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Developmental Biology

Research into normal development, developmental diseases and the function and potential uses of stem cells.

All Labs in This Area

 Sarki Abdulkadir Lab

Studying the mechanisms of prostate cancer initiation, progression and recurrence and strategies to therapeutically target these processes

Research Description

Our laboratory focuses on understanding the molecular mechanisms that drive prostate cancer initiation, progression and recurrence with the ultimate goal of developing therapeutic strategies that target these processes. Our approach includes the genomic analysis of human tumors, cell culture studies and the use of genetically engineered mouse models. We have a strong interest in genomics and gene regulation, oncogenic kinases as potential molecular therapeutic targets and the use of in vivo lineage tracing to define the fates of specific cell populations in tumorigenesis.

Specific projects include:

The role of the oncogenic serine/threonine kinase PIM1 in prostate cancer - PIM1 is coexpressed with c-MYC and dramatically enhances c-MYC-driven prostate tumorigenesis in a kinase-dependent manner. Notably, PIM1 is induced in tumors by hypoxia, radiation and treatment with docetaxel, a common but largely ineffective option for patients with advanced castration-resistant prostate cancer. PIM1 induction by hypoxia/radiation/docetaxel promotes prostate cancer cell survival and therapeutic resistance. Therefore, PIM1 may represent a valuable therapeutic target in prostate cancer. We are using new mouse models of prostate cancer for testing the efficacy of novel PIM1 kinase inhibitors in treating prostate cancer and reversing therapeutic resistance. We have also identified novel candidate PIM1-interacting proteins in prostate epithelial cells. Among the proteins identified are a MYC transcriptional cofactor and a prostate stem cell marker/regulator. We are investigating how PIM1 promotes prostate tumorigenesis by phosphorylating these substrates involved in regulating MYC transcriptional activity and stem cell function.

Cellular and molecular determinants of prostate cancer recurrence - A major clinical problem in prostate cancer is that of tumor recurrence following initial apparently successful therapy. Recurrent tumors may arise from a small number of "cancer stem-like cells" that survive the initial therapeutic intervention and have the capacity to regenerate the tumor. We are using lineage tracing to examine the competence of specific prostate epithelial cell types to regenerate tumors following therapy in mice.

Targeting lethal prostate cancer – We are using our mouse model of lethal prostate cancer based on alterations in Myc, Pten and Tp53 to develop new targeted therapies. One current project involves the targeting of EphB4 receptor tyrosine kinase using an antagonist as a therapeutic strategy.

For more information, see Dr. Abdulkadir's faculty profile.


Chalmers ZR, Burns MC, Ebot EM, Frampton GM, Ross JS, Hussain MHA, Abdulkadir SA. Early-onset metastatic and clinically advanced prostate cancer is a distinct clinical and molecular entity characterized by increased TMPRSS2-ERG fusions. Prostate Cancer Prostatic Dis. 2021 Jun;24(2):558-566.

Unno K, Chalmers ZR, Pamarthy S, Vatapalli R, Rodriguez Y, Lysy B, Mok H, Sagar V, Han H, Yoo YA, Ku SY, Beltran H, Zhao Y, Abdulkadir SA. Activated ALK Cooperates with N-Myc via Wnt/β-Catenin Signaling to Induce Neuroendocrine Prostate Cancer. Cancer Res. 2021 Apr 15;81(8):2157-2170.

Sagar V, Vatapalli R, Lysy B, Pamarthy S, Anker JF, Rodriguez Y, Han H, Unno K, Stadler WM, Catalona WJ, Hussain M, Gill PS, Abdulkadir SA. EPHB4 inhibition activates ER stress to promote immunogenic cell death of prostate cancer cells. Cell Death and Disease. November 2019.

Han H, Jain AD, Truica MI, Izquierdo-Ferrer J, Anker JF, Lysy B, Sagar V, Luan Y, Chalmers ZR, Unno K, Mok H, Vatapalli R, Yoo YA, Rodriguez Y, Kandela I, Parker JB, Chakravarti D, Mishra RK, Schiltz GE, Abdulkadir SA. Small-Molecule MYC Inhibitors Suppress Tumor Growth and Enhance Immunotherapy. Cancer Cell.  November 2019.

Njoroge RN, Vatapalli RJ, Abdulkadir SA. Organoids increase the predictive value of in vitro cancer chemoprevention studies for in vivo outcome. Frontiers in Oncology. January 2019.


See Dr. Abdulkadir's publications in PubMed.

Contact Us

Dr. Abdulkadir
Lab Telephone: 312-503-5031

 Rajeshwar Awatramani Lab

Investigating dopamine neurogenesis and subtypes; studying the role of microRNAs in Schwann cell (SC) differentiation.

Research Description

Topic 1. Mechanisms underlying dopamine neurogenesis
The floor plate, the ventral organizing center in the embryonic neural tube, patterns the neural tube by secreting the potent morphogen Shh. Using genetic fate mapping, we have recently shown that the midbrain floor plate, unlike the hindbrain and spinal cord floor plate, is neurogenic and is the source of midbrain dopamine neurons (Joksimovic, et al, 2009 Nature Neuroscience, Joksimovic et al. 2009 PNAS). We are interested in understanding pathways that are involved in floor plate neurogenesis and production of dopamine neurons. We have shown that Wnt signaling is critical for the establishment of the dopamine progenitor pool and that miRNAs may modulate the dosage and timing of the Wnt pathway (Anderegg et al, PloS Genetics 2013).

Topic 2. Deconstructing Dopaminergic Diversity
The neurotransmitter dopamine, produced mainly by midbrain dopaminergic neurons, influences a spectrum of behaviors including motor, learning, reward, motivation and cognition. In accordance with its diverse functions, dopaminergic dysfunction is implicated in a range of disorders affecting millions of people, including Parkinson’s disease (PD), schizophrenia, addiction and depression. How a small group of neurons underpins a gamut of key behaviors and diseases remains enigmatic. We postulated that there must exist several molecularly distinct dopaminergic neuron populations that, in part, can account for the plethora of dopaminergic functions and disorders. We are currently working to test this hypothesis and define dopamine neuron subtypes.

Topic 3. MicroRNAs in Schwann cell (SC) differentiation
MicroRNAs, by modulating gene expression, have been implicated as regulators of various cellular and physiological processes including differentiation, proliferation and cancer. We have studied the role of microRNAs in Schwann cell (SC) differentiation by conditional removal of the microRNA processing enzyme, Dicer1 (Yun et al, 2010, J Neurosci) . We reveal that mice lacking Dicer1 in SC (Dicer1 cKO) display a severe neurological phenotype resembling congenital hypomyelination. SC lacking Dicer1 are stalled in differentiation at the promyelinating state and fail to myelinate axons. We are beginning to determine the molecular basis of this phenotype. Understanding this will be important not only for congenital hypomyelination, but also for peripheral nerve regeneration and SC cancers.

For more information, please see Dr. Awatramani's faculty profile.


View Dr. Awatramani's complete list of publications in PubMed.

