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244Anilkumar Gopalakrishnapillai, Ph.D. <p>Head, Cancer Stem Cell Laboratory </p>(302) 652-4833 (302) 651-4827 anil.g@nemours.org 5211, Building 400, Nemours Biomedical Research Nemours Biomedical Research Experimental Station 200 Powder Mill Road, Building 400, Wilmington, DE 19803 <ul> <li><strong>B.S.</strong> – University of Kerala, India </li><li><strong>M.S.</strong> – Cochin University of Science and Technology, India </li><li><strong>Ph.D.</strong> – Indian Institute of Science, India </li><li><strong>Postdoctoral</strong> – University of California, Los Angeles<br>  </li></ul><p>Children with Down syndrome (DS) possess an extra copy of chromosome 21 and are at a high risk for different types of leukemia.  A mutation in the gene coding for an important protein called GATA1 induces a pre-leukemic condition 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. Another major project is developing patient derived xenograft models of DS-AML and using such models for preclinical testing.</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. </li><li>Testing the efficacy of metformin as a neoadjuvant for the treatment of pediatric leukemia and other hematologic malignancies. </li></ul><ol> <li><strong>Gopalakrishnapillai A</strong>, Kolb EA, Dhanan P, Mason RW, Napper A, Barwe SP. Disruption of annexin II/p11 interaction suppresses leukemia cell binding, homing and engraftment, and sensitizes leukemia cells to chemotherapy. PLoS ONE, October 14, 2015 </li><li><strong>Gopalakrishnapillai A</strong>, Kolb EA, Dhanan P, Bojja AS, Mason RW, Corao D, Barwe SP Generation of Pediatric Leukemia Xenograft Models in NSG-B2m Mice: Comparison with NOD/SCID Mice.. Front Oncol, Jun 27;6:162, 2016.   </li><li>Quagliano A, <strong>Gopalakrishnapillai A</strong>, Barwe SP. Epigenetic drug combination overcomes osteoblast-induced chemoprotection in pediatric acute lymphoid leukemia.   Leuk Res. 56;36-43, 2017. </li><li><strong>Gopalakrishnapillai A</strong>, Kolb EA, McCahan SM, Barwe SP. Epigenetic drug combination induces remission in mouse xenograft models of pediatric acute myeloid leukemia. Leuk Res, 58:91-97, 2017. </li><li>Bloh, K., Bilak P. A., <strong>Gopalakrishnapillai A.</strong>, Kolb E. A., & Kmiec E. B.  CRISPR/Cas9-Directed Reassignment of the GATA1 Initiation Codon in K562 Cells to Recapitulate AML in Down Syndrome. Molecular Therapy - Nucleic Acids. 7, 288-98, 2017 </li><li>Barwe SP, Quagliano A, <strong>Gopalakrishnapillai A.</strong> Eviction from the sanctuary: Development of targeted therapy against the cell adhesion molecules in acute lymphoblastic leukemia. Seminar in oncology. 2017 44(2):101-112. PMID: 28923207. </li><li><strong>Gopalakrishnapillai A</strong>, Kolb EA, Barwe SP. Metformin suppresses pediatric acute myeloid leukemia cell viability and clonogenicity. Cancer Metab, 2:P23, 2014. PMCID: PMC4072943.<br>  </li></ol><img alt="" src="/Images%20Bios/anilg.png" style="BORDER:0px solid;" />

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