The Committee on Cancer Biology has over 100 affiliated faculty that you can choose to work with. Here, we highlight the faculty who are currently mentoring CCB students. See full list of faculty here!


Lev Becker, PhD

Macrophage dysfunction is a hallmark of chronic sterile inflammatory diseases including cancer, atherosclerosis, and obesity/type 2 diabetes. Because macrophages are highly influenced by their environment, it is essential to understand how disease-specific changes to tissues trigger specific pathways in macrophages to drive pathogenesis. Moreover, the relationship between disease-producing macrophage pathways to those required for pathogen clearance is largely unknown, which is important because attempts to therapeutically target macrophages must preserve their host defense function. Comparing and contrasting macrophages across a spectrum of diseases is therefore required to elucidate disease-specific mechanisms, and to develop therapeutics that are both efficacious and safe.


Our long-term goal is to develop a robust research program that uses a multi-disease approach to develop a comprehensive understanding of macrophage biology, and translate this mechanistic understanding to develop therapeutics across a spectrum of human disease. To this end, we are developing a new biologic for the treatment of many cancers, a small molecule that restores anti-cancer immunity, and small molecules that attenuate the deleterious inflammation during metabolic diseases while preserving the inflammation required for host defense.


Shannon Elf, PhD

Although the genes that drive the development of myeloid blood cancers have largely been defined, there are currently few effective targeted treatment strategies for these diseases. The development of imatinib to treat BCR/ABL-­positive chronic myeloid leukemia remains the only true success story, with the majority of targeted therapies for myeloid malignancies demonstrating unimpressive clinical activity. This illuminates the need to exploit the molecular understanding that has been gained in the last decade through cancer exome sequencing to identify novel therapeutic vulnerabilities in myeloid malignancies. 


Research in the Elf Lab focuses on identifying unique molecular dependencies in myeloid blood cancers that can be targeted for therapeutic intervention, with the long­-term goal of improving upon current treatment regimens for these diseases. Currently, our work focuses on understanding the role of the unfolded protein response (UPR) in myeloproliferative neoplasms (MPN) and acute myeloid leukemia (AML). Using molecular, biochemical, and cellular approaches in both in vitro and in vivo models, we aim to dissect the molecular mechanisms underlying UPR activation in specific subsets of MPN and AML, and to use this mechanistic insight to develop rationally designed therapies to target the UPR in these challenging diseases.


Thomas Gajewski, MD, PhD

The Gajewski laboratory has long explored fundamental aspects of anti-tumor immunity, with an emphasis on translating laboratory discoveries into clinical applications. While working on melanoma vaccine strategies, my lab uncovered a role for downstream resistance pathways employed by tumor cells to evade immune responses. Gene expression profiling and immunohistochemistry have identified key elements of the T cell-inflamed and non-T cell-inflamed tumor microenvironment phenotypes. T cell-inflamed tumors contain tumor antigen-specific T cells but also negative regulatory pathways that we have advanced as drug targets. We have focused on the development of STING pathway agonists to promote T cell priming and infiltration into non-T cell-inflamed tumors, an event that could make tumors more susceptible to immunotherapy. One of our candidate drugs is now in phase I clinical testing. Genomic characterization of non-T cell-inflamed tumors in my lab has also revealed oncogene pathways that mediate T cell exclusion, the first of which is the Wnt/β-catenin pathway. Recent work has also identified germline polymorphisms and evidence for commensal microbiota that regulate anti-tumor immunity, suggesting additional approaches to improving immunotherapy outcomes.


Lucy Godley, MD, PhD

Dr. Lucy Godley is an expert in the care and treatment of patients with diseases of the bone marrow, including leukemias, lymphomas, and multiple myeloma. She also cares for patients undergoing stem cell transplantation and patients with benign hematologic conditions.


Dr. Godley has a special interest in the molecular basis of bone marrow malignancies and is an active researcher in the field. In her laboratory, Dr. Godley studies the basis for cancer cells’ abnormal patterns of DNA methylation, as well as inherited forms of bone marrow cancers.

Dr. Godley’s goal is to improve health through a deeper understanding and appreciation of science by integrating knowledge about fundamental networks within cancer cells and by bringing novel insights into the pathophysiology of her patients’ diseases while offering them new treatment options.


