PRISM Mentors

Early neural progenitors respond to extrinsic cues that maintain and support their potency. These stem/ progenitor cells are in direct contact with the cerebrospinal fluid (CSF), which acts as part of their niche. Our research program encompasses the early neural stem cell niche, neural tube closure, CSF, metabolism, and cortical neuronal development. We are dedicated to broad collaboration focused on translating an understanding of neurodevelopment and CSF biology into regenerative strategies.

The Poston Lab seeks to understand the biological underpinnings of non-motor symptoms in patients with Lewy Body diseases, such as Parkinson's disease and Lewy Body Dementia. While our primary focus is understanding cognition and dementia, we also study other prominent non-motor symptoms such as psychosis/hallucinations, sleep disruption, orthostatic dysregulation, and others.  A major focus is on the role of co-pathologies, such as Alzheimer's and vascular co-pathologies, and the role of neuro-inflammation, in the development of Lewy Body disease associated non-motor symptoms.  We collect clinical, motor, neuropsychological, biological, genetic, and imaging data on patients and healthy older adults to perform our studies. 

Mitochondria move and undergo fission and fusion in all eukaryotic cells. The accurate allocation of mitochondria in neurons is particularly critical due to the significance of mitochondria for ATP supply, Ca++ homeostasis and apoptosis and the importance of these functions to the distal extremities of neurons. In addition, defective mitochondria, which can be highly deleterious to a cell because of their output of reactive oxygen species, need to be repaired by fusing with healthy mitochondria or cleared from the cell. Thus mitochondrial cell biology poses critical questions for all cells, but especially for neurons: how the cell sets up an adequate distribution of the organelle; how it sustains mitochondria in the periphery; and how mitochondria are removed after damage. The goal of our research is to understand the regulatory mechanisms controlling mitochondrial dynamics and function and the mechanisms by which even subtle perturbations of these processes may contribute to neurodegenerative disorders.

Dr. Bhalla received his training in molecular biology at UC San Francisco. His postdoctoral work centered on the regulation of aldosterone-mediated sodium transport in health and disease. In his laboratory he uses both in vitro and in vivo approaches for several projects related to the role of the kidney in health, diabetes, and hypertension. (1) Diabetic kidney disease is costly and consequential. Diabetic kidney disease is the most common form of chronic kidney disease in the world, yet no curative therapy is available. Studies of the susceptibility of diabetic kidney disease led to the discovery of differential regulation of endothelial-specific molecule-1, Esm-1 (endocan) in susceptible strains of mice. Esm-1 is a secreted proteoglycan that is enriched in glomerular endothelium and inhibits interferon signaling in glomeruli in the setting of diabetes and other inflammatory diseases. Ongoing rescue and deletion experiments explore the role of Esm-1 in diabetes and diabetic kidney disease. We also study the regulation of Esm-1 transcription and protein stability. (2) Investigation of the mechanisms of hypertension in the setting of obesity and insulin resistance using renal tubular epithelial insulin receptor deletion challenged the role of insulin in the hypertension of obesity, insulin resistance, and the metabolic syndrome. These studies also shed light on the role of insulin in control of glucose reabsorption via SGLT2. Ongoing studies focus on molecular mechanisms of insulin-regulated SGLT2 and its contrast with insulin resistant pathways in other cell types and tissues. (3) Inhibition of sodium reabsorption using diuretics is a mainstay of therapy for hypertension and edema-forming states. Study on the consequences of diuretic therapy using tubular morphometry and single cell approaches have led to additional work on mechanisms of tubular remodeling in vivo.

Amyloidosis, heart failure, transplantation

The lifetime risk of developing cardiovascular disease (CVD) is determined by the genetic makeup and exposure to modifiable risk factors. The Cardiovascular Link to Environmental ActioN (CLEAN) Lab is interested in understanding how various environmental pollutants (eg. tobacco, e-cigarettes, air pollution and wildfire) interact with genes to affect the transcriptome, epigenome, and eventually disease phenotype of CVD. The current focus is to investigate how different toxic exposures can adversely remodel the vascular wall leading to increased cardiac events. We intersect human genomic discoveries with animal models of disease, in-vitro and in-vivo systems of exposure, single-cell sequencing technologies to solve these questions. Additionally, we collaborate with various members of the Stanford community to develop biomarkers that will aid with detection and prognosis of CVD. We are passionate about the need to reduce the environmental effects on health through advocacy and outreach. We strongly believe that the mechanistic understanding of the adverse health effects of harmful exposures will help to devise a targeted approach towards reduction of environmental toxins as well as to identify areas in need of improving environmental equity.

