Eric Sweet-Cordero

Associate Professor (Research) of Pediatrics (Cancer Biology)
I completed by undergraduate studies at Stanford (BA-Anthropology, BS-Biology). I went to medical school at completed a pediatric residency at UCSF. My fellowship training in pediatric oncology was done at the Dana Farber Cancer Institute/Boston Children's Hospital. I then did a research fellowship under the mentorship of Tyler Jacks at MIT, after which I was recruited to join the faculty at Stanford in 2005.

Professional Education

Residency: Univ of California San Francisco (1998) CA

Internship: Univ of California San Francisco (1996) CA

Fellowship: Dana-Farber Cancer Institute (2002) MA

Medical Education: UCSF School of Medicine (1995) CA

B.A., Stanford University, Anthropology (1989)

B.S., Stanford University, Biology (1989)

MD, UC San Francisco, Medicine (1995)

Residency, UC San Francisco, Pediatrics (1998)

Fellowship, Boston Children's/Dana Farber, Hematology and Oncology (2002)

Honors & Awards

Innovative Research Award, SU2C (6/2011-6/2014)

member, American Society for Clinical Investigation (2010)

Scholar Award, Rita Allen Foundation (2008-2011)

Clinical Scientist Development Award, Doris Duke Foundation (2007-2010)

Sidney Kimmel Scholar, Sidney Kimmel Foundation (2006-2008)

Clinical Trials

Clinical trials are research studies that evaluate a new medical approach, device, drug, or other treatment. As a Stanford Health Care patient, you have access to the latest, advanced clinical trials.

Open trials refer to studies currently accepting participants. Closed trials are not currently enrolling, but may open in the future.

A Meta-analysis of Lung Cancer Gene Expression Identifies PTK7 as a Survival Gene in Lung Adenocarcinoma
Chen, R., Khatri, P., Mazur, P. K., Polin, M., Zheng, Y., & Sweet-Cordero, E. A. (2014). A Meta-analysis of Lung Cancer Gene Expression Identifies PTK7 as a Survival Gene in Lung Adenocarcinoma. CANCER RESEARCH, 74(10), 2892-2902.

A Rare Population of CD24(+)ITGB4(+)Notch(hi) Cells Drives Tumor Propagation in NSCLC and Requires Notch3 for Self-Renewal
Zheng, Y., de la Cruz, C. C., Sayles, L. C., Alleyne-Chin, C., Vaka, D., & Sweet-Cordero, E. A. (2013). A Rare Population of CD24(+)ITGB4(+)Notch(hi) Cells Drives Tumor Propagation in NSCLC and Requires Notch3 for Self-Renewal. CANCER CELL, 24(1), 59-74.

Mathematical Modeling of Tumor Cell Proliferation Kinetics and Label Retention in a Mouse Model of Lung Cancer
Zheng, Y., Moore, H., Piryatinska, A., Solis, T., & Sweet-Cordero, E. A. (2013). Mathematical Modeling of Tumor Cell Proliferation Kinetics and Label Retention in a Mouse Model of Lung Cancer. CANCER RESEARCH, 73(12), 3525-3533.

Cross-Species Functional Analysis of Cancer-Associated Fibroblasts Identifies a Critical Role for CLCF1 and IL-6 in Non-Small Cell Lung Cancer In Vivo
Vicent, S., Sayles, L. C., Vaka, D., Khatri, P., Gevaert, O., & Sweet-Cordero, E. A. (2012). Cross-Species Functional Analysis of Cancer-Associated Fibroblasts Identifies a Critical Role for CLCF1 and IL-6 in Non-Small Cell Lung Cancer In Vivo. CANCER RESEARCH, 72(22), 5744-5756.

Wilms tumor 1 (WT1) regulates KRAS-driven oncogenesis and senescence in mouse and human models
Vicent, S., Chen, R., Sayles, L. C., Lin, Cw., Walker, R. G., & Sweet-Cordero, E. A. (2010). Wilms tumor 1 (WT1) regulates KRAS-driven oncogenesis and senescence in mouse and human models. JOURNAL OF CLINICAL INVESTIGATION, 120(11), 3940-3952.

Chronic cisplatin treatment promotes enhanced damage repair and tumor progression in a mouse model of lung cancer
Oliver, T. G., Mercer, K. L., Sayles, L. C., Burke, J. R., Mendus, D., & Sweet-Cordero, E. A. (2010). Chronic cisplatin treatment promotes enhanced damage repair and tumor progression in a mouse model of lung cancer. GENES & DEVELOPMENT, 24(8), 837-852.

Two is better than one: combining IGF1R and MEK blockade as a promising novel treatment strategy against KRAS-mutant lung cancer.
Chen, R., & Sweet-Cordero, E. A. (2013). Two is better than one: combining IGF1R and MEK blockade as a promising novel treatment strategy against KRAS-mutant lung cancer. Cancer discovery, 3(5), 491-493.