Geoffrey Greene, PhD

The overall objective of my research is to determine the molecular distinctions between estrogen/androgen/progestin/glucocorticoid agonism and antagonism in hormone dependent tissues and cancers and to use this information to identify, develop and characterize novel compounds that can be used as breast and prostate cancer chemopreventatives and chemotherapeutics. My lab has considerable experience and expertise with the identification and characterization of compounds (SERMs, SARMs, SPRMs, GRMs) that selectively target the two estrogen receptors, ERα and ERβ, as well as the androgen receptor (AR), the progesterone receptor (PR) nd the glucocorticoid receptor (GR). One of our major goals is to test and develop known and novel SERMs for their ability to selectively alter ER recruitment of co-regulator subsets that reflect differential responses to these ligands.  We are also actively characterizing ERα somatic mutations that have been observed in up to 40% of endocrine therapy resistant metastatic breast cancers, with the goal of targeting these mutant ERs with next generation SERMs/SERDs. An additional area of investigation is the previously unrecognized and extensive cross talk between estrogen and progestin signaling in ER+/PR+ breast cancers and how to selectively target both receptors in patients with these cancers. We are also exploring the role of GR/ER cross talk in breast cancers that express both receptors to better understand and exploit this combination as a potential therapeutic target. For many of these studies, we are creating and studying patient derived xenograft (PDX) mouse models that can serve as avatars for ER+/PR+/GR+ breast cancers. Our most recent PDX model is the mammary intraductal (MIND) model, which better reflects the environment in human DCIS and infiltrating ductal breast cancers. Derived organoid cultures are also being established for mechanistic and drug testing studies. Currently, two chemically distinct SERMs are being investigated in preclinical MIND models as potential therapeutics in endocrine therapy resistant ER+ metastatic breast cancers that express mutant ERs. One of these SERMs, lasofoxifene, is actively being tested in a phase 2 clinical trial involving patients with ERa+ metastatic breast cancers that have failed first line endocrine therapy. More such preclinical and clinical studies are planned.


Justin Kline, MD

Dr. Kline is a medical oncologist who specializes in the treatment of patients with Hodgkin and non-Hodgkin lymphoma, including stem cell transplantation and CAR T cell therapy. He has expertise in the development and use of immunotherapy, and his lab research is focused on overcoming immune evasion pathways activated in blood cancers and on improving the effectiveness of immune-based treatments for people with lymphoma.


Stephen Kron, PhD

The Kron laboratory is a diverse and collaborative group of cell biologists, geneticists, biochemists, chemists and computer scientists. Our current basic research and technology efforts include 1) defining roles for chromatin dynamics and cell cycle regulation in DNA damage checkpoint response and cellular senescence, 2) dissecting cross-talk between metabolism and DNA damage response, 3) developing novel molecular assays to interrogate cell signaling in cancer, and 4) implementing novel mass spectrometry approaches to enable quantitative proteomics. We also pursue translational projects directed at 1) discovering inhibitors of cellular response to DNA double strand breaks as an approach to radiosensitization, 2) examining DNA damage and repair in tissues and tumors, and 3) exploiting DNA damage responses to induce anti-tumor immune responses.


James LaBelle, MD, PhD

The major goal of the laboratory is to dissect and pharmacologically target intracellular proteins to induce cancer cell death and manipulate the immune response.  We are currently applying new research tools and prototype therapeutics that we, and others, have developed to target the BCL-2 family of proteins and other cell signaling proteins in immune cells.


A large part of our lab focuses on using portions of the actual proteins, or peptides, as drugs and biological tools to uncover specific molecular pathways in diseased and normal cells. Peptide-based therapeutics have enormous potential for immune modulation and direct cancer treatment but have traditionally lacked efficient stabilization and delivery within patients, and thereby, have had limited clinical applications. We are working to overcome these barriers within the lab and through collaboration with nanotechnologists and chemical engineers.


Overall, we are committed to translation of our findings to pediatric and adult patients with cancer and immune system disease. While performing research at the University of Chicago, we are in close proximity to scientists, clinicians, and patients and are deeply committed to working collaboratively with these groups to make significant inroads in treating those suffering from refractory disease.


Kay Macleod, PhD

The deadliest aspect of the majority of human cancers is metastasis, the multi-step process by which cancer cells escape the confines of the primary site (such as breast, pancreas or other organs) and travel in the circulation to distant sites (such as brain, liver or lungs) where they can lodge, invade and grow out as secondary tumors or metastases.


Many factors play into cancer metastasis including how disseminating tumor cells respond to stresses such as nutrient deprivation and altered cellular attachments. These stresses are known to activate a process known as autophagy and research in the Macleod Lab seeks to understand and clarify the role of autophagy in tumor growth and progression to metastasis. In particular, we are interested in understanding how defects in the turnover of mitochondria (the energy factory of the cell) by autophagy, leads to tumor invasion and metastasis.


Using a variety of approaches from biochemical, molecular, cellular as well as genetic models to in vivo imaging and primary human patient sample analysis, research on the role of autophagy in cancer metastasis in the Macleod Lab is focused on breast cancer, pancreatic cancer and liver cancer. By examining and comparing similarities and differences between how metastasis develops from each of these organ sites, we can appreciate what new molecular targets may be most relevant to understanding and ultimately treating these deadly diseases.