The research interests of the molecular imaging instrumentation lab are to create novel instrumentation and software algorithms for in vivo imaging of molecular signatures of disease in humans and small laboratory animals. These new cameras efficiently image radiation emissions in the form of positrons, annihilation photons, gamma rays, and/or light emitted from molecular contrast agents that were introduced into the body and distributed in the subject tissues. These contrast agents are designed to target molecular pathways of disease biology and enable imaging of these biological signatures in tissues residing deep within the body using measurements made from outside the body.

The goals of the instrumentation projects are to advance the sensitivity and spatial, spectral, and/or temporal resolutions, and to create new camera geometries for special biomedical applications. The computational modeling and algorithm goals are to understand the physical system comprising the subject tissues, radiation transport, and imaging system, and to provide the best available image quality and quantitative accuracy.

The work involves designing and building instrumentation, including arrays of position sensitive sensors, readout electronics, and data acquisition electronics, signal processing research, including creation of computer models, and image reconstruction, image processing, and data/image analysis algorithms, and incorporating these innovations into practical imaging devices.

The ultimate goal is to introduce these new imaging tools into studies of molecular mechanisms and treatments of disease within living subjects.

My laboratory's overall goal is to (i) understand the mechanisms of right heart failure in children and adults with congenital heart disease and (ii) to develop biomarkers as a plasma signature of myocardial events to better understand the mechanisms of heart failure, improve monitoring of disease progression, early detection of heart failure and risk-stratification.

We have focused on tetralogy of Fallot population and single ventricle heart disease. As the survival continues to improve, so also has the incidence of heart failure. However, the underlying cellular mechanisms of heart failure are poorly understood as a result of which no targeted therapy is available. Since it is not possible to obtain heart muscle biopsies routinely on patients, we have taken a novel strategy of using Multi-Omics to better understand disease mechanisms and to follow patients over time comparing their Omics signature to themselves thereby personalizing their care. The goal is to create a targeted biomarker panel for clinical utility to be used in conjunction with imaging data to improve overall prediction of risk. Based on our work to date, we are also interested in understanding myocardial mitochondrial and vascular dysfunction as these have the potential to serve as novel therapeutic targets.

Lab website is in creation. Link will be updated when it is ready.

Our lab works on biological mechanisms of patient-specific and disease-specific induced pluripotent stem cells (iPSCs). The main goals are to (i) understand basic cardiovascular disease mechanisms, (ii) accelerate drug discovery and screening, (iii) develop “clinical trial in a dish” concept, and (iv) implement precision cardiovascular medicine for prevention and treatment of patients. Our lab uses a combination of genomics, stem cells, cellular & molecular biology, physiological testing, and molecular imaging technologies to better understand molecular and pathophysiological processes.

My laboratory seeks to identify mechanisms responsible for human congenital heart disease, the most common cause of still-births in the U.S. and one of the major contributors to morbidity and mortality in infants and toddlers. We believe that by understanding the mechanisms regulating growth and differentiation of heart precursor stem/progenitor cells during early embryonic development we can then apply these principles to understand the pathogenesis heart malformation during fetal development and to leverage them for treating adult onset heart diseases such as heart failure and arrhythmia. We currently use both genetically-modified mice as our in vivo model to understand the biology of heart development as well as induced pluripotent stem cells (iPSCs) as a in vitro model to study the process of heart cell formation. Our major areas of interests include cardiovascular developmental biology, disease modeling, tissue engineering, and regenerative biology. Within each of these areas we are particularly focused on understand the major genes that regulate the proper formation of heart chambers and the consequesnces of disrupting the normal expression of these genes and how that may lead to the development of congenital heart diseases. While mouse models are useful for studying the process of heart formation, they are not exactly like the human hearts in various ways. Since human heart fetal tissue are diffulty to obtain, we have chosen to use iPSCs derived from patients with particular congenital heart diseases to study steps involved in human heart malformation. Furthermore, to bring our work closer to treating heart disease patients, we have combined our expertise in stem cell biology with 3D biopring to make engineered functional heart tissue for screening drugs and to serve as replacement tissues for damaged heart muscles.