The phosphatase PP2A links glutamine to the tumor suppressor p53.
Gwinn, D., & Sweet-Cordero, E. A. (2013). The phosphatase PP2A links glutamine to the tumor suppressor p53. Molecular cell, 50(2), 157-158.

Blocking NRG1 and Other Ligand-Mediated Her4 Signaling Enhances the Magnitude and Duration of the Chemotherapeutic Response of Non-Small Cell Lung Cancer
Hegde, G. V., de la Cruz, C. C., Chiu, C., Alag, N., Schaefer, G., & Jackson, E. L. (2013). Blocking NRG1 and Other Ligand-Mediated Her4 Signaling Enhances the Magnitude and Duration of the Chemotherapeutic Response of Non-Small Cell Lung Cancer. SCIENCE TRANSLATIONAL MEDICINE, 5(171).

Residual Tumor Cells That Drive Disease Relapse after Chemotherapy Do Not Have Enhanced Tumor Initiating Capacity
Hegde, G. V., de la Cruz, C., Eastham-Anderson, J., Zheng, Y., Sweet-Cordero, E. A., & Jackson, E. L. (2012). Residual Tumor Cells That Drive Disease Relapse after Chemotherapy Do Not Have Enhanced Tumor Initiating Capacity. PLOS ONE, 7(10).

Discovery and Preclinical Validation of Drug Indications Using Compendia of Public Gene Expression Data
Sirota, M., Dudley, J. T., Kim, J., Chiang, A. P., Morgan, A. A., & Butte, A. J. (2011). Discovery and Preclinical Validation of Drug Indications Using Compendia of Public Gene Expression Data. SCIENCE TRANSLATIONAL MEDICINE, 3(96).

Expression and Silencing of the Microtubule-Associated Protein Tau in Breast Cancer Cells
Spicakova, T., O'Brien, M. M., Duran, G. E., Sweet-Cordero, A., & Sikic, B. I. (2010). Expression and Silencing of the Microtubule-Associated Protein Tau in Breast Cancer Cells. MOLECULAR CANCER THERAPEUTICS, 9(11), 2970-2981.

Hypoxia in Models of Lung Cancer: Implications for Targeted Therapeutics
Graves, E. E., Vilalta, M., Cecic, I. K., Erler, J. T., Tran, P. T., & Giaccia, A. J. (2010). Hypoxia in Models of Lung Cancer: Implications for Targeted Therapeutics. CLINICAL CANCER RESEARCH, 16(19), 4843-4852.

HIF-2 alpha deletion promotes Kras-driven lung tumor development
Mazumdar, J., Hickey, M. M., Pant, D. K., Durham, A. C., Sweet-Cordero, A., & Keith, B. (2010). HIF-2 alpha deletion promotes Kras-driven lung tumor development. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 107(32), 14182-14187.

Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma
Schaffer, B. E., Park, K.-S., Yiu, G., Conklin, J. F., Lin, Cw., & Sage, J. (2010). Loss of p130 Accelerates Tumor Development in a Mouse Model for Human Small-Cell Lung Carcinoma. CANCER RESEARCH, 70(10), 3877-3883.

Differential effects of oncogenic K-Ras and N-Ras on proliferation, differentiation and tumor progression in the colon
Haigis, K. M., Kendall, K. R., Wang, Y., Cheung, A., Haigis, M. C., & Jacks, T. (2008). Differential effects of oncogenic K-Ras and N-Ras on proliferation, differentiation and tumor progression in the colon. NATURE GENETICS, 40(5), 600-608.

Requirement for Rac1 in a K-ras-induced lung cancer in the mouse
Kissil, J. L., Walmsley, M. J., Hanlon, L., Haigis, K. M., Kim, C. Fb., & Jacks, T. (2007). Requirement for Rac1 in a K-ras-induced lung cancer in the mouse. CANCER RESEARCH, 67(17), 8089-8094.

Comparison of gene expression and DNA copy number changes in a murine model of lung cancer
Sweet-Cordero, A., Tseng, G. C., You, H., Douglass, M., Huey, B., & Jacks, T. (2006). Comparison of gene expression and DNA copy number changes in a murine model of lung cancer. GENES CHROMOSOMES & CANCER, 45(4), 338-348.

MicroRNA expression profiles classify human cancers
Lu, J., Getz, G., Miska, E. A., Alvarez-Saavedra, E., Lamb, J., & Golub, T. R. (2005). MicroRNA expression profiles classify human cancers. NATURE, 435(7043), 834-838.

An oncogenic KRAS2 expression signature identified by cross-species gene-expression analysis
Sweet-Cordero, A., Mukherjee, S., Subramanian, A., You, H., Roix, J. J., & Jacks, T. (2005). An oncogenic KRAS2 expression signature identified by cross-species gene-expression analysis. NATURE GENETICS, 37(1), 48-55.