Alex Muir, PhD

The Muir lab is interested in understanding the metabolic adaptations that allow cancer cells to grow and proliferate, causing tumor growth. To understand how cancer cell metabolism works to fuel tumor growth, we use metabolomics techniques to catalog what nutrients are in the microenvironment of tumors. This provides us with a "menu" of nutrients that cancer cells could potentially metabolize to fuel their growth. Once we know the "menu" for different tumor types, we then use a variety of experimental tools from metabolomics to CRISPR gene editing to determine which nutrients cancer cells actually consume from the "menu", and which metabolic pathways process these nutrients. From these experiments, we are delineating the biochemical underpinnings of cancer cell growth.


Megan McNerney, MD, PhD

Our overarching goal is to improve the outcome for patients with myeloid neoplasms, particularly the high-risk subset unresponsive to current treatment protocols.  In the last decade, the somatic mutations in myeloid malignancies have been well characterized.  Many of these genetic changes impact tumor suppressor genes encoding transcription factors and epigenetic regulators.  This presents a challenge for the field, as restoring the normal level or activity of an inactivated tumor suppressor gene has remained therapeutically elusive.  Our lab is taking several different approaches to circumvent this problem in the context of -7/del(7q), a cytogenetic change present in half of high-risk myeloid neoplasms.  CUX1 is a non-clustered homeobox transcription factor encoded on 7q and is recurrently mutated in hematopoietic and solid tumors.  We reported that loss of CUX1 is sufficient to cause myeloid malignancies in mice.  We are taking several approaches to identify druggable partners or pathways to target CUX1-deficient malignancies.  In addition, we are identifying other tumor suppressor genes on 7q to understanding the molecular pathogenesis of 7q deletions and reveal new therapeutic vulnerabilities of chemoresistant disease.


In parallel, accomplishing this work will yield insight into several outstanding questions in developmental biology, cancer biology, and gene regulation.  Our research program is investigating: i) transcriptional mis-regulation in cancer, and how transcription factor haploinsufficiency is interpreted at the cis-regulatory level; ii) the role of transcription factors in genome architecture and differentiation; iii) the probabilistic nature of stem cell fate determination; iv) chromatin remodeling in DNA repair; v) the contribution of en bloc genic haploinsufficiency due to large segmental deletions, ie. “contiguous gene syndromes” in cancer; and vi) how genetics and environmental exposures interact to promote cancer, with the goal of ultimately preventing this disease.


Raymond Moellering, PhD

The Moellering Lab is a multi-disciplinary group of scientists with training in chemistry, biochemistry, cell biology and mass spectrometry. We are uniquely situated in both the Department of Chemistry and the Institute for Genomics and Systems Biology at the University of Chicago – thus figuratively and physically bridging the physical and biological sciences. 


Research in the Moellering Lab lies at the interface of chemistry and biology, with an eye towards understanding and intervening in human disease. By integrating chemical synthesis, cell biology and mass spectrometry platforms, our research aims to identify novel biological mechanisms underlying diseases such as diabetes and cancer, and to subsequently develop innovative diagnostic and therapeutic modalities to impact these disorders. We are specifically interested in developing new chemical tools and technologies to study complexity and dynamics in the proteome, thus enabling targeted manipulation of protein targets and the pathways they govern.


Scott Oakes, MD

The Oakes laboratory studies how mammalian cells commit “suicide” in response to various forms of damage and what goes wrong with this process in cancer and other diseases. In particular, they focus on a type of stress that occurs when the cell’s protein folding factory—an organelle called the endoplasmic reticulum—is overwhelmed and protein quality control fails. He is actively engaged in developing drugs to control cell fate under these conditions, which have potential to benefit patients with diseases from cancer to neurodegeneration.


Marsha Rosner, PhD

At the Rosner Lab, we are working on transformative therapy on patients with metastatic tumors for whom treatment is lacking.

The current focus of my laboratory is to understand fundamental signaling mechanisms leading to the generation of tumor cells and their progression to metastatic disease, particularly in triple-negative breast cancer that lacks targeted therapies. We use systems level approaches including activity-based proteomics, RNAseq, ChIPseq, and mass spectrometry as well as computational, molecular, biophysical, cellular and mouse model-based methodologies to identify and characterize key regulators of tumor growth and metastasis. As an additional tool, we have utilized a specific physiological suppressor of metastasis, Raf Kinase Inhibitory Protein (RKIP or PEBP1), and a downstream target of RKIP in cells, BACH1, to identify both molecular and cellular mediators of metastasis.