Contact Us

Rajeshwar Awatramani, PhD at 312-503-0690


 Irina Budunova Lab

Studying the role of the glucocorticoid receptor in carcinogenesis  and stem cell maintenance. Involved in development GR-targeted therapies in skin.

Research Description

The current projects in Dr. Budunova’s lab are centered on the role of the glucocorticoid receptor (GR) as a tumor suppressor gene in skin. We showed that skin-specific GR transgenic animals are resistant to skin carcinogenesis and GR KO animals are more sensitive to skin tumor development.  We are also interested in the role of GR in the maintenance of skin stem cells (SC). We found that GR/glucocorticoids inhibit the expression of numerous SC markers in skin including CD34- a marker of hair follicular epithelial SC and reduce the proliferative potential of skin SCs.

The glucocorticoids remain among the most effective and frequently used anti-inflammatory drugs in dermatology. Unfortunately, patients chronically treated with topical glucocorticoids, develop side effects including cutaneous atrophy. GR controls gene expression via (i) transactivation that requires GR dimerization and binding as homo-dimer to gene promoters and (ii) transrepression that is chiefly mediated via negative interaction between GR and other transcription factors including pro-inflammatory factor NF-kB. In general, GR transrepression is the leading mechanism of glucocorticoid anti-inflammatory effects, while many adverse effects of glucocorticoids are driven by GR transactivation.

Our laboratory has been involved in delineation of mechanisms underlying side effects of glucocorticoids in skin. Using GRdim knockin mice characterized by impaired GR dimerization and activation, we found that GR transactivation plays an important role in skin atrophy. These data suggested that non-steroidal selective GR activators (SEGRA) that do not support GR dimerization, could preserve therapeutic potential of classical glucocorticoids but have reduced adverse effects in skin.  We are testing effects of the novel SEGRA called Compound A– a synthetic analog of natural aziridine precursor from African bush Salsola Botch in skin. We have also established anti-cancer GR-dependent activity of Compound A in epithelial and lymphoma cells.

Using knockout mice for the major GR target genes including Fkbp5 (GR chaperone) and DDIT4/REDD1 (one of the major negative regulators  of mTORC), we discovered that blockage of Fkbp5 and REDD1 significantly changes GR function and greatly protects skin against glucocorticoid-induced atrophy. This suggests a novel GR-targeted anti-inflammatory therapy where glucocorticoids are combined with inhibitors of GR target genes.

For more information, please see Dr. Budunova’s faculty profile.


See Dr. Budunova's publications in PubMed.

Contact Budunova Lab

Contact the Budunova Lab at 312-503-4669 or visit in the Montgomery Ward Building, 303 E. Chicago Avenue, Ward 9-015, Chicago, IL 60611


Irina Budunova, MD, PhD

Research Associates

Pankaj Bhalla, PhDGleb Baida, PhDAnna Klopot, PhD

 Paul Burridge Lab

Investigating the application of human induced pluripotent stem cells to study the pharmacogenomics of chemotherapy off-target toxicity and efficacy

Research Description

The Burridge lab studies the role of the genome in influencing drug responses, known as pharmacogenomics or personalized medicine. Our major model is human induced pluripotent stem cells (hiPSC), generated from patient's blood or skin. We use a combination of next generation sequencing, automation and robotics, high-throughput drug screening, high-content imaging, tissue engineering, electrophysiological and physiological testing to better understand the mechanisms of drug response and action.

Our major effort has been related to patient-specific responses to chemotherapy agents. We ask the question: what is the genetic reason why some patients have a minimal side effects to their cancer treatment, whilst others have encounter highly detrimental side-effects? These side-effects  can include cardiomyopathy (heart failure or arrhythmias), peripheral neuropathy,  or hepatotoxicity (liver failure). It is our aim to add to risk-based screening by functionally validating genetic changes that predispose a patient to a specific drug response.

Recent Findings

  • Human induced pluripotent stem cells predict breast cancer patients’ predilection to doxorubicin-induced cardiotoxicity
  • Chemically defined generation of human cardiomyocytes

Current Projects

  • Modeling the role of the genome in doxorubicin-induced cardiotoxicity using hiPSC
  • Investigating the pharmacogenomics of tyrosine kinase inhibitor cardiotoxicity
  • hiPSC reprogramming, culture and differentiation techniques
  • High-throughput and high-content methodologies in hiPSC-based screening

For lab information and more, see Dr. Burridge’s faculty profile and lab website.


See Dr. Burridge's publications on PubMed.


Contact Dr. Burridge at 312-503-4895.

Lab Staff

Postdoctoral Fellows

Malorie Blancard, Hananeh Fonoudi, Mariam Jouni, Davi Leite, Tarek Mohamed, Disheet Shah

Graduate Students

Liora Altman-Sagan, Raymond Copley, K. Ashley Fetterman, Phillip Freeman, Donald McKenna, Emily Pinheiro, Marisol Tejeda, Carly Weddle

Technical Staff

Ali Negahi Shirazi

 Gemma Carvill Lab

Genetic causes and pathogenic mechanism that underlie epilepsy

Research Description

The primary goal of our research is to use gene discovery and molecular biology approaches to identify new treatments for epilepsy. We aim to 1) identify the genetic causes of epilepsy, 2) use stem cell models to understand how genetic mutations can cause epilepsy, 3) develop and test new therapeutics for this condition. Our work is based on the promise of precision medicine where knowledge of an individual’s genetic makeup shapes a personalized approach to care and management of epilepsy.

Current Projects

  • Next generation sequencing in patients with epilepsy
  • Alternative exon usage during neuronal development
  • Identify the regulatory elements that control expression of known epilepsy genes
  • Stem cell genetic models for studying the epigenetic basis of epilepsy

For more information, see Dr. Carvill's faculty profile or the Carvill Lab Website.


Please see Dr. Caraveo Piso's publications on PubMed.

Contact Information

Gemma L. Carvill, PhD

 Shi-Yuan Cheng Lab

Cancer stem cell biology, cellular signaling and therapy responses in human brain tumors, in particular, glioblastoma (GBM)

Research Description

      Integrated genomic analysis by TCGA revealed tat GBMs can be classified into four clinically relevant subtypes, proneural (PN), neural, mesenchymal (Mes) and classical GBMs with each characterized by distinct gene expression signatures and genetic alterations. We reported that PN and Mes glioma stem cells (GSCs) subtypes also have distinct dysregulated signaling pathways. Our current research focuses on novel mechanisms/cellular signaling of GSC biology, tumorigenesis, progression, invasion/metastasis, angiogenesis and therapy responses of GSCs and GBMs.

