Northwestern University Feinberg School of Medicine
Department of Biochemistry and Molecular Genetics
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Basic Science Labs

Following are descriptions of the lab work done within in the Department of Biochemistry and Molecular Genetics, listed by principal investigator. Learn about the broader goals for study within the labs as well as details on individual faculty labs and teams.

 Issam Ben-Sahra Lab

Decoding connections between signaling and metabolic networks

Research Description

The Ben-Sahra lab seeks to identify novel connections between oncogenic and physiological signals and cellular metabolism. My previous studies revealed new connections between mTORC1 (mechanistic Target of Rapamycin Complex I) signaling and de novo nucleotide synthesis pathways.

Using isotopic tracing experiments and genetic approaches, my lab investigates whether the additional signaling pathways such as PI3K/Akt, RAF/Erk, Hippo/Yap or AMPK could regulate metabolic pathways that supply small metabolites to sustain nucleotide synthesis independently of mTORC1 signaling. Furthermore, we are also interested in understanding how cells can sense changes in nucleotide levels. In addition to nucleotide metabolism, we also study connections between signaling pathway and global cancer cell metabolism. I predict that there could be points of regulations which could give selective advantages to cancer cells to grow and proliferate. The initial discovery that cancer cells exhibit atypical metabolic characteristics can be traced to the pioneering work of Otto Warburg, over the first half of the twentieth century.

Deciphering the interplay between oncogenic processes and metabolic pathways that contribute to metabolic reprogramming in a given setting may serve as a critical factor in determining therapeutic targets that yield greatest drug efficacy with marginal harmful effect on normal cells. Our research will enable further progress in the exploitation of unusual metabolic features in cancer as a means of therapeutic intervention.

For lab information and more, see Dr. Ben-Sahra's faculty profile and lab website.

Publications

See Dr. Ben-Sahra's publications on PubMed.

Contact

Contact Dr. Ben-Sahra.

 Jason Brickner Lab

Studying how the spatial organization of DNA within the nucleus impacts gene expression and chromatin structure.

DNA and proteins are non-randomly localized within the nucleus of the cell.  The Brickner lab studies how cells control the position of genes within the nucleus, and how gene positioning affects gene expression.  When genes are activated or repressed, their position in the nucleus often changes.  The lab has identified DNA "zip codes" in the promoters of genes that control their positioning, transcription and, through an epigenetic mechanism, chromatin structure.

Selected Publications

Selected Honors

  • 2014 Soretta and Henry Shapiro Research Professor in Molecular Biology
  • W.M. Keck Young Scholar in Medical Research
  • Baldwin Award for Biomedical Research
  • Helen Hay Whitney Postdoctoral Fellowship

Lab Staff

Leads

Jason Brickner, PhD

Donna Brickner, PhD

Graduate Students

Augustina D'Urso

Carlo Randise-Hinchliff

Varun Sood

Postdoctoral Fellow

Defne Egecioglu

Undergraduate Students

Robert Coukos

Teresa Kim

Jessica Marone

Nitin Walia

Contact Information

For more information, please see Dr. Brickner's faculty profile or lab website.

 Jaehyuk Choi Lab

Genetic basis of inherited and acquired immunological disorders and skin cancer.

Research Description

We employ cutting-edge genomics approaches to identify the genetic basis of inherited and acquired immunological disorders and skin cancer.

As an example, we have recently identified the genes and mutations underlying cutaneous T cell lymphoma, an incurable non-Hodgkin lymphoma of skin-homing T cells. The genes are components of the DNA damage, chromatin modifying, NF-kB and the T cell receptor signaling pathways. We are currently employing a comprehensive approach using human tissues and animal models to investigate the functions of these genes. We are confident these studies will allow us to elucidate the pathophysiology of this cancer and lead to the identification of novel therapeutic targets.

Work in the lab is funded by National Cancer Institute, Dermatology Foundation, American Skin Association and American Cancer Society. See the work of the Choi lab in the news. For further information, please also see Dr. Choi's faculty profile or visit the Choi Laboratory site.

Publications

See Dr. Choi's publications on PubMed.

Contact

Contact Dr. Choi.

 John Crispino Lab

The Crispino laboratory studies the mechanisms of normal and malignant blood cell growth.

