School of Medicine
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Assistant Professor of Pediatrics (Hematology/Oncology)
BioSneha Ramakrishna obtained her B. A. from the University of Chicago and her M.D. from the Cleveland Clinic Lerner College of Medicine at Case Western Reserve University. In medical school, through the Howard Hughes Medical Research Scholar Award, she joined Dr. Crystal Mackall’s laboratory, where she designed and developed various GD2 CAR-Ts and tested them in preclinical models. During her residency training in Pediatrics at the Children’s Hospital of Philadelphia, she cared for some of the first patients treated with CD19 CAR T cells, learning the power of this therapy first-hand. During her fellowship in Pediatric Hematology/Oncology at the Johns Hopkins/National Cancer Institute combined program, she worked with Dr. Terry Fry. She evaluated the mechanism of CD22 CAR T cell relapse in patients by developing an antigen escape model and establishing a deeper understanding of the effects of antigen density on CAR-T phenotype, expansion, and persistence (Fry…Ramakrishna…Mackall Nat Med, 2018; Ramakrishna, et al., Clinical Cancer Research, 2019). Since arriving at Stanford, Dr. Ramakrishna leads an interdisciplinary team that designs, develops, and successfully implements a robust correlative science platform for our novel CAR-T therapies. Analyzing patient samples from our first-in-human GD2 CAR-T trial (NCT04196413) treating a universally fatal cancer, diffuse midline glioma (DMG), we identified that intracerebroventricular CAR-T administration correlates with enhanced pro-inflammatory cytokines and reduced immunosuppressive cell populations in cerebrospinal fluid as compared to intravenous CAR-T administration (Majzner*, Ramakrishna*, et al., Nature 2022 *co-first authors). Her research program evaluates unique sets of patient samples using novel single-cell immune profiling to identify the drivers of CAR-T success or failure. Building on these findings, her team will assess approaches to enhance CAR-T efficacy and translate these findings to the clinic.
Clinically, Dr. Ramakrishna cares for children with solid tumors and treats hematologic, solid, and brain tumor pediatric patients with CAR T cell therapies in the Cancer Cellular Therapies program.
Clinical Professor, Medicine - Oncology
Current Research and Scholarly InterestsMy research focuses on innovative models of care delivey to understand how to integrate primary and specialist palliative care. We also do work in palliative care education and how to scale our education to be impactful and sustainable. We are evaluating online models.
In cancer care I do research on novel therapeutics in thoracic malignancies including immunotherapy, new targeted agents, and new sequencing of approved drugs.
Professor of Radiology (Molecular Imaging Program at Stanford) and, by courtesy, of Chemistry
Current Research and Scholarly InterestsProbe chemistry and nanotechnology for molecular imaging and diagnostics
Lawrence Recht, MD
Professor of Neurology and, by courtesy, of Neurosurgery
Current Research and Scholarly InterestsOur laboratory focuses on two interrelated projects: (1) assessment of glioma development within the framework of the multistage model of carcinogenesis through utilization of the rodent model of ENU neurocarcinogenesis; and (2) assessment of stem cell specification and pluripotency using an embryonic stem cell model system in which neural differentiation is induced.
Bev Redfield Currie
Associate Director of Finance and Administration, Stanford Cancer Institute Core
Current Role at StanfordDirector of Finance
Associate Professor of Epidemiology and Population Health, of Medicine (Primary Care and Population Health) and, by courtesy, of Sociology, of Pediatrics and of Health Policy
BioI am a social epidemiologist and serve as an Associate Professor in the Department of Epidemiology and Population Health and in the Department of Medicine in the Division of Primary Care and Population Health. I joined the faculty at Stanford School of Medicine in 2011.
I am Director of the Stanford Center for Population Health Sciences. In this position, I am committed to making high-value data resources available to researchers across disciplines in order to better enable them to answer their most pressing clinical and population health questions.
My own research is focused on understanding the health implications of the myriad decisions that are made by corporations and governments every day - decisions that profoundly shape the social and economic worlds in which we live and work. While these changes are often invisible to us on a daily basis, these seemingly minor actions and decisions form structural nudges that can create better or worse health at a population level. My work demonstrates the health implications of corporate and governmental decisions that can give the public and policy makers evidence to support new strategies for promoting health and well-being. In all of his work, I have a focus on the implications of these exposures for health inequalities.
Since often policy and programmatic changes can take decades to influence health, my work also includes more basic research in understanding biological signals that may act as early warning signs of systemic disease, in particular accelerated aging. I examine how social and economic policy changes influence a range of early markers of disease and aging, with a particular recent focus on DNA methylation. I am supported by several grants from the National Institute on Aging and the National Institute on Minority Health and Health Disparities to develop new more sensitive ways to understand the health implications of social and economic policy changes.
David A. Relman
Thomas C. and Joan M. Merigan Professor and Professor of Microbiology and Immunology
Current Research and Scholarly InterestsMy investigative program focuses on human-microbe interactions and human microbial ecology, and primarily concerns the ecology of human indigenous microbial communities; a secondary interest concerns the classification of humans with systemic infectious diseases, based on features of genome-wide gene transcript abundance patterns and pther aspects of the host response.