I am a Professor of Medicine-Oncology and Pathology and the Director of TRAM, ARTS and CTNT Programs.

My laboratory studies how oncogenes such as MYC initiate and maintain cancer.  In partic ular we have shown that shutting down oncogenes even for a brief time can revese cancer or elicit "Oncogene Addiction"  For a recent review of our work please see:

The MYC oncogene - the grand orchestrator of cancer growth and immune evasion Nature Reviews Clinical Oncology, 2022

Members of my laboratory are studying basic mechanisms of Oncogene Addiction, the role of Self-renewal/Stemness, Metabolism, Host Immune System, Protein 
Biogenesis, Microbiome, Extracellular Vesicles.  

We are developing novel therapuetics using small molecules, nanoparticles, proteins/peptides that can be used to target oncogenes and/or restore the immune response against cancer.

We are developing new diagnostic and imaging agents using PET, Mass Spec, Nanoproteomics, MIcrofluidics.

For recent examples of our work please see: Casey et al, Science, 2016; Gouw et al, Cell Metabolism, 2019; Dhanasekaran et al eLife, 2020; Swaminathan et al, Nat Comm 2020.

The Itakura Lab has an immediate opening for a creative and motivated postdoctoral scholar to conduct applied research in the areas of machine learning and pattern/feature detection with a focus on either computer vision/image or genomic/molecular data processing and analysis. The lab focuses on implementing machine learning frameworks and radiogenomic approaches on heterogeneous, multi-scale cancer data (e.g., clinical, imaging, histopathologic, genomic, transcriptomic, epigenomic, proteomic) to accelerate discoveries in cancer diagnostics and therapeutics. Projects include prediction modeling of survival and treatment responses, biomarker (feature) discovery, cancer subtype discovery, and identification of new therapeutic targets. Guided by critical and relevant problems in oncology, these projects have the potential to lead to clinically actionable or translatable findings.

The successful candidate will join the Department of Medicine, Division of Oncology and work. The job description:

• Build and implement algorithms in machine learning applied to either imaging data (computer vision) or genomic/molecular data (computational biology)
• Develop software tools for integrative analysis of heterogeneous, multi-omic cancer data using machine learning
• Publish and present research findings in journals and conferences

Required Qualifications:

• PhD (or MD/PhD) in Computer Science, Engineering, Informatics, Statistics, Applied Physics, or a related field with strong skills in data mining, machine learning, or statistics
• Experience in modeling, integrative analyses, parallel computing, and/or software development desirable
• Biomedical knowledge or research experience is not a requisite
• Demonstrated ability to work independently, problem-solve, author manuscripts, strive for innovation, and be highly self-motivated
• Strong interpersonal and communication skills, and ability to work as part of a multi-disciplinary team

The overall goal of our laboratory is to uncover new regulatory mechanisms in signaling systems, to understand how these mechanisms are damaged in disease states and how to devise new new strategies to repair their function.  Specific areas are highlighted below:

1. The Hedgehog and WNT pathways, two cell-cell communication systems that regulate the formation of most tissues during development. These same pathways play central roles in tissue stem-cell function and organ regeneration in adults. Defects in these systems are associated with degenerative conditions and cancer.

2. Signal transduction at the primary cilium and the mechanism of cilia-associated human diseases. Primary cilia are solitary hair-like projections found on most cells in our bodies that function as critical hubs for signal transduction pathways (such as Hedgehog). Over fifty human genetic diseases, called “ciliopathies,” are caused by defects in cilia. Patients with ciliopathies can show phenotypes in nearly all organ systems, suffering from abnormalities ranging from birth defects to obesity.

