 papers in PubMed, as of December 2017.
Peptide-enabled receptor-binding-quantum dots for enhanced detection and migration inhibition of cancer cells
Published in Journal of Biomaterials Science, Polymer Edition, 2020
Ruijuan Zu, Xiaocui Fang, Yuchen Lin, Shilin Xu, Jie Meng, Haiyan Xu, Yanlian Yang, Chen Wang
Dedicated efforts have been reported on studying chemokine receptor CXCR4 as a potential therapeutic target for cancer diagnosis and treatment [10]. One small molecule antagonist named as plerixafor (also termed as AMD3100) has been approved by the U.S. Food and Drug Administration (FDA) for non-Hodgkin’s lymphoma and multiple myeloma treatment [11,12]. Several other CXCR4 antagonist candidates are currently being evaluated in various stages of clinical development. In our previous study, we selected a series of potential peptide antagonists with designated sequences in our original experiments according to the extracellular domain of CXCR4. The binding strengths between peptide antagonists and CXCR4 were examined using flow cytometry, surface plasmon resonance (SPR), and confocal microscopy methods. Our results demonstrated that, peptide E5 (GGRSFFLLRRIQGCRFRNTVDD) shows high binding affinity and selectivity towards CXCR4-overexpressed cancer cells [13]. E5 was observed to inhibit the migration and adhesion of cancer cells, and increase the sensitivity of cancer cells to chemotherapeutic agents by antagonizing CXCR4/CXCL12 chemokine axis [13–15].