1. MicroRNAs (miRs) and non-coding RNAs in GSCs and GBMs – miRs and other small non-coding RNAs act as transcription repressors or inducers of gene expression or functional modulators in all multicellular organisms.  Dysregulated miRs/noncoding RNAs plays critical roles in cancer initiation, progression and responses to therapy. We study the mechanisms by which deregulated expression of miRs influence GBM malignant phenotypes through interaction with signaling pathways, that in turn, influence proneural (PN)- and mesenchymal (Mes)-associated gene expression in GSCs and GBM phenotypes. We study the molecular consequences and explore clinical applications of modulating miRs and signaling pathways in GBMs.  We are establishing profiles of non-coding RNAs in these GSCs and study mechanisms and biological influences of these non-coding RNAs in regulating GSC biology and GBM phenotypes. In addition, we explore novel therapeutic approaches of delivery of tumor suppressive miRs into GSC brain xenografts in animals.

2.  Autophagy in GBMs. (Macro)autophagy is an evolutionally conserved dynamic process whereby cells catabolize damaged proteins and organelles in a lysosome-dependent manner. Autophagy principally serves as an adaptive role to protect cells and tissues, including those associated with cancer. Autophagy in response to multiple stresses including therapeutic treatments such as radiation and chemotherapies provides a mechanism for tumor cell to survive and acquire resistance to therapies. Tumors can use autophagy to support and sustain their proliferation, survival, metabolism, invasiveness, metastasis and resistance to therapy. We study mechanisms by which phosphorylation, acetylation and ubiquitination of autophagy proteins regulate GSC and GBM phenotypes and autophagic response, which, in turn contributes to tumor cell survival, growth and resistance to therapy. We investigate whether disruption of these post-translational processes on autophagy proteins inhibits autophagy and enhances the efficacy of combination therapies for GBMs. We examine whether cross-talks between miRs, autophagy and oncogenic signaling pathways regulate GSC stemness and phenotypes.

3. Heterogeneity, epigenetic regulation, DNA damage and metabolic pathways in GSCs and GBMs. Intratumoral heterogeneity is a characteristic of GBMs and most of cancers. Phenotypic and functional heterogeneity arise among GBM cells within the same tumor as a consequence of genetic change, environmental differences and reversible changes in cell properties. Subtype mosaicism within the same tumor and spontaneous conversion of human PN to Mes tumors have been observed in clinical GBMs. We explore an emerging epigenetic marker with distinct functions such as DNA methylation together with genetic mapping of these markers to assess their contributions to GBM heterogeneity. In addition, compared with PN GSCs, DNA damage and glycolytic pathways are aberrant active in Mes GSCs. We investigate the mechanisms by which these pathways regulate GSC and GBM phenotypes and responses to therapies.

4. Oncogenic receptor tyrosine kinase (RTKs) signaling, small Rho GTPase regulators in GBM and GSCs: Small Rho GTPases such as Rac1 and Cdc42 modulate cancer cell migration, invasion, growth and survival. Recently, we described mechanisms by which EGFR and its mutant EGFRvIII and PDGFR alpha promote glioma growth and invasion by distinct mechanisms involving phosphorylation of Dock180, a Rac-specific guanidine nucleotide exchange factor (GEF) and DCBLD2, an orphan membrane receptor. We are currently investigating involvement of other modulators/GEFs and other Rho GTPases in modulating GSC and GBM phenotypes and responses to therapy.

For more information, please see Dr. Cheng's faculty profile and lab website.


View Dr. Cheng's complete list of publications in PubMed.

Contact Us

Shi-Yuan Cheng, PhD at 312-503-5314

Visit us on campus in the Lurie Building, Room 6-119, 303 E Superior Street, Chicago, Illinois 60611.


 Erica Davis Lab

Multidisciplinary studies to elucidate the genetic architecture of rare pediatric disease with emphasis on ciliopathies, undiagnosed rare congenital disorders, and neurodevelopment disorders

Research Description

We are focused primarily on the study of pediatric genetic disorders, and our mission is to: a) improve our knowledge of genetic variation that causes these disorders and modulates their severity; b) discover pathomechanisms at the cellular and biochemical level; and c) develop cutting-edge therapeutic modalities that will improve the health and well-being of affected individuals and their families. Our research themes focus on but are not limited to:

  1. Acceleration of gene discovery in proximal and global pediatric cohorts.
  2. Understanding the contextual effect of genetic variation to explain pleiotropy, variable expressivity, and epistasis.
  3. Development and application of experimentally tractable models to delineate underlying pathomechanism.
  4. Establishing in vitro and in vivo assays for human disease modeling that are suitable for medium and high throughout drug screening.
  5. Synthesis of clinical investigation and basic experimental biology to advance molecular diagnosis and identify suitable treatment.

For more information, please see Dr. Davis's faculty profile.


See Dr. Davis's publications in PubMed.


Email Dr. Davis

Phone 312-503-7662

 Francesca Duncan Lab

Mammalian ovarian and gamete biology and reproductive aging

Research Description

Aging is associated with cellular and tissue deterioration and is a prime risk factor for chronic
diseases and declining health. The female reproductive system is the first to age in humans, with
a decline in egg quantity and quality beginning at ~35 years of age and menopause ensuing at
~50 years of age. Female reproductive aging has significant health consequences as it results in
endocrine function loss and is a leading cause of infertility, miscarriages, and birth defects.
Although aging hallmarks and mechanisms have been enumerated across multiple organ
systems and species, they have not been investigated in the context of mammalian reproductive

My research program integrates and builds upon my 18-year history in the field of reproductive
science and medicine to investigate the overarching hypothesis that deterioration of oocyte-intrinsic
cellular pathways together with alterations in the ovarian environment underlie the age-associated
decline in female gamete quantity and quality. Our work is at the interface of
reproductive aging and systemic aging; physiologic and iatrogenic reproductive aging; gamete,
follicle, and ovarian biology; and reproductive science and medicine. Our comprehensive insights
will help us design targeted interventions to potentially slow or counteract reproductive aging,
laying the foundation to simultaneously improve women’s fertile-span and health-span across
generations. In addition, reproductive aging mechanisms may inform those that precipitate
general aging, which occur up to decades later in life. Moreover, the mechanisms involved in
reproductive aging that we are investigating - aneuploidy, protein metabolism dysregulation,
and fibrosis and inflammation – are also central to other conditions such as cancer
pathogenesis. Thus, our research has broad impact and collaborative opportunities across
disciplines, which already include biochemistry, biophysics, toxicology and pharmacology, and
reproductive endocrinology and infertility.

Ultimately our work in reproductive aging will have direct impacts on public health in two ways.
First, reproductive aging affects all women, and menopause and premature aging of the ovary
accelerates aging in general. Such health consequences occur because ovarian hormones such
as estrogen, for example, are critical for cardiovascular, bone, immune, and cognitive functions.
Second, reproductive aging is associated with age-associated infertility, which has significant
societal, clinical, and health ramifications as more women globally are delaying childbearing.

For lab information and more, see Dr. Duncan's faculty profile.

Visit the Duncan Lab website


See Dr. Duncan's publications on PubMed.