3. Regulation of signaling pathways by endogenous lipids. The landscape of endogenous small-molecules and their biological functions remains a terra incognita, one that provides many opportunities to discover new regulatory layers in signaling pathways and other membrane dependent processes.

4. Biomolecular condensates in cancer and cancer therapeutics. The formation of reversible, membrane-less compartments in cells by the segregation of proteins into liquid phases, hydrogels or amyloid-like assemblies is an emerging principle of cellular organization. Emerging evidence shows that some cytotoxic drugs used in oncology can accumulate in and disrupt the biophysical properties of these condensates. A future challenge is to develop strategies to target such membraneless compartments (such as the nucleolus) for effective and safe cancer therapies.

5. Cellular adaptation to extreme tissue environments. Many cells in our bodies can be considered “extremophiles,” charged with maintaining homeostasis in the face of an environment containing markedly non-physiological concentrations of ions, small molecules and toxins. For instance, cells in the kidney medulla face tissue concentrations of ions, urea and other small molecules that are several-fold higher than blood.

A central focus of our laboratory is to uncover new regulatory mechanisms in cell-cell communication system, understand how these mechanisms are damaged in disease states and devise strategies to repair their function. We are actively recruiting post-doctoral fellows to join projects in the following areas:
--Signaling pathways implicated in birth defects, cancer and regeneration.
--Regulation of signaling and development by primary cilia.
--Genetic and biochemical dissection of lipid pathways that regulate signaling, development and cancer.
--The role of biomolecular condensates in cancer and cancer therapeutics.
We strive to provide a supportive, inclusive, organized and collaborative lab environment that maximizes the ability to tackle important biomedical problems. Career development is a priority. Nearly all prior lab members have obtained multiple publications and top-level competitive positions in academics or in the biotech industry.

Department URL:
https://biochemistry.stanford.edu/

Vast amounts of molecular data characterizing the genome, epi-genome and transcriptome are becoming available for a wide range of complex disease such as cancer and neurodegenerative diseases. In addition, new computational tools for quantitatively analyzing medical and pathological images are creating new types of phenotypic data.  Now we have the opportunity to integrate the data at molecular, cellular and tissue scale to create a more comprehensive view of key biological processes underlying complex diseases. Moreover, this integration can have profound contributions toward predicting diagnosis and treatment. The Gevaert lab focuses on achieving progress in multi-scale modeling by tackling challenges in biomedical multi-scale data fusion. Applications are in the area of complex diseases with most projects in the lab focused on oncology, and possible new directions studying neuro-degenerative & cardiovascular diseases.

Multi-omics, multi-modal, multi-scale data fusion for precision medicine

Vast amounts of biomedical data are now routinely available for patients ranging from sequencing of tissues to liquid biopsies. In addition, new computational tools for quantitatively analyzing radiographic images are now available. Multi-scale data is now available for complex diseases at molecular, cellular and tissue scale to establish a more comprehensive view of key biological processes. Intra and inter individual heterogeneities are often quoted as the main challenge for studying complex diseases. These heterogeneities exist at all scales, from microscopic to macroscopic. We develop multi-scale modeling approach to counter heterogeneity and uncover potentially untapped synergies between different data modalities by integrating information across spatial scales. Multi-scale modeling involves linking information from molecules, cells, tissues, and organs all the way to the organism and the population. We propose to use high dimensional molecular data with tissue scale image data to develop a statistical multi-scale modeling approach in the context of multi-modal & multi-scale modeling. Such modeling can contribute toward predicting diagnosis and treatment by revealing synergies and previously unappreciated relationships. Multi-scale modeling also can contribute to a more fundamental understanding of disease development and can reveal novel insights in how data at different scales are linked to each other.