Research in the Crispino laboratory is focused on investigating the regulatory mechanisms governing normal and malignant blood cell development, with an emphasis on understanding the growth of erythroid cells (red blood cells) and megakaryocytes (platelet-producing cells). Major areas of focus include: 1) Understanding the link between Down syndrome and leukemia. We are investigating how mutations in GATA1, a key transcription factor that regulates megakaryocyte growth contribute to leukemia. We are also studying the mechanisms by which trisomy 21 promotes the development of leukemia with a long-term goal of unraveling the mystery of why children with DS are predisposed to leukemia. Our current efforts are focused on characterizing the contributions of two chromosome 21 genes: DYRK1A, a kinase and ERG, a transcription factor. 2) Development of novel therapeutics for human megakaryocytic malignancies. In collaboration with the Broad Institute, we identified several small molecules that induce proliferation arrest, polyploidization and maturation of malignant megakaryocytes. By a three-pronged target identification approach, we discovered that a key target of these small molecules is Aurora A Kinase. We are currently investigating the utility of AURKA inhibitors as potential new, targeted therapies for acute megakaryocytic leukemia. In addition, we have completed extensive pre-clinical studies to support the testing of AURKA inhibitors in a related blood disease named primary myelofibrosis, a subtype of the MPNs. 3) Investigating the mechanisms of red blood cell development. We are currently studying two aspects of red blood cell development. First, based on our previous discovery that the coalescence of cytoplasmic vesicles is required for enucleation of erythroblasts, we are probing the requirements for specific motor proteins in enucleation and identifying small molecules that enhance enucleation in culture. This research will aid in the development of new strategies to generate red blood cells for transfusion in vitro from stem cells. Second, in line with our expertise and significant interest in GATA1 biology, we are studying the effects of GATA1 mutations on erythropoiesis. We are using state of the art approaches to identify essential, direct GATA1 target genes whose expression depends on the presence of the full-length wild-type protein. This research is relevant to rare red blood cell disorders such as Diamond Blackfan Anemia. Overall, the lab seeks to make seminal basic science discoveries while simultaneously translating these discoveries in ways that will benefit patients with hematologic malignancies.

Publications

View lab publications via PubMed.

For more information, visit the faculty profile page of John Crispino, PhD.

Contact Us

Contact Dr. Crispino at 312-503-1504 or the Crispino Lab at 312-503-1433.

Lab Staff

Gina Kirsammer, PhD
Research Assistant Professor
312-503-1433

Paul Lee, MD, PhD
Pediatric Hematology/Oncology Fellow
312-503-1433

Maureen McNulty
DGP Student
312-503-1433

Rachael Schultz
Research Technologist
312-503-1433

Monika Stankiewicz, PhD
Post-Doctoral Fellow
312-503-1433

Praveen Suraneni, PhD
Post-Doctoral Fellow
312-503-1433

Benjamin Thompson, MD/PhD
Post-Doctoral Fellow
312-503-0827

Qiang (Jeremy) Wen, MD/PhD
Research Assistant Professor
312-503-1434

Andrew Volk
Post-Doctoral Student
312-503-1434

Qiong Yang, MD/PhD
Visiting Scholar
312-503-1433

 Daniel Foltz Lab

Epigenetic control of centromere assembly and chromosome segregation.

Research Description

My research program is focused on the important basic question of how chromosomes are segregated during cell division to ensure the complete and accurate inheritance of the genome. Chromosome instability is a hallmark of cancer and can drive tumorigenesis. Therefore, how centromere specification is controlled is a basic biological question with great therapeutic potential. Centromeres are specified by the incorporation of a histone variant CENP-A in a centromere specific nucleosome. The stable inheritance of this locus is controlled by an epigenetic pathway and does not depend on the underlying DNA sequence. My research program is using a combination of cell biology, biochemical purification and in vitro reconstitution of centromeric chromatin to discover the mechanisms of epigenetic inheritance and CENP-A function during mitosis. A key to understanding the epigenetic inheritance of centromeres is determining the process by which new CENP-A nucleosomes are deposited. Our lab is studying how activity of the CENP-A chromatin assembly factor HJURP is coupled to existing centromeres. Non-coding RNAs, as well as chromatin modifying enzymes have been implicated in the process and we are exploring how these factors contribute to specific assembly of the CENP-A nucleosomes. We have identified novel post translational modifications of the CENP-A amino-terminus and we are working to determine how these modifications contribute to genomic stability and accurate chromosome segregation. Our immediate goal is to determine the mechanism of epigenetic centromere inheritance, with a long-term goal of delineating the role of this process in tumorigenesis so as to translate our basic understanding of the enzymes and proteins involved in this process into therapeutic approaches for genomic instability in cancer.

