Research

Dr. Wendy Woodward leads an internationally recognized research program at MD Anderson Cancer Center focused on understanding and improving treatment outcomes for inflammatory breast cancer (IBC) — one of the most aggressive and understudied subtypes of breast cancer. 

As a physician-scientist, her work bridges the clinic and the laboratory, leveraging patient insights, preclinical modeling and translational studies to drive innovations in cancer biology, radiation therapy and therapeutic targeting.

1. Inflammatory breast cancer (IBC): Microenvironment and clinical biology
   Dr. Woodward's lab has helped redefine the biological underpinnings of IBC by demonstrating that the tumor microenvironment plays a central role in the pathogenesis and therapy resistance of the disease. Her landmark Lancet Oncology Personal View (2015) proposed a novel framework positioning the stroma as a critical driver of IBC’s unique clinical phenotype. Subsequent studies have confirmed increased macrophage infiltration and stem-like cell populations in IBC tumors (Reddy J et al), as well as distinct immunologic features via multiplexed immunofluorescence (Reddy S et al). Ongoing work seeks to better stratify IBC patients based on “IBC-likeness” (Balema et al), with the goal of refining diagnostic and therapeutic approaches in partnership with the Susan G. Komen Foundation.
   
   
2. Cholesterol metabolism, radiation sensitivity and IBC
   Dr. Woodward’s group was the first to link cholesterol metabolism to radiation response in IBC. Her clinical and preclinical research has demonstrated that statins, particularly simvastatin, enhance radiation sensitivity and reduce tumor recurrence in both IBC and triple-negative breast cancer models (Lacerda et al). Her team identified HDL as a mediator of these effects and established a mechanistic connection through miR-33a, ABCA1 and the FOXO3a tumor suppressor (Wolfe et al). This work supports new avenues for metabolic targeting in radiosensitization strategies and integrates metabolic biology with tumor microenvironment and immune signaling.
   
   
3. Radiation resistance in stem and stromal cells
   Building on her early discoveries in mammary progenitor cell resistance to radiation (Woodward et al, Chen et al), Dr. Woodward has elucidated key molecular mechanisms that enable both cancer stem cells and stromal elements to evade therapy. Notably, her group uncovered that tumor-associated macrophages confer radioprotection in IBC via Protein Kinase C zeta signaling (Rahal et al), highlighting potential combinatorial targets to overcome treatment resistance.
   
   
4. Modeling IBC and Brain Metastasis
   A hallmark of Dr. Woodward’s program is the development of preclinical models that accurately recapitulate IBC biology and metastatic behavior. Her lab was the first to show that mesenchymal stem cells can induce IBC phenotypes in vivo, dependent on macrophage interactions and STAT3 activation (Lacerda et al, Wolfe et al). These studies led to the creation of novel cell lines and brain metastasis models, used to uncover drivers like NDRG1 (Villodre et al) and miR-141 (Debeb et al), and to apply mathematical modeling for predicting therapeutic response in the CNS.
   
   
5. Translational leadership and collaborative infrastructure
   As Executive Director of the Morgan Welch IBC Clinic and Research Program, Dr. Woodward oversees a campus-wide initiative integrating clinical trials, tissue banking, translational science and collaborative grant development. Her team recently launched a consensus-driven strategic plan aligning biospecimen use with unmet clinical questions and driving new investigator-led trials. Her program’s biobank, the largest of its kind for IBC, underpins multiple national collaborations and serves as a resource for the global IBC research community.