Research into the physiologic functioning and diseases of the reproductive system. Many of these investigators are part of Northwestern's Center for Reproductive Sciences.
Labs in This Area
Studying the mechanisms of prostate cancer initiation, progression and recurrence and strategies to therapeutically target these processes
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.
See Dr. Abdulkadir's publications in PubMed.
Meejeon Roh, Research Assistant Professor
Yvonne Feeney, Lab Manager
Younga Yoo, Postdoc
Tanushri Sengupta, Research Associate
Kenji Unno, Research Associate
Rose Njoroge, Graduate Student
Rajita Vatapalli, Graduate Student
Lab Telephone: 312-503-5031
Transcriptional regulators of inflammation and metabolism
The burgeoning epidemic of obesity and type 2 diabetes mellitus presents a major health and therapeutic challenge. Transcriptional regulation is the fundamental control mechanism for metabolism, but a gap remains in our knowledge of gene regulatory pathways that control lipid and glucose homeostasis. Thus, we seek to identify modulable pathways that may be leveraged to counteract diabetes mellitus and its comorbidities, particularly cardiovascular disease. In this effort, we use a variety of genetic, molecular, next-generation sequencing, biochemical methods and physiological models. Our recent work has helped to reveal the genomic architecture for transcriptional regulation in innate immunity, which plays a key role in both diabetes mellitus and atherosclerosis. Surprisingly, although macrophage regulatory elements are often at significant linear distance from their associated genes, we identified interplay between transcriptional activators and repressors that is highly proximate, occurring at shared nucleosomal domains (Genes & Development, 2010). Moreover, we discovered a powerful role for the BCL6 transcriptional repressor to maintain macrophage quiescence and prevent atherosclerosis (Cell Metabolism, 2012).
Currently, we are exploring the impact of activator–repressor interactions on enhancer function and transcription, the signal-dependent control of repression and the functional impact of transcriptional activators and repressors on inflammatory and metabolic disease. In particular, we strive to further understand the role for B cell lymphoma 6 (BCL6), a C2H2-type zinc finger repressor, in innate immunity and metabolism.
In related work, we are developing new methods for cell-specific isolation of RNA and chromatin from tissues composed of mixed cell populations. These genetic tools will allow us to explore transcriptional regulation in living animals with unprecedented precision and global scope using transcriptome sequencing and ChIP-sequencing. We anticipate that these approaches will identify new candidate regulators and mechanisms underlying cardiovascular and metabolic disease.
For more information, please see Dr. Barish's faculty profile.
See Dr. Barish's publications in PubMed.
Estrogen metabolism in breast cancer, endometriosis and uterine fibroids.
The laboratory research of Serdar E. Bulun, MD, focuses on studying estrogen biosynthesis and metabolism, in particular aromatase expression, in hormone-dependent human diseases such as breast cancer, endometriosis and uterine fibroids.
A team of investigators works on understanding the epithelial-stromal interactions and aromatase overexpression in breast cancer tissue. Because aromatase inhibitors treat breast tumors primarily via suppressing intratumoral estrogen biosynthesis, these efforts are important for discovering new targets of treatment.
Another team studies endometriosis. Basic data from this laboratory led to the introduction of aromatase inhibitors into endometriosis treatment. Human tissues and a primate model are used to elucidate cellular and molecular mechanisms responsible for the development of endometriosis.
Regulation of aromatase expression is also studied in uterine fibroids, benign tumors that are dependent on estrogen for growth, by a third team.
A fourth team is investigating the link between progesterone action and estrogen inactivation in normal endometrium and endometriosis.
Lastly, a fifth team has identified novel mutations that cause familial excessive estrogen formation syndrome. This syndrome is characterized by short stature, gynecomastia and hypogonadism in males and early breast development and irregular menses in females. In this syndrome, heterozygous inversions in chromosome 15q21, which cause the coding region of the aromatase gene to lie adjacent to constitutively active cryptic promoters that normally transcribe other genes, result in estrogen excess owing to the overexpression of aromatase in many tissues.
For more information, please see Dr. Bulun's faculty profile.
See Dr. Bulun's publications in PubMed.
Transcriptional and Epigenetic Regulatory Mechanisms in Nuclear Hormone Signaling and Cancer Cell Function
The Chakravarti laboratory is interested in understanding the roles of nuclear hormone signaling and epigenetic modifications in regulating normal cell and organ physiology and how altered transcriptional and epigenetic signaling contributes to cancer development and metastasis. To pursue these overall goals, we are currently focusing on three research areas which are of significant current interests in biomedical field.
Research Area 1: Transcriptional Regulation of Tumor Development: Cancer is a complex disease and remains poorly understood. In particular, how altered transcriptional and epigenetic regulation contributes to cancer development and progression is not clear. We have recently discovered and characterized a new family of proteins termed the THAP family. Using xenograft mouse model, next generation mRNA and ChIP deep sequencing, extensive analysis of human progressive cancer tissue samples and state-of-the-art molecular techniques, members of the laboratory are determining the role of this novel THAP domain transcription factor and its cofactor HCF1 in cell cycle regulation and cancer progression. These studies should advance our knowledge of cancer progression and may provide a molecular target for therapeutic intervention.
Research Area 2: Nuclear Hormone Receptor Signaling in Physiology and Uterine Fibrosis: Alterations of receptor/hormone function and coactivator and corepressor proteins have been implicated in several human diseases including cancer and fibrotic diseases. We are currently determining the role of epigenetic changes and novel cofactors in hormone signaling and prostate and breast cancer. Tissue fibrosis is a major health problem in the world. We have profiled all 48 human nuclear receptors in uterine fibroids and found profound changes of receptor expression in normal and fibroid uterine tissues. Laboratory members are currently using biochemical, bioinformatics, ChIP, deep sequencing and molecular techniques to determine epigenetic cross talk in hormone signaling and human cancer and uterine fibroids.