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

Publications

See Dr. Foltz's publications on PubMed.

Contact

Contact Dr. Foltz at 312-503-5684.

 Douglas Freymann Lab

Structural Biology, X-ray Crystallography, Macromolecular Structure/Function-GTPase mechanism, Signal Recognition Particle (SRP) targeting complex and Mitochondrial protein Miro, among others

molecules

a. Tetrameric galectin from cynachyrella sp.
b. Hydrogen bonding structure at the N/G domain interface of Ffh.
c. The Ffh/FtsY GTPase heterodimer highlighting its buried nucleotide pair.

Research Description

We determine the three-dimensional structures of proteins in order to understand the structural basis for and functional mechanisms of interactions between proteins and between proteins and small molecules that play important roles cell biology.

One focus is the GTPases of the Signal Recognition Particle (SRP), Ffh and FtsY. We currently seek to understand the structural basis for regulation of assembly of their heterodimeric targeting complex. The complex is mediated by a remarkable composite GTPase active site, but how this “GTPase core” regulates (and is regulated by) cotranslational targeting remains an important focus of research. Key publication: Focia (2004) Heterodimeric GTPase Core of the SRP Targeting Complex Science 303 p373-7

We have collaborated with the laboratory of Geoffrey Swanson (Northwestern University, Pharmacology) and Ryuichi Sakai (Hokkaido University) to determine the structure of a novel tetrameric galectin from a marine sponge. Key publication: Freymann (2012) Structure of a tetrameric galectin from Cinachyrella sp. Acta Cryst D68 p1163-74

Currently we are collaborating with Sarah Rice (Northwestern University, Cell & Molecular Biology) to understand the mitochondrial protein Miro, a key regulator of Ca-dependent mitochondrial transport. The protein comprises unusually coupled Ca-binding EF hand / GTPase-fold pairs.  We seek to determine the structural role for small molecule ligands (i.e. calcium, GTP) in the regulation of this important protein. Key publication: Klosowiak (2013) Structural coupling of the EF hand and C-terminal GTPase domains in the mitochondrial protein Miro EMBO Rep. 14 p968-74

We have also initiated a proposal to determine structures of novel members of the bloodstream trypanosome surface coat proteins (VSGs) in order to understand a previously unrecognized minimal structural motif that is widely conserved among unrelated trypanosomal surface proteins.

For more information, visit the faculty profile of Douglas Freymann, PhD.

Publications

See Dr. Freymann's publications in PubMed.

Lab Staff

Research Assistant Professor:
Pamela Focia Structural Biology Facility Manager, Robert H. Lurie Comprehensive Cancer Center

Contact Us

Dr. Freymann
Phone: 312-503-1877

 Elizabeth McNally Lab

Genetic mechanisms responsible for inherited human diseases

Research Description

My laboratory studies genetic mechanisms responsible for inherited human diseases including heart failure, cardiomyopathy, muscular dystrophy, arrhythmias, aortic aneurysms. Working with individuals and families, we are defining the genetic mutations that cause these disorders. By establishing models for these disorders, we can now begin to develop and test new therapies, including genetic correction and gene editing.


For lab information and more, see Dr. McNally's faculty profile or visit the McNally Laboratory site.

Publications

See Dr. McNally's publications on PubMed.

Contact

Email Dr. McNally

Phone  312-503-5600

 Xiaolin He Lab

Mechanisms of signal transmission across the membrane via the cell-surface receptors

Research Description

This laboratory is interested in cancer, neural development and reproduction-related structural mechanisms of how extracellular signals (e.g., growth factors, adhesion molecules and morphogens) are translated into intracellular signals by plasma membrane receptors. We use biophysical methods (crystallography, calorimetry, surface plasmon resonance, analytical ultracentrifugation, etc.) in combination with functional studies to define the physiological states and binding processes of these receptors and their complexes with ligands. Our research targets include receptor tyrosine kinases, Semaphorin and its receptors and leucine-rich-repeat-containing G-protein coupled-receptors.

