- Why Research
- Our Impact
- Get Involved
- About BCRF
- Contact Us
You are here
Christina Curtis, PhD, MSc
Assistant Professor, Medicine and Genetics
Co-director, Molecular Tumor Board, Stanford Cancer Institute
Stanford University, School of Medicine
Goal: To understand the causes of drug resistance in breast cancers in order to develop preventive strategies or curative treatments for patients with metastatic ER-positive breast cancer.
Impact: Dr. Curtis’ work is aimed at understanding what happens at the molecular level that makes tumor cells resistant to therapy. Her findings may help define new therapeutic targets and better treatments for patients with advanced breast cancer.
What’s next: She and her team will expand their research to develop new ways to target patients who are at high risk of relapse so they can receive well-timed and appropriate treatment.
During cancer therapy, some cancer cells change their characteristics in ways that make them resistant to the drug(s) being administered. Because these cells do not die, they can form a new tumor in the future, which will also likely be resistant to therapies. Dr. Curtis has been studying genetic alterations harbored by breast tumors that cause them to be resistant to therapy. This year, she and her colleagues will focus on preventing and treating metastasis in patients with estrogen receptor-positive breast cancer who have a high risk of relapse.
Full Research Summary
Research area: Examining what makes breast tumor cells resistant to therapy in order to improve outcomes for patients with breast cancer.
Impact: Tumors are composed of a mixture of cells that are genetically unique and have different properties. This intra-tumor complexity poses many clinical challenges, including drug resistance. Drug resistance represents a major cause of breast cancer mortality and the underlying mechanisms of this phenomenon remain poorly understood. Dr. Curtis is using a variety of technologies to understand what happens at the molecular level to make tumor cells resistant to therapy. Her work will enable the development of patient-tailored treatment strategies, leading to more precise treatment decisions—thereby sparing patients ineffective therapy.
Current investigation: Dr. Curtis is continuing her investigations into the drivers of drug resistance to identify new targets that could prevent breast cancer recurrence and metastasis.
What she’s learned so far: Dr. Curtis and her team have described and validated 11 breast cancer subgroups within the ER-positive classification and further defined four high-risk ER-positive/HER2-negative breast cancer subgroups with a high-risk of relapse up to 20 years post diagnosis. These high-risk subgroups accounted for one quarter of all ER-positive breast cancers they studied and the majority of distant relapses. Moreover, these subgroups harbor characteristic molecular drivers, some of which are therapeutically actionable. They have developed patient-derived organoid models of the four high-risk subgroups to be used in follow up studies. Her group has also developed a powerful machine learning approach which they will employ in the coming year to facilitate these studies.
What’s next: Dr. Curtis and her colleagues will continue to fully characterize the organoid models of the four high-risk subgroups. Using the newly developed machine learning approach, they will evaluate the prevalence of these subgroups in patients with metastatic breast cancer compared to those with early stage disease and evaluate the association between the high-risk subgroups and treatment response. The results of these studies will elucidate the drivers and dynamics of relapse and treatment response. This will inform strategies for personalized breast cancer treatment and risk prediction with the long-term goal of improving outcomes for high-risk breast cancer subtypes.
Dr. Curtis is an Assistant Professor of Medicine and Genetics in the School of Medicine at Stanford University where she leads the Cancer Systems Biology Group and serves as Co-Director of the Molecular Tumor Board at the Stanford Cancer Institute. She received her doctorate in Molecular and Computational Biology in 2007 and completed a postdoctoral fellowship in Computational Biology at the University of Cambridge in 2010. Dr. Curtis was the recipient of several young investigator awards, including the 2012 V Foundation for Cancer, V Scholar Award and the 2012 STOP Cancer Research Career Development Award.
Dr. Curtis’s laboratory pursues innovative experimental approaches and data-driven modeling to address outstanding questions in cancer systems biology. In particular, her research seeks to delineate mechanisms of tumor progression and therapeutic resistance. For example, she and her team have developed an experimental and computational framework to interrogate tumor evolutionary dynamics and the timeline of neoplastic progression. They are also developing approaches to model therapeutic resistance. By coupling this approach with high-resolution genomic profiling of patient samples, this research will enable a paradigm shift in patient stratification and will ultimately inform optimal treatment strategies.
Another aspect of her research has focused on the integration of diverse genomic data types to elucidate inter-individual variation and mechanisms of tumorigenesis. For example, she leads a seminal study that redefined the molecular map of breast cancer through a detailed characterization of the genomic and transcriptomic landscape of 2,000 breast cancers. Using integrative genomics and statistical approaches, this work identified novel subtypes of breast cancer with distinct clinical outcomes and subtype-specific driver genes. Ongoing efforts in this area will guide the development of novel targeted therapeutics and improved prognostic signatures.