Our recent studies have shown that regulators of metastasis control multiple processes within the tumor cell microenvironment including metabolism, redox state, extracellular matrix, and recruitment and programming of tumor-associated macrophages. These factors also direct extracellular vesicles (exosomes) secreted by tumor cells to reprogram other cells in the body toward a pro-metastatic phenotype.  Correlating omic-generated data from these studies with clinical data from cancer patients led to the identification of novel signaling modules that we used to build gene signatures that predict the metastatic potential of a tumor. More recently, our studies have led us to potential therapeutic treatments based on the concept of targeting key regulators of tumorigenesis, mimicking the action of metastasis suppressors such as RKIP or reprogramming signaling networks in cells to sensitize tumors to therapeutic agents.


Russell Szmulewitz, PhD

Dr. Szmulewitz is a physician scientist whose primary academic focus is on characterizing and controlling the process of metastatic progression in men with prostate cancer. He has a laboratory working with proteins called “metastasis suppressors” to slow down the growth of disseminated tumors in models of metastatic prostate cancer. In addition, Dr. Szmulewitz’s translational laboratory is using novel techniques to isolate and characterize prostate cancer cells from the blood of men with advanced prostate cancer. It is his goal to use these techniques to better personalize targeted therapies for metastatic prostate cancer.


Yingming Zhao, PhD

The Zhao lab’s main research interests lie in developing and applying mass spectrometry-based proteomics technologies to discovery of previously undescribed cellular pathways with current focus on metabolites-mediated epigenetic pathways. He uses an integrated approach, involving proteomics, biochemistry, molecular biology, and cell biology to decode protein post-translational modification (PTM) networks that have implications for human health and are not amenable to conventional techniques.


Our lab carried out first few proteomic studies of lysine acetylation that led to identifying thousands of acetyllysine substrate peptides. These landmark works challenge a long-standing notion that lysine acetylation is restricted to nuclei and catalyze extensive investigation of non-nuclear functions of this modification pathway.  Our lab recently discovered 10 types of new lysine acylation pathways: propionylation, butyrylation, crotonylation, malonylation, succinylation, glutarylation, 2-hydroxyisobutyrylation, 3-hydroxybutyrylation, benzoylation and lactylation. We identified about 600 new histone marks, which more than doubles the tally of the previous known histone marks discovered during the first forty years of chromatin biology. We revealed numerous enzymes for the new PTM pathways (acyltransfersases and deacylases, such as SIRT5 as a desuccinylase, demalonylase, and deglutarylase), as well as specific binding proteins (or “readers’) for the novel histone marks. His laboratory demonstrates that the new PTM pathways have critical roles in epigenetic regulation and cellular metabolism, and contribute to multiple inborn metabolic diseases.


Xiaoyang Wu, PhD

Given their pivotal role in tissue homeostasis and regenerative medicine, somatic/adult stem cells are of tremendous interest to both biomedical research field and the public. Skin and its appendages provide a protective barrier that keeps harmful microbes out and essential body fluids in. To perform these functions while confronting the physicochemical traumas from the outside world, human skin must undergo rejuvenation through homeostasis and wound repair. Both processes rely on the essential activities of skin somatic stem cells, including the activation and migration of epidermal stem cells upon wounding, as well as the delicate balance of epidermal stem cell proliferation, self-renewal and differentiation during tissue homeostasis. Understanding the underlying mechanisms is important, because dysregulation of these processes leads to many skin diseases including cancers. Research in my laboratory is dedicated to understanding the dynamics, signaling, and clinical applications of epidermal stem cells. Particularly, we are interested in three fundamental questions in this field: 1) regenerative medicine and tissue engineering with epidermal stem cells; 2) migration and cytoskeletal dynamics of epidermal stem/progenitor cells; and 3) molecular mechanisms controlling stemness and differentiation of epidermal stem cells.


Lixing Yang, PhD

With continuing advances in high-throughput sequencing technologies, the amount of genomic and epigenetic data is increasing exponentially, giving us a great opportunity to boost our understanding of complex biological systems.


Genomic rearrangements, also known as structural variations (SVs), are large scale alterations that changes the DNA structure. They include deletions, duplications, insertions, and other forms that are accompanied by copy number changes as well as inversions, translocations, and other copy-neutral forms. They are an important type of variation, affecting an order of magnitude more base pairs than single nucleotide variations (SNVs) in normal human population. In cancer, several chromosomal translocations have been identified and subsequently became targets of successful treatments. However, the functional impact of genomic rearrangements and their roles in treatment response are largely unexplored. We are developing new computational methods and exploring large scale cancer omics data to infer the mutational mechanisms leading to these alterations, to identify potential disease-driving events, and to study how they affect treatments.