For more information, visit the faculty profile of Xiaolin He, PhD.

Publications

See Dr. He's publications in PubMed.

Staff Listing

Research Associate:
Xiaoyan Chen

Graduate Student:
Po-Han Chen

Contact Us

Contact Dr. He at 312-503-8030 or the He Lab at 312-503-8029.

 James Lab

The research activities of my laboratory are directed towards elucidating the molecular and biological consequences of specific gene alterations in CNS cancer, with particular emphasis on malignant glioma, the most common type of primary CNS tumor, and towards identifying actionable/druggable molecular characteristics of these tumors.

For more information about the James Lab, please visit the James Laboratory website.

 Neil Kelleher Lab

The Kelleher Group has three primary lines of research focused on Top Down Proteomics, Natural Products Discovery and Biosynthesis and Chromatin Oncobiology and DNA-Damage.  An underlying focus, driving all lines of research, is our continued push towards optimizing instrumentation and bioinformatic approaches to best suit the unique needs of a Top Down analysis.

Research Description

The main focus for our Top Down Proteomics subgroup is to push the limits for whole proteome analysis of mammalian cells, striving for a future in which Top Down analysis rivals that of Bottom Up in the number of protein identifications per run. Recently, we have seen progress toward this very goal with the introduction of a separation platform specifically designed to minimize the most common problem in Top Down Proteomics, intact protein separations. This platform effectively reduces sample complexity and separates proteins depending on size, resulting in an opportunity for the scientist to select the optimal analysis method for the sample.

Our Natural Products subgroup is focused on the discovery and biosynthesis of novel natural products. Developments from this subgroup include the introduction of the PrISM platform, geared towards the identification of natural products synthesized by nonribosomal peptide synthetases (NRPSs) and polyketide synthases (PKSs) without prior knowledge of a gene sequence. This is made possible by our ability to detect a phosphopantetheinyl (Ppant) ejection marker ion for NRPS/PKS thiolation domains. We also work in collaboration with groups from other universities to provide mass spectrometry analysis of novel biochemical systems.

We also have a long-standing interest in histone analysis. Our Chromatin Oncobiology and DNA-Damage subgroup continues to dig deeper into the "histone code", a complex mixture of post-translational modifications that together determine a host of cellular processes. We are interested in visualizing dynamic histone PTM changes simultaneously on multiple sites. Through application of technology developed in our Top Down Proteomics subgroup, we are able to apply "Precision Proteomics" to histone analysis.


Publications

View lab publications via PubMed.

For more information, visit the Kelleher Lab Web Page or see Dr. Kelleher's faculty profile.

Contact Us

Contact the Kelleher Lab at 847-467-1086 or 847-467-4362

 Liming Li Lab

Structural properties of prion proteins using yeast as a model organism

Research Description

Prion diseases belong to a class of fatal, infectious neurodegenerative diseases known as transmissible spongiform encephalopathies (TSEs), including the bovine spongiform encephalopathies (BSE or mad cow disease) in cattle and Creutzfeldt-Jakob disease (CJD) in human. It is generally accepted that the infectious agent of prion disease is a normal host protein (PrPC) that has adopted a pathogenic conformation that is infectious (PrPSc). Remarkably, there are several atypical yeast proteins capable of existing in multiple stable conformations, each of which is associated with distinct phenotypes. Intriguingly, some of the conformations are able to self-propagate and are “infectious.” They are thus referred to as yeast prions. Our laboratory is interested in study this fascinating prion phenomenon using yeast as a model organism. Yeast offers a powerful system that is amenable to biochemical, cell biological and genetic manipulations. We want to obtain information on the structural properties of yeast prions, their mutual interactions and their interactions with other cellular factors, particularly, with molecular chaperones. We have recently discovered that the yeast heat-shock transcription factor (HSF), a master regulator of molecular chaperones’ production, plays an important role in governing the de novo formation and “strain” determination of yeast prion [PSI+]. We are working toward to identify novel cellular factors that are HSF targets and important for yeast prion formation and inheritance. The function of HSF is evolutionally conserved from yeast to human. We hope that results from our yeast prion studies will provide valuable information on the complex etiology of the devastating prion diseases.