Email Dr. Duncan


 Jaime García-Añoveros Lab

Development, function, dysfunction and degeneration of sensory receptor cells and neurons

Research Description

We investigate sensory organs and particularly the uniquely specialized cells that detect external signals (the sensory receptor cells) and communicate this information to the brain (the primary sensory neurons). Our approach is to identify and characterize novel genes involved in the formation (during development or regeneration), function (as sensory transducers), dysfunction and death (causing diseases like deafness or neuropathic pain) of these cells. The genes we have studied so far encode ion channels (of the Deg/ENaC and TRP families) and transcriptional regulators (zinc-finger proteins; these studied in collaboration with Anne Duggan). We are interested in all forms of sensation but, as of now, have primarily explored the somatic (touch and pain), auditory and nasal sensory organs.

Sensory Neuron Development: We found Insm1, a zinc-finger gene regulator that determines the number of olfactory receptor neurons. Insm1 is expressed in the olfactory epithelium, as it is everywhere else in the developing nervous system, in late (but not early) progenitors and nascent (but not mature) neurons. It functions by promoting the transition of neuroepithelial progenitors from apical, proliferative and uncommitted (i.e., neural stem cells) to basal, terminally dividing and neuron-producing (Duggan et al., 2008; Rosenbaum, Duggan & García-Añoveros 2011). We are currently determining the role of Insm1 in other sensory organs, as well as elucidating the role of other novel neurodevelopmental genes.

Sensory Transduction: We pioneered a molecular model of how certain neurons can detect touch using DEG/ENaC channels and structural components of the extracellular matrix and the cytoskeleton (García-Añoveros et al., 1995; 1996), characterized a major pain transduction channel (TRPA1; Nagata et al., 2005), and continue searching for sensory transducers, particularly ion channels.

Sensory Neuron Degeneration: We found a form of cell death caused by mutations on ion channels that leave them open, generating lethal currents (García-Añoveros et al., 1998). In this way, we found how dominant mutations in the Mcoln3 (Trpml3) gene cause loss of mechanosensory cells of the inner ear and deafness (Nagata et al., 2008; Castiglioni et al., 2011). We continue exploring he role of TRPML3 and other ion channel in inner ear function and disease.

For more information, view the faculty profile of Jaime García-Añoveros, PhD or visit the Añoveros & Duggan lab site.


See Dr. García-Añoveros' publications on PubMed.

Staff Listing

Graduate Students

Chuan Foo
Teerawat Wiwatpanit

Post-doctoral Fellows

Research Assistant Professor

Technical Staff

Contact Info

Dr. García-Añoveros

Lab Phone: 312-503-4246
Office Phone: 312-503-4245

 Vladimir Gelfand Lab

Discovering how multiple motors on the surface of the same cargo work together in organelle movement, how these motors are attached to the surface of organelles and what regulates their activity

Research Description

One of the remarkable features of eukaryotic cells is their ability for rapid transport of intracellular organelles in the cytoplasm. Examples of such transport include segregation of chromosomes during cell division and the transport of organelles in neurons from the cell body into axons and dendrites. Movements of organelles are powered by molecular motors. Microtubule motors(kinesins and dyneins) move along microtubules and myosins move along microfilaments.

We use two cellular models to discover how multiple motors on the surface of the same cargo work together in organelle movement and how these motors are attached to the surface of organelles and what regulates their activity. One model is cultured pigment cells (melanophores). These cells activate movement of pigment organelles in response to hormone-modulated changes of cAMP concentration. The movement of pigment organelles is powered by three different motors (two microtubule motors of different polarity and a myosin) and this system is very convenient for analysis of motor regulation. A second model is cultured Drosophila cells that we use to individual components of transport machinery by using RNAi. In our work, we employ techniques of cell and molecular biology and computer-assisted microscopy of living cells and purified organelles as well as high-resolution and high-sensitivity biophysical methods.

For lab information and more, see Dr. Gelfand's faculty profile and lab website.


See Dr. Gelfand's publications on PubMed.


Contact Dr. Gelfand at 312-503-0530.

Lab Staff

Postdoctoral Fellows

Urko Del Castillo, Anna Gelfand, Wen Lu, Rosalind Norkett, Bhuvanasundar Ranganathan, Amelie Robert

Graduate Student

Yinlong Song

Technical Staff

Margot Lakonishok

 Jeffrey Goldstein Lab

Placental diagnosis and deep phenotyping using machine learning and artificial intelligence.

Research Description

Area: Placenta diagnosis and deep phenotyping by machine learning:
Diagnosis of placental abnormalities relies on microscopic examination of glass slides. Digitizing the slides to form whole slide images opens several avenues for applying machine learning techniques. Avenues of research include studies to improve interobserver reliability, decrease vulnerability to artifacts, aid humans in diagnosing, and produce explainable predictions. Machine learning techniques can be used to probe basic problems in placental biology and pathophysiology, quantifying changes that evade routine human detection.
Area: Placental diagnosis using AI on placental photographs:
 Placental examination can provide insight into future maternal and child health, but preparation of slides and expert examination are expensive and time consuming. Many diagnoses can be made in whole or in part from the photographic appearance of the placentas. An AI algorithm, installed on smart phones, could make placental examination feasible for all births, everywhere. Bioinformatic studies of electronic health records can identify new associations between placental features and outcomes.

For lab information and more, see Jeffrey Goldstein, MD,PhD, faculty profile.


See Dr. Goldstein's publications


Email Dr. Goldstein


 Alicia Guemez-Gamboa Lab

Identifying and investigating novel molecular bases of cellular recognition that govern neuronal circuit assembly during human development and disease.

Research Description

Developing neurons integrate into functional circuits through a series of cell recognition events, which include neuronal sorting, axon and dendrite patterning, synaptic selection, among others. Our research focuses on cell-surface recognition molecules that mediate interactions between neurons to discriminate and select appropriate targets in the developing brain. Additionally, we seek to uncover novel mechanisms of neural recognition that lead to brain connectivity defects in humans. To explore the broader roles for cell recognition molecules and their pivotal function in neural circuit development, our lab takes advantage of a battery of modern laboratory techniques. These approaches include animal and stem cell disease modeling, as well as next-generation sequencing and CRISPR/Cas9 gene editing. Identifying fundamental principles of cellular recognition in wiring circuits contributes to our understanding of neurological disorders and how neuronal dysfunction arises from aberrations during development of the human brain.

For lab information and more, see Dr. Guemez-Gamboa's faculty profile and lab website.


See Dr. Guemez-Gamboa's publications on PubMed.


Contact Dr. Guemez-Gamboa at 312-503-0752.

Lab Staff

Postdoctoral Fellows

Nadya Gabriela Languren, Jennifer Rakotomamonjy

Technical Staff

Devin Davies, Sean McDermott, Niki Sabetfakhri, Davis Thomas

Temporary Staff

Ian Quiroz

 Peng Ji Lab

Role of MDia1 in the pathogenesis of del(5q) myelodysplastic syndromes

Research Interests

Our lab is interested in how cytoskeletal signaling, motor proteins and adhesion systems are integrated with chemical signaling pathways to regulate cell behavior and tissue differentiation and disease. The Ji lab studies small G proteins and downstream actin regulatory effectors that participate in enucleation during red cell development.

