Postdoctoral Fellowship, MD Anderson Cancer Center
PhD, University of Texas Health Science Center, San Antonio
BS, Zoology, University of Texas, Austin
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. In breast and many other solid tumor types, residual tumor is still present at the time of surgery following chemotherapy treatment. Funded by a DoD BCRP Breakthrough Award, the lab investigates how the tumor suppressor p53 is paradoxically associated with poor responses to chemotherapy treatment in breast cancer. p53, 'the guardian of the genome', is a transcription factor that is activated in response to cellular stressors and DNA damage, and initiates cell cycle arrest or apoptosis. p53 is mutated in ~30% of breast tumors.
Dr. Jackson’s lab has shown that breast cancer patients with tumors capable of undergoing senescence (those that are p53 wild type) had dramatically worse survival following chemotherapy, but that addition of a hormone receptor targeting drug was highly beneficial in these patients (Ungerleider et al, 2018).
In further investigations, Dr. Jackson’s lab discovered a novel cannibalism phenotype used by cells that enter senescence to survive chemotherapy and drive relapse (Tonnessen-Murray CA et al, 2019). This research was covered by more than 25 news outlets, the NIH Director’s blog, Scientific American, and highlight sections of Journal of Cell Biology, Trends in Cancer, and Nature.
Recently, the lab showed that a new class of drugs termed “senolytics” could selectively induce apoptosis in some breast cancer cell lines and mouse mammary tumors that survive chemotherapy by entering senescence. Drugs that target the anti-apoptotic protein BCLXL were highly effective in many cases, but low expression of the pro-apoptotic gene NOXA conferred resistance in some cells, necessitating additional MCL1 inhibition (Shahbandi, Rao et al; 2020).
Breast cancer tumorigenesis and drug response, cellular senescence, mouse models, mouse genetics, tumor suppressor mechanism of action, p53
Cellular senescence, including mechanisms of induction, chromatin changes and consequences to organisms.
A full bibliography of the lab’s research can be found at https://www.ncbi.nlm.nih.gov/sites/myncbi/1j3h16qYex45m/bibliography/public/