Our laboratory is also interested in investigating how common the prion phenomenon in biology is. We wish to identify potential prion proteins from yeast and other non-yeast model organisms through a combined approach of bioinformatics and genetic screenings. Our ultimate goal is to uncover the mechanisms governing the prion conformational switch and to understand the biological significance of the protein conformation based prion-like inheritance.

For more information, visit the faculty profile of Liming Li, PhD.

Publications

See Dr. Li's publications in PubMed.

Contact

Email Dr. Li

 Elizabeth McNally Lab

Genetic mechanisms responsible for inherited human diseases

Research Description

My laboratory studies genetic mechanisms responsible for inherited human diseases including heart failure, cardiomyopathy, muscular dystrophy, arrhythmias, aortic aneurysms. Working with individuals and families, we are defining the genetic mutations that cause these disorders. By establishing models for these disorders, we can now begin to develop and test new therapies, including genetic correction and gene editing.


For lab information and more, see Dr. McNally's faculty profile or visit the McNally Laboratory site.

Publications

See Dr. McNally's publications on PubMed.

Contact

Email Dr. McNally

Phone  312-503-5600

 Marc Mendillo Lab

Cellular stress response systems in malignancies

Research Description

The cellular stress response systems guard the proteome from diverse endogenous and environmental insults to maintain the fitness of the organism. Ironically, this pro-survival system can act to the detriment of the host to enable tumor cells accommodate to the myriad stresses associated with malignancy. Our long-term goals are to identify and characterize the systems that promote protein homeostasis, understand how these systems are co-opted and perturbed in malignancy, and ultimately identify means to manipulate them for therapeutic benefit. To accomplish these goals our group bridges biochemical, genetic and chemical biology approaches with systematic high-throughput and genomic methods.

For lab information, publications and more, see Dr. Mendillo’s faculty profile.

Publications

View Dr. Mendillo's publications at PubMed

Contact

Email Dr. Mendillo

Phone 312-503-6061

 Panagiotis Ntziachristos Lab

Studying Molecular Mechanisms of Oncogenesis In Acute Leukemia

Research Description

This is an exciting time for cancer biology especially with the advent of epigenetics and chromatin biology. New molecules with tumor suppressive or oncogenic roles are currently identified and characterized paving the way for new therapeutic ways but at the same time, posing new challenges for researchers. This area of cancer epigenetics is my personal and laboratory's focus. To study this perplexing biology we use patient samples and disease-relevant mouse models.

The Ntziachristos laboratory studies the mechanistic aspects of oncogenesis with an emphasis on transcriptional and epigenetic regulation of acute leukemia. Important questions are related to how oncogenes interact with each other and with epigenetic modulators to influence gene expression programs as well as how their function is related to tri- dimensional (3D) structure of the nucleus and other biological aspects of cancer cells, like metabolism. To address these questions we use high-throughput molecular and cell biology techniques like ChIP-Seq, RNA-Seq, 4C-Seq and HiC, fluorescent in situ hybridization, biochemical analysis e.t.c. in cell lines and primary cells of human origin and tissues of mouse models of disease. In addition to understanding cancer biology these finding help us design and test targeted therapies in preclinical models of leukemia.

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

Publications

See Dr. Ntziachristos's publications at PubMed.

Contact

Contact Dr. Ntziachristos at 312-503-5225 or Searle 6-523

 Marcus Peter Lab

The lab of Dr. Marcus E. Peter studies various forms of cell death including apoptosis, which is a fundamental process to regulate homeostasis of all tissues and to eliminate unwanted cells specifically in the immune system.

Apoptosis is a fundamental process to regulate homeostasis of all tissues and to eliminate unwanted cells specifically in the immune system. Various parts of apoptosis signaling pathways have been characterized. Specifically in apoptosis pathways initiated by members of the death receptor family such as CD95 (APO-1/Fas) proteins that either contain a death domain (DD) or a death effector domain (DED) have been found to be essential. In addition, it has become clear in recent years that death receptors such as CD95 and all of its signaling components have nonapoptotic activities that in the context of cancer can cause tumor promotion and progression. The group of Marcus Peter studies the activities of death receptors and their signaling components in apoptosis and the relevance of their nonapoptotic activities in cancer development. In addition, the Peter lab is interested in the role of microRNAs in various aspects of carcinogenesis.