At the level of the nucleus, the Ji laboratory studies genes involved in erythroid lineage commitment, chromatin condensation and enucleation towards understanding how congenital red cell disorders and leukemia develop. 

For more information, visit the faculty profile of Peng Ji, MD, PhD.


See Dr. Ji's publications in PubMed.


Dr. Ji

 Geoff Kansas Lab

T helper cell differentiation and trafficking.

Research Description

My laboratory is interested in signaling mechanisms which control T helper cell differentiation and traffic. We are currently focused on two areas: functions of p38 MAP kinases (MAPK) and the role of a transcription factor KLF2 in these processes. Toward this end, we have produced novel mouse models which will allow us to test the role of the different isoforms of p38 (of which there are 4) in T helper differentiation and expression of key leukocyte adhesion molecules; and to determine the role of KLF2 downregulation in T helper biology generally.

For lab information and more, see Dr. Kansas's faculty profile.


See Dr. Kansas's publications on PubMed.


Contact Dr. Kansas at 312-908-3237 or the lab at 312-908-3752.

Lab Staff

Technical Staff

Caroline Patel

 John Kessler Lab

Focusing on the biology of neural stem cells and growth factors and their potential for regenerating the damaged or diseased nervous system.

Research Description

The Kessler laboratory focuses on the biology of neural stem cells and growth factors and their potential for regenerating the damaged or diseased nervous system. A major interest of the laboratory has been the role of bone morphogenetic protein (BMP) signaling in both neurogenesis and gliogenesis and in regulating cell numbers in the developing nervous system.  Both multipotent neural stem cells and pluripotent embryonic stem cells are studied in the laboratory. Recent efforts have emphasized studies of human embryonic stem cells (hESC) and human induced pluripotent stem cells (hIPSC). The Kessler lab oversees the Northwestern University ESC and IPSC core and multiple collaborators use the facility. In addition to the studies of the basic biology of stem cells, the laboratory seeks to develop techniques for promoting neural repair in animal models of spinal cord injury and stroke. In particular, the lab is examining how stem cells and self-assembling peptide amphiphiles can be used together to accomplish neural repair. The lab is also using hIPSCs to model Alzheimer’s disease and other disorders. 

For more information see the faculty profile of John A Kessler, MD.


View Dr. Kessler's full list of publications in PubMed.


John Kessler, MD

 Dimitri Krainc Lab

Understanding the mechanisms of neuronal dysfunction in neurodegenerative disorders that affect children and adults.

Research Description

The overarching goal of my laboratory is to study rare diseases such Huntington’s and genetic forms of Parkinson’s disease, as a window to understanding neurodegeneration across the lifespan. More recently, we have focused on rare lysosomal diseases such as Gaucher’s in order to identify specific targets and mechanisms that contribute to neurodegeneration in Parkinson’s and related synucleinopathies. It is expected that such defined targets will facilitate mechanism-based development of targeted therapies for children with neuronopathis Gaucher’s disease as well as adult-onset synucleinopathies such as Parkinson’s disease. To validate and study these targets and novel therapies in human neurons, we have utilized induced pluripotent stem cells (iPS) generated by reprogramming of patient-specific skin fibroblasts. These iPS cells are differentiated into specific neuronal subtypes in order to characterize the contribution of genetic, epigenetic and environmental factors to disease mechanisms and to test novel therapeutic approaches.

For more information see the faculty profile of Dimitri Krainc or visit the Krainc Lab website.

Recent Publications

View Dr. Krainc's full list of publications in PubMed.

Contact information

Dimitri Krainc, MD, PhD
Ward Professor and Chairman

 Tsutomu Kume Lab

The Kume Lab’s research interests focus on cardiovascular development, cardiovascular stem/progenitor cells and angiogenesis.

Research Description

Cardiovascular development is at the center of all the work that goes on in the Kume lab. The cardiovascular system is the first functional unit to form during embryonic development and is essential for the growth and nurturing of other developing organs. Failure to form the cardiovascular system often leads to embryonic lethality and inherited disorders of the cardiovascular system are quite common in humans. The causes and underlying developmental mechanisms of these disorders, however, are poorly understood. A particular emphasis in our laboratory has recently been the study of cardiovascular signaling pathways and transcriptional regulation in physiological and pathological settings using mice as animal models, as well as embryonic stem (ES) cells as an in vitro differentiation system. The ultimate goal of our research is to provide new insights into the mechanisms that lead to the development of therapeutic strategies designed to treat clinically relevant conditions of pathological neovascularization.


View Dr. Kume's publications on PubMed.

For more information, visit the faculty profile for Tsutomu Kume, PhD.

Contact Us

Contact Dr. Kume at 312-503-0623 or the Kume Lab at 312-503-3008.

Staff Listing

Austin Culver
MD Candidate

Anees Fatima
Research Assistant Professor

Christine Elizabeth Kamide
Senior Research Technologist

Erin Lambers
PhD Candidate

Ting Liu
Senior Research Technologist

Jonathon Misch
Research Technologist

 Monica Laronda Lab

Pediatric Fertility & Hormone Preservation & Restoration

Research Description

Our research addresses fundamental regenerative medicine questions through the lens of reproductive biology. The main objective of our lab is to develop a patient-specific ovarian follicle niche that will support systemic endocrine function and fertility in women and girls who were sterilized by cancer treatments, have disorders of sex development or were exposed to other factors that could result in premature ovarian failure or sex hormone insufficiency. This research is a part of the Ann & Robert H Lurie Children’s Hospital Fertility and Hormone Preservation and Restoration Program that bridges basic science, translational research and clinical practice.


See Dr. Laronda's publications in PubMed.


Email Dr. Laronda

 Yan Liu Lab

Hematopoietic stem cell self-renewal and pathogenesis of myeloid malignancies

Research Description

The Liu laboratory is interested in investigating the molecular mechanisms governing normal and malignant hematopoiesis, with an emphasis on understanding hematopoietic stem cell (HSC) self-renewal and pathogenesis of myeloid malignancies, including myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). Our long-term goals are to identify novel regulators of HSC self-renewal, understand the molecular mechanisms regulating their function, and develop novel therapeutic strategies to eliminate leukemia stem cells (LSCs) and improve leukemia treatment. We utilize molecular, genetic, immunological, biochemical, and pharmacological approaches as well as unbiased genome wide studies, including RNA-seq, ChIP-seq, ATAC-seq, and cytokine arrays, to investigate the molecular basis of HSC self-renewal and leukemogenesis. Major areas of focus include: 1) The role of tumor suppressor p53 in CHIP progression and pathogenesis of MDS; 2) Phosphatase PRL2 in HSC self-renewal and leukemogenesis; 3) Polycomb Repressive Complex 1 (PRC1) in HSC self-renewal and terminal differentiation.

For more information, visit Dr. Liu's faculty profile page.


View Dr. Liu's publications at PubMed.


