Dr. Jackson received his BS in Zoology from the University of Texas, Austin, and then worked in the laboratories of Douglas Yee, MD, and Michael Brattain, PhD, on growth factor signal transduction in breast and colon cancer at the University of Texas Health Science Center at San Antonio. For his PhD research at the University of Texas Health Science Center at San Antonio (mentor: Olivia Pereira-Smith, PhD), he published studies describing the chromatin modifications that drive cellular senescence in both normal human fibroblasts and in breast cancer cell lines treated with DNA damaging chemotherapy. For his postdoctoral fellowship, he extended this work into mouse models of breast cancer at MD Anderson Cancer Center in the laboratory of Gigi Lozano, PhD. Dr. Jackson showed that p53 mutant mammary tumors responded better to chemotherapy than p53 wild type tumors and that induction of cellular senescence was responsible for the poor responses (Jackson JG et al, 2012, Cancer Cell, 21(6):793-806).
In 2015, Dr. Jackson joined the faculty in the Biochemistry Department at Tulane School of Medicine to continue studies on how cellular senescence causes a poor response to cancer treatment. Recent studies from our lab have shown that chemotherapy treated patients with breast cancers that were wild type for the tumor suppressor TP53 have much worse survival than patients with TP53 mutant tumors (Ungerleider et al, 2018). We showed that TP53 wild type tumors enter a program of arrest and cellular senescence that prevents the tumor cells from dying by apoptosis or mitotic catastrophe (Shahbandi et al, Cell Death & Differentiation, (2020) 27: 3097–3116; Tonnessen-Murray et al, Translational Oncology (2018) May 28;11(4):930-940; Jackson JG et al, 2012, Cancer Cell, 21(6):793-806). Further research by our lab identified a novel phenotype used by some chemotherapy treated cells to survive and persist: senescent tumor cells engulf and break down neighboring cells [Tonnessen-Murray et al Journal of Cell Biology, (2019) 218(11) 3827–3844; Frey et al, PLoS Biology, (2022) 24;20(10):e3001858]. We have recently identified how breast cancers activate programs of immune evasion to survive chemotherapy [Shahbandi et al, Nat Cancer 3, 1513–1533 (2022)].