Publications

View lab publications via PubMed.

For more information, visit the faculty profile page of Marcus Peter, PhD or the laboratory's website.

Contact Us

Contact Dr. Peter at 312-503-1291 or the Peter Lab at 312-503-2883.

Lab Staff

Paolo Ceppi
Postdoctoral Fellow
312-503-2883

Andrea Murmann
Research Assistant Professor
312-503-2883

Monal Patel
Postdoctoral Fellow
312-503-2883

Will Putzbach
Graduate Student
312-503-2883

Nandini Rayindran
Research Technician
312-503-2883

Xiang (Kevin) Rui
Graduate Student
312-503-2883

Qadir Syed
Postdoctoral Fellow
312-503-2883

 Leonidas C. Platanias Lab

Dr. Platanias’ research laboratory focuses on understanding the signaling pathways in different types of cancers in order to develop novel therapies to specifically kill cancer cells.

Cell signaling is part of an intricate system of events activated by various stimuli that coordinate cell responses. Our laboratory is interested in unveiling pathways involved in cancer development in order to target them and control cancer progression. For over two decades, Dr. Platanias’ laboratory has identified several cellular cascades activated by IFN, ATRA and arsenic. Our research on Type I IFN found an essential role for SKAR protein in the regulation of mRNA translation of IFN-sensitive genes and induction of IFN-α biological responses. We also provided evidence for unique function of mTORC2 complex in inducing Type I IFN response. Our studies on arsenic signaling revealed a direct binding of this compound to a kinase called AMPK as a mechanism underlying its anti-leukemic activity. Other work included the activation of biological responses by BCR-ABL oncoprotein through the mTOR pathway. Dr. Platanias’ laboratory is also involved in testing new compounds in combination with approved therapies in order to identify synergy and improve the risk/benefit ratios of current therapeutic regimens for patients.

Publications

View lab publications via PubMed.

For more information, visit the faculty profile page of Leonidas Platanias, MD, PhD.

Contact Us

Contact Dr. Platanias at 312-908-5250 or the Platanias Lab at 312-503-4500.

Lab Staff

Dirim Arlsan, PhD
Post-Doctoral Fellow
312-503-4500

Elspeth Beauchamp, PhD
Post Doctoral
312-503-4500

Jonathan Bell
Graduate Student
312-503-0292

Gavin Timothy Blyth
Lab Technician
312-503-4500

Dany Curi
Post Doctoral Fellow
312-503-0292

Frank Eckerdt
Research Assistant Professor
312-503-0292

Asneha Iqbal
Post Doctoral Fellow
312-503-0292

Ewa Kosciuczuk
Post Doctoral Fellow
312-503-4500

Barbara Kroczynska
Research Assistant Professor
312-503-4500

Swarna Mehrotra
Research Associate
312-503-4500

Diana Saleiro
Post Doctoral Fellow
312-503-4500

Antonella Sassano
Research Assistant Professor
312-503-4500

 Ali Shilatifard Lab

Molecular machinery for histone modifications in yeast, Drosophila and human cells

Research Description

Chromosomal rearrangements resulting in alterations of gene expression are a major cause of hematological malignancies. Our goal is to advance the understanding of the biochemical and molecular mechanisms of rearrangement-based leukemia and to provide insights into how translocations affect cellular division by altering gene expression. Using mammalian model systems such as tissue culture and mouse genetics, we plan to explore the regulation of gene expression via the MLL gene and its translocation partners found in human leukemia. We are currently defining the molecular composition of the MLL complexes and how translocations alter its biochemical function and integrity, resulting in leukemic pathogenesis. We are also planning to define the mechanism of the targeting of the MLL complex and its histone methyltransferase activity to chromatin to determine its normal cellular functions and its mistargeting and disregulation in leukemogenesis.

One fusion partner of MLL in acute myelogenous leukemia (AML) is the ELL protein. We show that human ELL functions as a transcription elongation factor. We have identified the Drosophila homolog of ELL and demonstrate it to be essential for development.  Drosophila ELL associates with elongating RNA polymerase II in vivo on chromosomes and is a regulator of the Notch signaling pathway.  This has suggested to us that human ELL might also participate in the same process.