Email Dr. Liu



 Yong-Chao Ma Lab

Regulation of Motor Neuron and Dopaminergic Neuron Function in Development and Disease

Postdoctoral fellow jobs and graduate student rotation projects are available.

Research Description

Spinal Motor Neurons and Spinal Muscular Atrophy (SMA)

SMA is characterized by the selective degeneration of spinal motor neurons. As the leading genetic cause of infant mortality, SMA affects one in every eight thousand live births. Our group is interested in studying mechanism regulating motor neuron development and function, as well as why motor neurons specifically degenerate in SMA. To address these questions, we use a combination of genetic, biochemical and cell biological approaches and utilize genetically modified mice, induced pluripotent stem (iPS) cells reprogrammed from fibroblasts and zebrafish as model systems. We focus on the regulation of mitochondrial functions in SMA pathogenesis. Based on our findings, we hope to develop new therapeutic strategies for treating SMA.

Dopaminergic Neurons and Parkinson's Disease

Dopaminergic neurons located in the ventral midbrain control movement, emotional behavior and reward mechanisms. Dysfunction of these neurons is implicated in Parkinson’s disease, drug addiction, depression and schizophrenia. Our group is interested in the genetic and epigenetic mechanisms regulating dopaminergic neuron functions in disease and aging conditions. We are particularly interested in how aging and mitochondrial oxidative stress contribute to dopaminergic neuron degeneration in Parkinson's disease through transcriptional and epigenetic regulations. We use mouse models, cultured neurons and iPS cells for these studies.

For more information visit Dr. Ma's faculty profile and Dr. Ma's lab website within the Children's Hospital Research Center.


View Dr. Ma's publications at PubMed


Email Dr. Ma

Phone 773-755-6339

Lab Staff

Nimrod Miller, PhD, Postdoctoral Fellow

Han Shi, Graduate Student

Brittany Edens, Graduate Student

Kevin Park, Graduate Student

Monica Yang, Undergraduate Student

Aaron Zelikovich, Undergraduate Student

 Brian Mitchell Lab

Our goal is to understand the integration of signaling and cytoskeletal dynamics on diverse developmental processes including centriole amplification, cell migration and cell polarity.

Research Description

Centrioles are microtubule based structures with nine fold symmetry that are involved in both centrosome organization and aster formation during cell division. During the normal cell cycle centrioles duplicate once, generating a mother/daughter pair and in most post-mitotic vertebrate cells the mother centriole then goes on to form the basal body of a sensory cilium. Abnormalities in the duplication of centrioles (and centrosomes) are prevalent in many cancers suggesting a link between centriole duplication and cancer progression. We study what factors limit centriole duplication from a novel direction with the use of Xenopus motile ciliated cells. Ciliated cells are unique among vertebrate cells in that they generate hundreds of centrioles (basal bodies) therefore providing a great system for studying the regulation of centriole duplication. Understanding how nature has overcome the typically tight regulation of centriole duplication will lend insight into the molecular mechanisms of cancer progression.

Tissue development and homeostasis requires dramatic remodeling as new cells migrate into an epithelium.  How migrating cells breakdown junctional barriers during development or during diseases processes such as metastasis is poorly understood at the molecular level.  During the early development of Xenopus embryos, distinct cell types join the outer epithelium in a process called radial intercalation.  We are interested in the molecular mechanisms that regulate both the migration of these cells as well as the tissue remodeling that occurs to accommodate them. 

The ability of ciliated epithelia to generate directed fluid flow is an important aspect of diverse developmental and physiological processes including proper respiratory function. To achieve directed flow, ciliated cells must generate 100-200 cilia that are polarized along a common axis both within and between cells. My lab is currently working towards understanding the molecular mechanisms for how cell polarity is coordinated as well as how individual cilia interpret the cells polarity. We have determined that ciliated cells receive polarity cues via the non-canonical Wnt/Planar Cell Polarity (PCP) pathway, but the details of this are still poorly understood. Additionally, the PCP pathway is known to influence a cells cytoskeleton dynamics and a main goal is to understand how this influences the ability of individual cilia to coordinate their polarity.


For lab information and more, see Dr. Mitchell's faculty profile and lab website.


See Dr. Mitchell's publications on PubMed.


Contact Dr. Mitchell at 312-503-9251.

Lab Staff

Postdoctoral Fellows

Caitlin Collins, Jennifer Mitchell, Rosa Ventrella

Technical Staff

Eva Brotslaw, Sun Kim, Ahmed Majekodunmi

 Guillermo Oliver Lab

Exploring how each specific cell type and organ acquires all its specific and unique morphological and functional characteristics during embryogenesis

Research Description

The Oliver Lab focuses on understanding how each specific cell type and organ acquires all its specific and unique morphological and functional characteristics during embryogenesis. Alterations in the cellular and molecular mechanisms controlling organ formation can result in major defects and pathological alterations. Our rationale is that a better knowledge of the basic processes controlling normal organogenesis will facilitate our understanding of disease. Our goal is to dissect the specific stepwise molecular processes that make each organ unique and perfect. Our major research interests are the forebrain, visual system and the lymphatic vasculature and to address those questions we use a combination of animal models and 3D organ culture systems, stem cells and iPS cells.

Related to the lymphatic vasculature, our lab identified years ago the first specific marker for lymphatic endothelial cells and generated the first mouse model devoid of lymphatics. We have characterized many of the critical steps leading to the formation of the lymphatic vasculature. We have also reported that a defective lymphatic vasculature can cause obesity in mice and we are currently trying to determine whether this is also valid in humans.

In case of the central nervous system, our focus is to characterize how complex structures such as the forebrain and eye are formed. For that we have started to apply 3D organ culture systems derived from stem cell and iPS that allow us to grow eyes in a petri dish. Using this approach we expect to dissect the genes and mechanisms controlling these developmental processes.

For more information, visit Dr. Oliver’s faculty profile or visit the Guillermo Oliver Lab Site.


View Dr. Oliver's publications at PubMed


Email Dr. Oliver

Phone 312-503-1651

 Susan Quaggin Lab

Uncovering the molecular mechanisms of diabetic vascular complications, thrombotic microangiopathy, glomerular diseases and glaucoma

Our lab focuses on the basic biology of vascular tyrosine kinase signaling in development and diseases of the blood and lymphatic vasculature.  Our projects include uncovering the molecular mechanisms of diabetic vascular complications, thrombotic microangiopathy, glomerular diseases and glaucoma.  Utilizing a combination of mouse genetic, cell biologic and proteomic approaches, we have identified key roles for Angiopoietin-Tie2 and VEGF signaling in these diseases.  Members of the lab are developing novel therapeutic agents that target these pathways.  

For more information, please see the faculty profile of Susan Quaggin, MD


See Dr. Quaggin's publication in PubMed


Email Dr. Quaggin

 Paul Schumacker Lab

Oxygen sensing in embryonic development, tissue responses to hypoxia and tumor angiogenesis.

