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244Anilkumar Gopalakrishnapillai, Ph.D. <p>Head, Cancer Stem Cell Laboratory <br></p>(302) 652-4833 (302) 651-4827 anil.g@nemours.org 5269, Building 400, Nemours Biomedical Research Nemours Biomedical Research Experimental Station 200 Powder Mill Road, Building 400, Wilmington, DE 19803 <p> <strong>Ph.D.</strong> – Indian Institute of Science, India<br> <strong>Postdoctoral</strong> – University of California, Los Angeles</p><p>Our laboratory focuses on understanding the initiation and progression of pediatric leukemia specifically leukemia seen among Down Syndrome (DS) children.  A mutation in the gene coding for an important protein called GATA1 induces a pre-leukemic condition in these children marked by a very high proliferation of myeloid cells. In approximately thirty percent of these cases, the pre-leukemic condition is not resolved and it progresses into Down Syndrome-Acute Myeloid Leukemia (DS-AML) by acquisition of additional mutations in genes falling under three major categories, those coding for signaling molecules, epigenetic modifiers and cell division regulators. We have little knowledge about how the interplay among these factors causes leukemia development in DS children. Currently a combination of induced pluripotent stems cells derived from Down syndrome children and CRISPR/Cas9 technologies are being used in the lab for the generation of different subtypes of DS-AML models to study the synergistic effect of factors causing DS-AML. We also develop patient derived xenograft models of DS-AML and using such models for preclinical testing. We mainly focus on immunotherapeutic and epigenetic approaches our preclinical testing to move these findings to clinical trial.  Another project of high importance to our lab is understanding unique features of cancer stem cells and its interaction with leukemia niche. ​</p><ul> <li>Developing DS-AML models by combining iPSCs and CRISPR/Cas9 approach </li><li>PDX models of DS-AML for preclinical testing. </li><li>Deciphering molecular mechanism of DS-AML biogenesis using transcriptomics and epigenomics approaches.​</li><li>AML stem cells and their role in developing leukemic niche​</li></ul><p></p><p></p><ul><li>​​Meredith Tavenner, MS, Research Associate</li><li>Pallashri Saha, Ph.D, Research Associate</li><li>Kara Lehner, Graduate Student (jointly with Sonali Barwe)</li><li>Kader Cicek, Graduate student</li></ul><p></p><p></p><p></p><p></p><p></p><ol><li>​Barwe SP1, Kisielewski A, Bonvini E, Muth J, Moncada JD3, Kolb EA <strong>Gopalakrishnapillai A</strong> 1, Efficacy of Flotetuzumab in Combination with Cytarabine in Patient-Derived Xenograft Models of Pediatric Acute Myeloid Leukemia. J. Clin. Med. 2022, 11, 1333. https://doi.org/10.3390/ jcm11051333</li><li>Barwe SP, Sebastian A, Sidhu I, Kolb EA, <strong>Gopalakrishnapillai A</strong> Modeling Down Syndrome Myeloid Leukemia by Sequential Introduction of <em>GATA1</em> and <em>STAG2</em> Mutations in Induced Pluripotent Stem Cells with Trisomy 21. Cells. 2022 11;11(4):628. doi: 10.3390/cells11040628.</li><li><strong>Gopalakrishnapillai A</strong>, Correnti CE, Pilat K, Lin I, Chan MK, Bandaranayake AD, Mehlin C, Kisielewski A, Kaeding A, Meshinchi S, Olson JM, Kolb EA, Barwe SP. Immunotherapeutic targeting of mesothelin positive pediatric AML using bispecific T cell engaging antibodies. Cancers, 2021 Nov 26;13(23):5964. doi: 10.3390/cancers13235964.</li><li>Sidhu I, Barwe SP, Kiick KL, Kolb EA, <strong>Gopalakrishnapillai A</strong>. A 3-D hydrogel-based system for modeling transient myeloproliferative disorder using GATA1s expressing induced pluripotent stem cells. Biomater Sci, Sep (18)6266-6281 (2021).</li><li>Heikamp EB, Henrich JA, Pemer F, Wong EM, Hatton C, Wen Y, Barwe SP, <strong>Gopalakrishnapillai A</strong>, Xu H, Julia H, Takao S, Kazansky Y, Pikman Y, McGeehan GM, Kolb EA, Kentsis A, Armstrong SA. The Menin-MLL1 interaction is a molecular dependency in <em>NUP98</em>-rearranged AML. Blood, 2022 Feb 10;139(6):894-906. doi: 10.1182/blood.2021012806.</li><li>Sidhu I, Barwe SP, <strong>Gopalakrishnapillai A</strong>. The extracellular matrix: a key player in the pathogenesis of hematologic malignancies. Blood Rev. 2021 Jul;48:100787. doi: 10.1016/j.blre.2020.100787.</li><li>Barwe SP, Sidhu I, Kolb EA, <strong>Gopalakrishnapillai A</strong>. Modeling transient abnormal myelopoiesis using induced pluripotent stem cells and CRISPR/Cas9 technology. Mol Ther Methods Clin Dev, Sep (19):201-209 (2020).</li></ol><img alt="" src="/Images%20Bios/anilg.png" style="BORDER:0px solid;" />

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