For lab information and more, see Dr. Shilatifard's faculty profile or visit the Shilatifard Laboratory site.

Publications

View Dr. Shilatifard's publications on PubMed.

Contact

Email Dr. Shilatifard

Phone 312-503-6061

 Xiao-Qu Wang Lab

Investigates novel biomarkers for metastatic melanomas and related mechanisms.

Research Description

The Wang research team is focused on the discovery of novel biomarkers for melanoma metastasis along with the study of how these novel biomarkers regulate metastasis in melanomas. 

 Wang’s research has provided evidence of ganglioside alteration in skin cancers. Dr. Wang and her research team have shown that manipulating ganglioside content profoundly affects cell function through binding directly to glycosylated receptors, such the epidermal growth factor receptor (EGFR), integrin a5β1 and urokinase-like plasminogen activator receptor (uPAR).

Gangliosides are glycosphingolipids that regulate tumor metastasis and growth at the plasma membrane. The Wang research team has recently discovered that deacetylate GM3 (d-GM3) is exclusively expressed in metastatic melanomas, but not in primary melanomas and benign nevi, suggesting that d-GM3 is a novel biomarker for melanoma metastasis. GM3 is the simplest ganglioside. Native classic GM3 (c-GM3) is the predominant ganglioside in most normal human cells, while its’ variant, d-GM3 has not been found in normal human cells. In addition, d-GM3 is immunologically distinguishable from c-GM3, which enables us to specific target d-GM3 and minimizes potential toxicity to normal cells.

Dr. Wang’s team also found that d-GM3 expression increases melanoma proliferation, migration and survival and has linked GM3 deacetylation 

Publications

For publication information and more, see Xiao-Qu Wang’s, MD/PhD, faculty profile.

Contact Wang Lab

Contact the Wang Lab at 312-503-0294 or visit us on campus in the Montgomery Ward Building, 303 E. Chicago Avenue, Ward 9-070, Chicago, Illinois, 60611(housed in the Paller Lab).

 Jindan Yu Lab

The Yu laboratory focuses on understanding the genetic and epigenetic pathways to prostate cancer.

The Yu lab focuses on cancer genomics and translational cancer research.  At the current stage, our primary research interest is to understand aberrant transcriptional and epigenetic regulation of prostate cancer and to translate such knowledge into clinical applications.  We utilize high-throughput genomic techniques in combination with bioinformatics/statistical analysis to generate testable hypothesis.   We then test these hypotheses using traditional molecular and/or cellular biological approaches and examine the functional relevance of these innovative regulatory pathways in vitro and in vivo using cell lines and mouse models.  Based on the genetic and epigenetic underpinning of the disease, we pursue translational research to develop new biomarkers and novel therapeutics strategies for advanced prostate cancer.

Publications

View lab publications via PubMed.

For more information, visit the faculty profile page of Jindan Yu, MD/PhD or visit the Yu Laboratory website.

Contact Us

Contact Dr. Yu at 312-503-2980 or the Yu Lab at 312-503-3041.

Lab Staff

Will Ka-Wing Fong
Postdoctoral Fellow
312-503-3041

Jung Kim
Graduate Student
312-503-3041

Shangze Li
Postdoctoral Fellow
312-503-3041

Bing Song
Postdoctoral Fellow
312-503-3041

Yeqing (Angela) Yang
Graduate Student
312-503-3041

Ali Zhang
Postdoctoral Fellow
312-503-3041

Changsheng (Jonathan) Zhang
Bioinformatician
312-503-3041

 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.

Publications

View publications by Ming Zhang in PubMed

Contact

Dr. Zhang

Phone 312-503-0449

 Lihua Zou Lab

Deciphering the cause and functional consequence of somatic mutations in cancer

Research Description

The overarching goal of my research lab is to utilize orthogonal genomic data to discover novel cancer drivers and understand their function and underlying mechanism. We are particularly interested in combining computation and experimental approaches (especially high-throughput sequencing) to understand the regulation and functional consequence of somatic mutations in cancer.

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

Contact

Contact Dr. Zou at 312-503-5643.

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