The QIAI lab focuses on cutting‐edge research at the intersection of imaging science and biomedical informatics, developing and applying AI methods to large amounts of medical data for biomedical discovery, precision medicine, and precision health (early detection and prediction of future disease). The lab develops novel methods in text and image analysis and AI, including multi-modal and multi-task learning, weak supervision, knowledge representation, natural language processing, and decision theory to tackle the challenges of leveraging medical Big Data. Our exciting work is bridging a spectrum of biomedical domains with multidisciplinary collaborations with top scientists at Stanford as well as with other institutions internationally. The QIAI lab provides a unique multidisciplinary environment for conducing innovative AI-based healthcare research with a strong record of scholarly publication and achievement. Core research topics in the laboratory include: (1) automated image annotation using unsupervised methods of processing associated radiology reports using word embeddings and related methods; (2) developing methods of analyzing longitudinal EMR data to predict clinical outcomes and best treatments, (3) creating multi-modal deep learning models integrating multi-dimensional EMR and other data to discover electronic phenotypes of disease, (4) developing AI models with noisy or sparse labels (weak supervision), and cross-modal, multi-task learning, and observational AI approaches, and (5) developing and implementing algorithms for distributed computation for training deep learning models that leverage multi-institutional data while avoiding the barriers to data sharing.

We analyze multiple types of health data (EHR, Claims, Wearables, Weblogs, and Patient blogs), to answer clinical questions, generate insights, and build predictive models for the learning health system. Our group runs the country's only bedside consult service to enable better medical decisions using aggregate EHR and Claims data at the point of care. Our team leads the Stanford Medicine Program for Artificial Intelligence in Healthcare, which makes predictions that allow taking mitigating actions, and studies the ethical implications of using machine learning in clinical care. We have built models for predicting future increases in cost, identifying slow healing wounds, missed diagnoses of depression and for improving palliative care.

Stanford Training Program in Ethical, Legal, and Social Implications (ELSI) Research

• Co-Principal Investigators and Program Co-Directors:  Mildred Cho, PhD, Holly Tabor, PhD
• Funding source: NIH National Human Genome Research Institute
• Appointment:  One year, renewable for up to three years
• Qualifications: The NIH requires that candidates must have a PhD or MD (JD or Master’s degree only not accepted) prior to starting the fellowship, and be a U.S. citizen or permanent resident to be eligible for funding.  We are seeking candidates with a background in social science, ethics, philosophy, history, health services research, public policy or other related disciplines.

Job description: 

The postdoctoral fellow will conduct independent research on ethical, legal and social considerations arising from genetics and genomics.  The fellow will be part of an interdisciplinary community including faculty and fellows from this program and other affiliated programs. Fellows are expected to gain practical experience in professional activities through programs such as the Stanford Benchside Ethics Consultation Service, a research ethics consultation program to assist life sciences researchers in the resolution of ethical concerns in their research, one of the Stanford-affiliated clinical ethics consultation services, and/or teaching.

In addition to participating in SCBE and CIRGE activities, fellows will have access to a full range of courses at Stanford University, which includes genetics, social science, humanities and law courses.  It is expected that the fellow may need formal coursework in genetics, ethics, or ELSI research methods.  Mentors will assist the fellow in formulating an individualized curriculum and career strategies.  All trainees will be expected to present their research in scholarly venues.  Fellowship support includes a stipend, tuition, and health insurance. Funds will be provided by the fellowship for each fellow to travel to one meeting per year.

For more information, please see our website. 

The Majeti lab focuses on the molecular/genomic characterization and therapeutic targeting of leukemia stem cells in human hematologic malignancies, particularly acute myeloid leukemia (AML). In parallel, the lab also investigates normal human hematopoiesis and hematopoietic stem cells. Our lab uses experimental hematology methods, stem cell assays, genome editing, and bioinformatics to define and investigate drivers of leukemia stem cell behavior. As part of these studies, we have led the development and application of robust xenotransplantation assays for both normal and malignant human hematopoietic cells. A major focus of the lab is the investigation of pre-leukemic hematopoietic stem cells in human AML.

Our basic research program focuses on understanding the roles of virus-host interactions in viral infection and disease pathogenesis via both molecular and systems virology/immunology single cell approaches. This program is combined with translational efforts to apply this knowledge for the development of broad-spectrum host-centered antiviral approaches to combat emerging viral infections, including dengue, encephalitic alphaviruses, SARS-CoV-2 and Ebola, and means to predict disease progression.