Research Description

Our lab is interested in the molecular mechanisms of oxygen sensing and the importance of this process for embryonic development, tissue responses to hypoxia and tumor angiogenesis. We are testing the hypothesis that the mitochondria play a central role in detecting cellular oxygenation and signal the onset of hypoxia by releasing reactive oxygen species (ROS). These signals trigger downstream signal transduction pathways responsible for the transcriptional and post-translational responses of the cell. Transcriptional activation of genes by Hypoxia-Inducible Factor-1 confers protection against more severe hypoxia by augmenting the expression of glycolytic enzymes, membrane glucose transporters and other genes that tend to augment tissue oxygen supply by increasing the release of vascular growth factors such as VEGF, erythropoietin and vasoactive molecules that augment local blood flow. Current experiments are aimed at improving our understanding of how oxygen interacts with the mitochondrial electron transport chain to amplify ROS production and clarifying the targets that they act on to stabilize HIF and activate transcription.

In specific tissues, oxygen sensing is essential for normal function, but it can also contribute to disease pathogenesis.  For example, during mammalian development, the lung tissue is hypoxic and blood flow is restricted in the pulmonary circulation in order to prevent escape of oxygen from the pulmonary capillaries to amniotic fluid.  At birth, inflation of the lung with air causes an increase in lung oxygen levels, which triggers relaxation of pulmonary arteries.  In Persistent Pulmonary Hypertension of the Newborn, failure of the pulmonary circulation to dilate results in elevated pulmonary arterial pressures and significant lung gas exchange dysfunction.  We are testing the hypothesis that pulmonary vascular cells sense O2 at the mitochondria and that ROS released from those organelles trigger an increase in cytosolic calcium, which causes smooth muscle cell contraction.  In adult patients with hypoxic lung disease, similar activation of hypoxic vasoconstriction can lead to chronic pulmonary hypertension, which can progress to right heart failure.  A fuller understanding of the mechanisms of oxygen sensing in health and disease may lead to insights into therapeutic inhibition of this response in disease states.

In solid tumors, consumption of oxygen by highly metabolic tumor cells leads to hypoxia and threatens glucose supplies.  Hypoxic tumor cells retain their oxygen sensing capacity and turn on expression of HIF-dependent genes, leading to tumor angiogenesis and increased blood supply, which permits further growth.  We are currently exploring the hypothesis that the mitochondrial oxygen sensor is required for this response using pursuing genetic models.  A better understanding of how tumor cells detect hypoxia could lead to the discovery of therapeutic approaches that would prevent detection of hypoxia and thereby prevent tumor progression.

For more information visit Dr. Schumacker's faculty profile page


View Dr. Schumacker's publications at PubMed


Email Dr. Schumacker

Phone 312-503-1476

 Hans-Georg Simon Lab

Development and regenerative repair of vertebrate limbs and hearts

Research Description

The development of organs during embryogenesis and their repair during adulthood are biological problems of very practical importance for regenerative medicine.

Using both newt and zebrafish model organisms that naturally rebuild lost structures as adults, we identified evolutionarily conserved gene activities indicative of a molecular signature of regeneration. Particularly, we found the dynamic remodeling of the extracellular matrix (ECM) to be key in instructing cell behaviors that are critical for initiating and maintaining regenerative processes. These findings point to new opportunities for the enhancement of regenerative wound healing in mammals through the manipulation of the local extracellular environment.

As a new research direction, we are studying an unexpected hyperactive blood clotting phenotype in mice deficient for the actin-associated protein Pdlim7. The Pdlim7 knockout mouse provides strong translational opportunities as a novel model to better understand the causes and possible treatments of hypercoagulopathies.

For more information visit the faculty profile of Hans-Georg Simon, PhD.


View all publications on PubMed


Email Dr. Simon

Phone Dr. Simon at 773-755-6391 or the Simon Lab at 773-755-6372.

 Greg Smith Lab

Cell and molecular biology of herpesvirus invasion of the nervous system

Research Description

We investigate the relationship between infection of the nervous system by herpesviruses and disease outcome. Some of the most traumatic diseases – including polio, rabies and encephalitis – result from infections of the nervous system.  In contrast, herpesviruses are highly proficient at infecting the nervous system, yet normally do not cause neurological disease.  This is achieved in part by self-imposed restrictions encoded within the viruses that limit viral reproduction and prevent dissemination into the brain.  For the individual, this results in a relatively benign infection, yet the virus becomes a life-long occupant of the nervous system that will periodically reemerge at body surfaces to infect others. Unfortunately, this infectious cycle can go awry resulting in several forms of severe disease (i.e. keratitis and encephalitis).

We have pioneered methods to genetically manipulate herpesviruses and visualize individual viruses in living neurons. Using these methods, we are studying the mechanisms by which the virus achieves its stringently controlled infectious cycle. Current genetic manipulations are based on a full-length infectious clone of the herpesvirus genome. The clone was made as a bacterial artificial chromosome (BAC) in E. coli. Transfection of purified E. coli BAC plasmid into permissive eukaryotic cells is sufficient to initiate viral infection, allowing for immediate examination of viral mutant phenotypes in a variety of biological assays.  For example, by fusing the green fluorescent protein (GFP) to a structural component of the viral capsid, individual viral particles can be tracked within the axons of living neurons during both entry and egress phases of the infectious cycle. Studies in culture can be complemented by examining the pathogenesis of mutant viruses in rodent models of infection.

Using these methods, we have discovered key aspects of cellular infection, viral assembly and intracellular transport. Looking forward, we are continuing to pursue our multidisciplinary approach of combining neuroscience, cell biology, bacterial genetics and virology to better understand these important pathogens.

For lab information and more, see Dr. Smith's faculty profile.


See Dr. Smith's publications on PubMed.


Contact Dr. Smith at 312-503-3745 or the lab at 312-503-3744.

Lab Staff

Research Faculty

Sarah Antinone 

Postdoctoral Fellows

Oana Maier

Graduate Students

Kennen Hutchison, DongHo Kim, Caitlin Pegg, Jen Ai Quan

Technical Staff

Austin Stults 

 Beatriz Sosa-Pineda Lab

The Sosa-Pineda lab studies studies the regulation of acinar cell development and plasticity in the pancreas, hepatic cell fate, and liver zonation. We also investigate mechanisms that promote pancreas metastasis.

Research Description

Using genetically modified mouse models and cutting-edge technologies, we investigate how the complex architecture of the mammalian pancreas and liver is established during development. We also investigate how acute or chronic injury affect liver zonation and exocrine pancreas homeostasis, and the role of chromosomal instability in pancreatic tumor formation and metastasis.


For more information, visit the faculty profile of Beatriz Sosa-Pineda, PhD or the Sosa-Pineda lab web site.


