Chris Benz was among the first to study why age is such an important risk factor for the development of breast cancer, the most common age-related malignancy. Breast cancer is especially prevalent among Marin County women, underscoring why he helped initiate the Marin Women’s Study (MWS) in 2006. Results from the MWS have since led to larger population-based studies and an exciting new breast cancer prevention project being undertaken at the Buck Institute.
Dr. Benz’s early career work explored the genetic and structural differences driving different types of breast cancers, followed by a comparison of these differences to the activated pathways driving other cancer types. This led to his national involvement in The Cancer Genome Atlas (TCGA) program in 2008, followed by a decade-long team collaboration between his lab and a group of very creative genomic and computer scientists at the University of California, Santa Cruz, supported by the National Cancer Institute. Over the past decade, their team’s accomplishments have earned international acclaim, most recently for leading an innovative international effort termed the Pan-Cancer Atlas project. This project molecularly characterized over 10,000 tumors across 33 different cancer types, producing a groundbreaking new understanding and classification of cancers that will enable better-informed clinical trials and more effective and personalized cancer treatments.
The Benz lab is also working to uncover a new subcellular mechanism altered during breast tumorigenesis that can be effectively targeted by existing and repurposed cancer drugs. The aim is to reverse the increased aggressiveness of cancer cells observed during metastatic progression and offer new hope to women struggling with more advanced stages of breast cancer.
Why it matters
Over the course of a lifetime, 1 in 8 women in the United States will develop breast cancer. It is the most common cancer among women worldwide. The risk of developing breast cancer dramatically increases after age 20, with 75 percent of all breast cancers arising after age 50. Yet, for unknown reasons, different molecular subtypes of breast cancer exhibit different age-specific patterns of incidence. We believe that understanding how aging increases the risk of developing each of the varying molecular subtypes of breast cancer will not only lead to novel prevention strategies and more sensitive and accurate early detection methods, but also uncover more effective and better tolerated treatments of breast cancer at all clinical stages, improving the outcomes and survival of younger and older women alike.
For women, aging is the single greatest risk factor for developing breast cancer. By understanding the different molecular and genetic subtypes of breast cancer and why aging affects the development of some but not others, new prevention strategies can be designed that will eliminate this deadly disease that primarily arises in women after age 50.
Chris Benz, MD
For more than 30 years, Dr. Benz’s translational research efforts in oncology have focused on identifying molecular strategies to improve breast cancer diagnostics and therapeutics. Dr. Benz holds faculty appointments at both the Buck Institute and University of California, San Francisco, and has published over 250 peer-reviewed studies. He continues to serve on multiple national and international review and oversight committees, including the National Cancer Institute’s DTP/DCTD Biological Resources Branch Oversight Committee, the American Association of Cancer Research’s Task Force on Cancer and Aging, and the national steering committees for the NCI/NHGRI-funded The Cancer Genome Atlas (TCGA) and Genome Data Analysis Network (GDAN) programs. Dr. Benz provides weekly care for breast cancer patients at the UCSF Carol Franc Buck Breast Care Center, where he also remains active in the nationwide I-SPY2 clinical trial network and the statewide UC Athena program.
Dr. Benz has successfully invented and brought into worldwide phase-2 clinical trial (Hermione) a new and first-in-human cancer therapeutic, HER2-targeted immunoliposomes, currently licensed as MM-302 to Merrimack Pharmaceuticals in Cambridge, Massachusetts. For nearly a decade, he has also co-led with University of California, Santa Cruz, computer scientists the Buck Institute-UCSC Genome Data Analysis Center (GDAC), serving both the national TCGA and GDAN networks and resulting in groundbreaking Pan-Cancer Atlas publications that have earned worldwide notoriety and international acclaim by introducing a new molecular understanding and classification of human cancers that will drive more personalized and effective cancer therapies.
- Hoadley, K. A., et al., including Benz, C. C. (2014 Aug 14). Multiplatform analysis of 12 cancer types reveals molecular classification within and across tissues of origin. Cell, 158, 929–944. DOI: 10.1016/j.cell.2014.06.049. PubMed PMID: 25109877.
- Hoadley, K. A., et al., including Benz, C. C. (2018 Apr 5). Cell-of-origin patterns dominate the molecular classification of 10,000 tumors from 33 types of cancer. Cell, 173, 291–304. DOI: 10.1016/j.cell.2018.03.022. PubMed PMID: 29625048.
- Scott, G. K., Chu, D., Kaur, R., Malato, J., Rothschild, D. E., Frazier, K., Eppenberger-Castori, S., Hann, B., Park, B. L., Benz, C. C. (2016 Oct 18). ERpS294 is a biomarker of ligand or mutational ER activation and a breast cancer target for CDK2 inhibition. Oncotarget. DOI: 10.18632/oncotarget.12735. PubMed PMID: 27765908.
- Prebil, L. A., Ereman, R. R., Powell, M. J., Kerlikowske, K., Shepherd, J. A., Hurlbert, M. S., Benz, C. C. (2014 Jul). First pregnancy events and future breast density: Modification by age at first pregnancy and specific VEGF and IGF1R gene variants. Cancer Causes and Control, 25, 859–868. DOI: 10.1007/s10552-014-0386-2. PubMed PMID: 24801045.
- Powell, M. J., Von Behren, J., Neuhausen, S., Reynolds, P., Benz, C. C. (2017 Oct). Functional IGF1R variant predicts breast cancer risk in women with preeclampsia in California Teachers Study. Cancer Causes and Control, 28, 1027–1032. DOI: 10.1007/s10552-017-0942-7. PubMed PMID: 28822014.