Vivienne I. Rebel, PhD

  • Rank: Associate Professor/Research
  • Department: Cellular & Structural Biology
  • Office: 3.100.20
  • Location: Greehey CCRI
  • Tel: 1.210.562.9096


The goal of our research is to understand the nature of the molecular events leading to the development of myelodysplastic syndrome (MDS). The incidence of MDS in children is very low, however, after chemotherapy or radiation, as many as 2-6% will develop MDS, with a median survival of only 13 months! Thus, MDS is a serious and common side-effect of anti-cancer treatment, one for which there are currently very few therapeutic options.


MDS - a stem cell disease in the bone marrow

Blood-forming stem cells in the bone marrow are the affected cells in MDS. Since these cells are responsible for the generation of mature red and white blood cells, both types of mature blood cells may show abnormalities in MDS, resulting in recurrent infections, recurrent bleedings and extreme fatigue. One of the chromosomal perturbations that have been found in children’s MDS involves the CREBBP gene. Our studies of the blood and marrow of mice with only one intact copy of Crebbp+/- (where there are normally two) show that at 9-12 months of age, these mice display all the clinical feature characteristic of human MDS, including abnormal blood stem cells and mature cell differentiation, and a high probability of developing leukemia.


MDS is associated with defective repair of damaged DNA

At the time of diagnosis, the majority of MDS patients show DNA abnormalities in their blood cells. As the disease progresses, MDS blood cells continue to accrue DNA abnormalities, suggesting that faulty DNA repair mechanisms plays a role in MDS development. Our Crebbp+/- mice also show evidence of abnormal DNA repair. Together with our collaborators in other UT Health San Antonio departments, we are currently investigating if prohibiting the accumulation of DNA abnormalities can be used as a novel therapeutic approach for treating MDS.


Small molecule therapeutics for treating adult and pediatric cancers.

We have developed several small molecule inhibitors that target factors critical for cancer cell growth and metastasis. Using orthotopic mouse tumor models as well as ex-vivo explants from breast cancer patients, we have recently shown that one of these inhibitors that targets proto-oncogene FOXM1 suppresses cancer growth and metastasis without inducing any toxicity in normal cells. We are currently performing detailed pharmacokinetics/pharmacodynamics studies and exploring the possibility of taking this molecule to clinical trial in near future.


Bone marrow stroma abnormalities in MDS

In addition to defects in blood stem cells, MDS is also affected by the cells that surround the stem cells in the bone marrow, the so-called stroma cells. These cells produce factors (e.g. sKITL and MMP9) that normally keep the stem cells from differentiating into abnormal myeloid cells. However, Crebbp+/- stroma cells produce less of these factors.



Vivienne Rebel joined the Greehey Children’s Cancer Research Institute in November of 2005 with major faculty responsibilities as a Principal Investigator in Hematologic Malignancies and Assistant Professor in the Department of Cellular and Structural Biology. She received her medical degree at the Free University in Amsterdam, The Netherlands. She completed her doctoral degree from Free University and the Terry Fox Laboratory in Vancouver, Canada. She completed a post-doctoral fellowship at Harvard Medical School at the Dana-Farber Cancer Institute, where she received the David Abraham Fellowship. She is currently an Instructor in the Department of Pediatrics at Harvard Medical School and the Department of Cancer Biology at the Dana-Farber Cancer Institute.

Dr. Rebel’s research focuses on elucidating the molecular mechanisms that govern stem cell regulation in vivo. Knowledge about stem cell regulation may also benefit our understanding of cancer cell development.



Stem Cell Biologist
My area of expertise is in basic hematopoietic stem cell (HSC) biology and malignant hematologic diseases, especially Myelodysplastic Syndrome (MDS). In my laboratory, we use mouse models to investigate HSC function, disease development and in vivo mutagenesis. Other often utilized technologies are fluorescence activated cell sorting, tissue culture, gene expression analysis, protein analysis, and lentiviral mediated gene transfer.




Funding Agency NIH/NIEHS
Title Study DNA repair in preventing MDS and AML after radiation and benzene exposure
Status Active Active
Period 7/2012-6/2017
Role Co-Principal Investigator
Grant Detail The purpose of this proposal is to determine if double strand DNA break repair (homologous recombination and non-homologous end-joining) are required to prevent MDS and AML development after benzene or radiation exposure. The grant is equally distributed between the Hasty and Rebel laboratories; I have a separate account (PID# 153348). My role is to oversee the in vivo mouse studies we proposed as well as the in vitro studies with primary stem and progenitor cells.


Funding Agency BioAffinity
Title Developing a Simple Non-Invasive Fluorescence-Based assay for early lung detection
State Active
Period 7/2015-7/2016
Role Principal Investigator
Funding Agency Edward P. Evans Foundation
Title TREX2: A Novel Target in the Treatment of MDS
Status Active
Period 9/2015-8/2016
Role Principal Investigator


Funding Agency Baylor College of Medicine/Cancer Prevention and Research Institute of Texas
Title Role of DNA Methyltransferase 3A in Hematologic Malignancies
Status Active Active
Period 8/2015-8/2016
Role Co-Principal Investigator