Our studies focus on the following emerging concepts that are transforming our understanding of virus-host interactions:

1. Understanding the pathogenesis of flaviviral infections via an integrative systems immunology single cell approach. The goal of this project is to elucidate the cellular and molecular factors contributing to increased severity of dengue and Zika disease in distinct patient populations (children, adults, pregnant women). To achieve this goal, we are advancing and utilizing various single-cell immunological approaches (virus-inclusive single cell RNA-seq, CyTOF etc) and samples from our large Colombia dengue cohort (>500 patients) and Zika cohort. We are mapping an atlas of viral immune cellular targets and studying critical protective and pathogenic elements of the host response to these viruses in multiple distinct infected and bystander cell subtypes with an unprecedented resolution. The translational goals of this project are to identify candidate biomarkers associated with infection outcome and candidate targets for antiviral therapy, as well as improve vaccine strategies.

2. Deciphering the intracellular membrane trafficking pathways essential for viral pathogens. We have used proteomic and genetic approaches to identify proteins that are critical for the replication of multiple globally relevant RNA viruses including dengue virus, Zika virus, encephalitis alphaviruses, SARS-CoV-2, hepatitis C virus, and Ebola virus. We are studying the molecular mechanisms by which these viruses hijack intracellular membrane trafficking pathways for mediating key steps in their viral life cycle and are characterizing the roles these factors play in cellular biology using viruses as complexed probes. Ongoing work focuses on the roles of cellular kinases and adaptor protein complexes in viral trafficking during viral entry, assembly, release, and direct cell-to-cell spread, the role of the ESCRT machinery in intracellular viral budding, and the roles of ubiquitin signaling pathways in the regulation of trafficking during viral assembly and release.

3. Advancing the development of small molecules targeting host functions as broad-spectrum antivirals. Most direct antiviral strategies targeting viral enzymes provide a “one drug, one bug” approach and are associated with the emergence of viral resistance. We have discovered several host functions exploited by multiple viruses as targets for broad-spectrum antivirals. We have demonstrated the utility of a repurposed approach that inhibits these factors in suppressing replication of multiple RNA viruses both in vitro and in mouse models and are advancing this approach into the clinic and studying its mechanism of action. In parallel, we are developing chemically distinct small molecules targeting various cellular functions as pharmacological tools to study cell biology and viral infection and as broad-spectrum antivirals to combat SARS-CoV-2, dengue virus, encephalitic alphaviruses and Ebola virus.

I am an infectious diseases physician and epidemiologist    OUr lab is well know internationally in two major areas:  1.  The role of infections in chronic diseases and 2.  Physiologic changes in humans over time, specifically the decrease in human body temperature.  3. Novel surveillance projects, especially serosurveys done through the mail and  the use of wastewater to track infections.  Right now, projects that could integrate a post-doctoral fellow include:  In addition, my research group works on gun violence prevention.  

1.  Analysis of a California population-based serosurvey on SARS-COV2 infection, including information on human behaviors (mask wearing, social , vaccination) and demographics (age, race, education),  We could expand this study to look at other infectious diseases as well.

2.  Research assessing the association between high normal body temperature and longevity.

3.  Gun violence prevention.  Gun violence is a national tragedy.  We have two major projects in this area:

     a.  A project with Santa Clara County Department of Public health that combines the many data sources on gun violence across the county (Police, hospitals,EMT, schools, health departments), bring together stakeholders at community organizations across the county fighting gun violence and work with health care workers to identify strategies to educate patients on gun violence prevention.

     b.  Educational project development to teach physicians across the county how to talk to patients about gun violence

The primary research focus of the Relman Lab is the human indigenous microbiota (microbiome), and in particular, the nature and mechanisms of variation in patterns of microbial diversity within the human body as a function of time (microbial succession), space (biogeography within the host landscape), and in response to perturbation, e.g., antibiotics (community robustness and resilience). One of the goals of this work is to define the role of the human microbiome in health and disease. We are particularly interested in measuring and understanding resilience in the human microbial ecosystem. Our work includes the human oral cavity, gut, and female reproductive tract, as well as an analysis of microbial diversity in marine mammals. This research integrates theory and methods from ecology, population biology, environmental microbiology, genomics and clinical medicine.