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Christina Curtis, PhD, MSc
Assistant Professor, Medicine and Genetics
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 on their research by developing 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 don’t 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: Discovering what happens at the molecular level to make breast tumor cells resistant to therapy 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 more precise treatment decisions—thereby sparing patients ineffective therapy—and inform the development of patient-tailored treatment strategies.
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: Her current work builds on their recent findings, which defined four high-risk ER-positive/HER2-negative breast cancer subgroups. These accounted for one quarter of all ER-positive breast cancers they studied and the majority of distant relapses. They are building on this new information to more fully characterize the drivers and dynamics of relapse and treatment response in order to inform strategies for personalized breast cancer treatment and risk prediction with the long-term goal of improving outcomes for high risk breast cancer subtypes.
What’s next: With the support of BCRF, Dr. Curtis will build upon her team’s prior description and validation of 11 breast cancer subgroups and recent identification of several estrogen receptor-positive subgroups with a high-risk of relapse up to 20 years post diagnosis. These subgroups harbor characteristic molecular drivers, some of which are therapeutically actionable. Dr. Curtis plans to more fully characterize these in order to inform strategies for personalized breast cancer treatment and risk prediction with the long-term goal of improving outcomes for patients with a high risk of recurrence.
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.
BCRF Investigator Since
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