Research Summary

Dr. Julie Saba is a pediatric oncologist and basic research scientist. Her research team is focused on elucidating novel biochemical and genetic mechanisms responsible for the development and progression of childhood cancers. Early in her career, Dr. Saba theorized that sphingolipids, a unique family of lipids that control cell growth and death, played a key role in carcinogenesis. Using a yeast genetic approach, she identified the first known genes of sphingolipid metabolism, opening the pathway to genetic manipulation. Now, three decades later, many hundreds of scientific studies have confirmed the contributions of sphingolipids to carcinogenesis, metastasis, and chemotherapy resistance. Dr. Saba’s group established that pro-inflammatory sphingolipids play a fundamental role in mediating cell transformation, the first step in carcinogenesis. They demonstrated that sphingolipids provide a biochemical link between inflammation and carcinogenesis. She has also shown the importance of dietary anti-inflammatory plant sphingolipids in cancer chemoprevention. 

The Saba team is currently focused on clarifying the role of an oncogene called AF1q in neuroblastoma, pediatric brain tumors, and adult cancers. Their group has found that AF1q is regulated by sphingolipids and acts through varied mechanisms to promote the growth and survival of different types of cancer, such as by suppressing cellular senescence (aging) and augmenting the cellular expression of other cancer-promoting genes.  Dr. Saba’s other projects focus on the discovery of a rare inborn error of sphingolipid metabolism in a cancer-related gene called SGPL1. Her group is developing gene therapy for the condition and exploring whether the affected individuals or their parents exhibit a cancer predisposition. 

The Saba Laboratory has been designated as a Swim Across America Laboratory for Pediatric Cancer Research by Swim Across America, a national non-profit organization dedicated to raising money and awareness for cancer research, prevention, and treatment.

Research Funding

  • April 1, 2022 - March 31, 2024 - Providing a cure for sphingosine phosphate lyase insufficiency syndrome (SPLIS) through adeno-associated viral mediated SGPL1 gene therapy , Principal Investigator . Sponsor: CIRM, Sponsor Award ID: DISC2-13072
  • February 1, 2022 - February 6, 2023 - SPLIS Patient Finding , Principal Investigator . Sponsor: Catalyst Program (UCSF), Sponsor Award ID: Catalyst Award
  • June 15, 2018 - May 31, 2022 - Endogenous and Dietary Sphingolipids as Modulators in Inflammatory Bowel Disease , Principal Investigator . Sponsor: NIH, Sponsor Award ID: R01DK115669
  • July 1, 2007 - January 31, 2018 - S1P Lyase in colon cancer , Principal Investigator . Sponsor: NIH, Sponsor Award ID: R01CA129438


The Johns Hopkins University, MD, B.S., 05/1981, Natural Sciences
University of Maryland, School of Medicine, MD, M.D., 05/1985, Medicine
The Johns Hopkins University, MD, M.A., 05/1986, Creative Writing
Duke University, NC, Ph.D., 05/1996, Cell Biology

Honors & Awards

  • 1997
    International Union of Biochemistry and Molecular Biology Satellite Symposium on Sphingoglycolipids as Mediators of Molecular Events: Young Investigator Award
  • 2012
    John and Edna Beck Chair in Pediatric Cancer Research
  • 2014
    Women's History Month Trailblazer in STEM, Alameda County
  • 2014
    STEM Woman of the Year, CA Assembly District 15
  • 2014
    Swim Across America National Pediatric Research Laboratory
  • 2016
    CHORI Lifetime Scientific Achievement Award

Selected Publications

  1. Zhao P, Aguilar AE, Lee JY, Paul LA, Suh JH, Puri L, Zhang M, Beckstead J, Witkowski A, Ryan RO, Saba JD. Sphingadienes show therapeutic efficacy in neuroblastoma in vitro and in vivo by targeting the AKT signaling pathway. Invest New Drugs. 2018 Oct;36(5):743-754. View on PubMed.
  2. Oskouian B, Sooriyakumaran P, Borowsky AD, Crans A, Dillard-Telm L, Tam YY, Bandhuvula P, Saba JD. Sphingosine-1-phosphate lyase potentiates apoptosis via p53- and p38-dependent pathways and is down-regulated in colon cancer. Proc Natl Acad Sci U S A. 2006 Nov 14;103(46):17384-9. View on PubMed.
  3. Degagné E, Pandurangan A, Bandhuvula P, Kumar A, Eltanawy A, Zhang M, Yoshinaga Y, Nefedov M, de Jong PJ, Fong LG, Young SG, Bittman R, Ahmedi Y, Saba JD. Sphingosine-1-phosphate lyase downregulation promotes colon carcinogenesis through STAT3-activated microRNAs. J Clin Invest. 2014 Dec;124(12):5368-84. View on PubMed.
  4. Fyrst H, Oskouian B, Bandhuvula P, Gong Y, Byun HS, Bittman R, Lee AR, Saba JD. Natural sphingadienes inhibit Akt-dependent signaling and prevent intestinal tumorigenesis. Cancer Res. 2009 Dec 15;69(24):9457-64. View on PubMed.
  5. Alvarez-Rueda N, Desselle A, Cochonneau D, Chaumette T, Clemenceau B, Leprieur S, Bougras G, Supiot S, Mussini JM, Barbet J, Saba J, Paris F, Aubry J, Birklé S. A monoclonal antibody to O-acetyl-GD2 ganglioside and not to GD2 shows potent anti-tumor activity without peripheral nervous system cross-reactivity. PLoS One. 2011;6(9):e25220. View on PubMed.
  6. Kumar A, Zamora-Pineda J, Degagné E, Saba JD. S1P Lyase Regulation of Thymic Egress and Oncogenic Inflammatory Signaling. Mediators Inflamm. 2017;2017:7685142. View on PubMed.

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