View Dr. Sosa-Pineda's publications at PubMed


Email Dr. Sosa-Pineda

Phone 312-503-2296

 Rui Yi Lab

Investigate mechanisms of skin development, stem cells, aging and cancer at the single-cell level

Research Description

Mammalian skin and its appendages function as the outermost barrier of the body to protect inner organs from environmental hazards and keep essential fluid within. Our research program studies mechanisms that govern cell fate specification, stem cell maintenance and aging as well as initiation and progression of cancer. We use single-cell genomics and computational tools, live animal imaging and genetically engineered mouse models to study gene expression regulation mediated by transcription factors, epigenetic regulators and post-transcriptional mechanisms mediated by miRNAs and RNA binding proteins at the single-cell resolution in mammalian skin. 

Our research aims to address several fundamental questions in stem cell biology: how the developmental potential of embryonic progenitors and adult tissue stem cells is transmitted or restricted in their progenies at the molecular level when they go through critical transitions such as cell fate specification, self-renewal of stem cells as well as stress response, and how these regulatory mechanisms go awry in aging and diseases. Answers to these questions will help to manipulate skin stem cells for regenerative medicine and discover new treatment for human skin diseases.​

View all lab publications via PubMed.

For more information, visit the faculty profile page of Rui Yi, PhD or visit the Yi Laboratory website.

Contact Us

Email Dr. Yi




 Ming Zhang Lab

Molecular Mechanisms of Tumorigenesis and Cancer Metastasis

Research Description

The Zhang laboratory is focused on two research directions: 1) determining role of tumor suppressors in development and cancer progression and 2) identifying immune components that control breast cancer metastasis.

The main focus of my research program is to study the roles of tumor suppressors in normal development and in breast and prostate cancer progression, focusing on maspin and an Ets transcription factor PDEF. Maspin is a unique member of the SERPIN family that plays roles in normal tissue development, tumor metastasis and angiogenesis. Genetic studies by my laboratory using maspin transgenic and knockout mice demonstrated an important role of maspin in normal mammary, prostate and embryonic development. Recently, we have identified several new properties of maspin. As a protein that is present on cell surface, maspin controls cell-ECM adhesion. This function is responsible for maspin-mediated suppression of tumor cell motility and invasion. We have also discovered that maspin is involved in the induction of tumor cell apoptosis through a mitochondrial death pathway. The long-term goals of these projects are to elucidate the molecular mechanisms by which maspin and PDEF control tumor metastasis and to identify their physiological functions in development. These analyses are not only important for basic biology and but also may lead to a therapy for cancer and other developmental diseases.

Another focus of research in Zhang lab is to identify immune components that control breast cancer metastasis. Chronic inflammation not only increases neoplastic transformation but also drives the inhibition of the immune response in a protective negative-feedback mechanism.  Suppressive immune cells are recruited to the sites of inflammation and function to inhibit both innate and adaptive immune responses, enabling tumor tolerance and unmitigated tumor progression. To study the interplay between tumor and immune cells, the Zhang lab has developed a unique animal model of breast cancer that reproduces different stages of breast cancer bone metastasis. Molecules that control tumor-immune cell interaction and immunosuppression have been identified. We are currently studying roles of these genes in tumor-driven evolution that control chronic inflammation and immunosuppression. We hypothesize that these key pro-inflammatory genes are upregulated during cancer progression, which function synergistically to recruit and activate suppressive MDSCs, TAMs and Tregs, inducing chronic inflammation and an immunosuppressive tumor microenvironment conducive to metastatic progression.

For more information visit Ming Zhang's faculty profile.


View publications by Ming Zhang in PubMed


Dr. Zhang

Phone 312-503-0449

 Youyang Zhao Lab

The Zhao Lab studies the molecular mechanisms of endothelial regeneration and resolution of inflammatory injury as well as endothelial and smooth muscle cell interaction in the pathogenesis of pulmonary vascular diseases.

Research Description

Recovery of endothelial barrier integrity after vascular injury is vital for endothelial homeostasis and resolution of inflammation. Endothelial dysfunction plays a critical role in the initiation and progression of vascular diseases such as acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) and atherosclerosis. A part of the research in the lab, employing genetically modified mouse models of human diseases, endothelial progenitor cells/stem cells, and translational research approach as well as nanomedicine, is to elucidate the molecular mechanisms of endothelial regeneration and resolution of inflammatory injury and determine how aging and epigenetics regulate these processes (J. Clin. Invest. 2006, 116: 2333; J. Exp. Med. 2010, 207:1675; Circulation 2016, 133: 2447).  We are also studying the role of endothelial cells in regulating macrophage functional polarization and resolving inflammatory lung injury. These studies will identify druggable targets leading to novel therapeutic strategies to activate the intrinsic endothelial regeneration program to restore endothelial barrier integrity and reverse edema formation for the prevention and treatment of ARDS in patients.

Pulmonary hypertension is a progressive disease with poor prognosis and high mortality. We are currently investigating the molecular basis underlying the pathogenesis.  We have recently identified the first mouse model of pulmonary arterial hypertension (PAH) with obliterative vascular remodeling including vascular occlusion and formation of plexiform-like lesions resembling the pathology of clinical PAH (Circulation 2016, 133: 2447). Our previous studies also show the critical role of oxidative/nitrative stress in the pathogenesis of PAH as seen in patients (PNAS 2002, 99:11375; J. Clin. Invest. 2009, 119: 2009). With these unique models and lung tissue and cells from idiopathic PAH patients, we will define the molecular and cellular mechanisms underlying severe vascular remodeling and provide novel therapeutic approaches for this devastating disease. 

The Zhao lab employs the state-of-the art technologies including genetic lineage tracing, genetic depletion, genetic reporter, and CRISPR-mediated in vivo genomic editing as well as patient samples to study the molecular mechanisms of acute lung injury/ARDS, and pulmonary hypertension and identify novel therapeutics for these devastating diseases. Current studies include 1) molecular mechanisms of endothelial regeneration and vascular repair following inflammatory lung injury induced by sepsis and pneumonia; 2) how aging and epigenetics regulate this process; 3) how endothelial cells regulate macrophage and neuptrophil function for resolution of inflammation and host defense; 4) stem/progenitor cells in acute lung injury and pulmonary hypertension and cell-based therapy; 5) mechanisms of obliterative pulmonary vascular remodeling; 6) molecular basis of right heart failure; 7) pathogenic role of oxidative/nitrative stress; 8) lung regeneration; 9) drug discovery; 10) nanomedicine.


View publications by Youyang Zhao in PubMed.

For more information, visit Dr. Zhao's Faculty Profile page


Email Dr. Zhao

Contact Dr. Zhao’s Lab at 773-755-6355

Lab Staff

Zhiyu Dai, PhD.
Research Assistant Professor

Xianming Zhang, PhD.
Research Assistant Professor

Narsa Machireddy, PhD.
Research Assistant Professor

Junjie Xing, PhD.
Research Scientist

Colin Evans, PhD.
Research Scientist

Varsha Suresh Kumar, PhD.
Research Scientist

Xiaojia Huang, PhD
Research Scientist

Hua Jin, PhD
Postdoctoral fellow

Yi Peng, PhD
Research Scientist

Mengqi Zhu, M.S.,
Graduate Student

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