Research Area 3: Epigenetic Modifications and Effectors of Chromatin Function: Combinatorial histone modifications including acetylation, methylation and phosphorylation play important regulatory roles in gene expression, chromatin function and cell cycle progression. We have recently demonstrated that the SR-proteins are critical cell cycle-dependent effector proteins for histone H3 serine 10 phosphorylation. We are also determining the role of histone H3 T11 phosphorylation and its effector protein WDR5 in androgen receptor function and in prostate cancer. Members in the laboratory are currently investigating the mechanisms by which these “effector-modification” interactions contribute to cell cycle progression and human diseases including cancer.
For more information, please see, visit the Dr. Chakravarti's faculty profile.
See Dr. Chakravarti's publications in PubMed.
Editorial Board: Molecular Endocrinology 2011- present, Mol. Cell. Biol. 2014-2017
The Editor of a Book volume on “Regulatory Mechanisms in Transcriptional Signaling” in Progress in Molecular Biology and Translational Science (Vol 87), published in Aug 2009, Academic Press, Chakravarti, D. Editor
Contact Chakravarti lab at 312-503-0782, 312-503-0783 or 312-503-0784. Our fax is 312-503-0095.
Mammalian ovarian and gamete biology and reproductive aging
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
Studying the posttranscriptional regulation of intronless viral messages
We study the posttranscriptional regulation of intronless viral messages. Intronless messages must be efficiently processed in the absence of splicing. Therefore, intronless messages must uncouple RNA processing and export from the splicing process making a simpler model system. We are currently focused on the posttranscriptional regulatory element (PRE) of the Hepadnaviruses, including hepatitis B virus (HBV) and woodchuck hepatitis virus (WPRE). Our goal is to understand the novel mechanism of the stimulation of heterologous gene expression by the WPRE. Understanding WPRE function will allow the development of even more efficient gene expression for a variety of applications from gene therapy to large scale protein production.
Although much is known about the molecular biology of HIV, little is known about the details of interactions between the virus and cellular components such as the cytoskeleton. To gain insights into these processes we are combining the disciplines of virology and cell biology to develop the field of cellular virology. We are especially excited by new methods we have developed – such as time-lapse analysis and fluorescent tagging – that allow for HIV to be visualized in living cells.
See Dr. Hope's publications on PubMed.
Contact Dr. Hope at 312-503-1360.
The role of progesterone receptor in uterine diseases
Progesterone is essential for the regulation of normal female reproductive function. Its mode of action is diverse and dependent on the target tissues. In my lab we are interested in delineating the molecular mechanisms of progesterone action through its receptor, PR in the uterus. This is done in the context of normal endometrial differentiation, specifically, decidualization, as well as in uterine pathologies, such as endometriosis, endometrial cancer and uterine fibroids. Interestingly, in these three diseases, progesterone responsiveness is aberrant.
Endometrial cancer is the most common gynecologic cancer diagnosed in the United States with an estimated 40,100 new cases and about 7,500 deaths in 2008. As risk factors for endometrial cancer increase, the incidence of this disease will also rise, with a paradigm shift to younger ages. In our laboratory, we investigate the role of progesterone receptor in endometrial cancer to understand why progestin therapy is not an effective treatment in all cases of endometrial cancer.
Endometriosis is an estrogen-dependent disorder affecting up to 10% of the female population and 30-50% of infertile women, with no cure and limited therapies. It is often associated with debilitating pelvic pain and infertility. This disease has also been referred to as a “progesterone resistant” disease since the ectopic and eutopic tissues do not respond to progesterone as it does in normal endometrial tissues. Our laboratory is investigating progesterone resistance in endometriosis and identifying specific biological targets for the future development of alternative therapies.
Leiomyoma, also known as uterine fibroids, are benign tumors originating from the myometrium. These tumors can range from a few millimeters to over 20 cm in size. Leiomyomas are common and can occur in up to 77% of women while up to 20% of women suffer from significant morbidity, pain and discomfort and excessive menstrual bleeding. Leiomyomas are the primary indication for over 200,000 hysterectomies in the United States. In our laboratory we are investigating how progesterone promotes growth of leiomyomas by focusing on the non-genomic signaling of progesterone on the PI3K/AKT pathway. These studies are translated to the identification of important signaling molecules that can be targeted using small molecule inhibitors.
See Dr. Kim's publications in PubMed.
Dr. Kim at 312-503-4762.
Investigating the roles of cell cycle-regulatory proteins in differentiation, senescence and tumorigenesis and the cell cycle control in endocrine and reproductive organs
We are interested in the basic mechanisms of cell cycle control, cellular senescence/immortalization and malignant transformation, with a focus on protein regulation by ubiquitination. We previously demonstrated that cell cycle regulators such as p27Kip1, CDK4 and CDC25A play highly tissue-specific roles in development and oncogenesis. Ubiquitination, the covalent modification of substrate proteins with the small 76-residue protein ubiquitin, exerts diverse regulation of the fate of substrates, including the cell cycle regulators, e.g, promoting proteolysis, altering subcellular localization and modulating enzymatic activities. Our current research is aimed at revealing novel functions of ubiquitination enzymes and their substrates in development and cancer, which is expected to identify new therapeutic targets against human diseases. The laboratory uses a combination of protein engineering, proteomics, bioinformatics, cell biological techniques such as time-lapse microscopy and 3-D culture and genetically engineered mouse models. Keywords: cell cycle, ubiquitin, ubiquitination, cancer initiation, cancer progression, knockout mice, transgenic mice, breast cancer, cyclin, diabetes, pituitary, development.
- There is a unique regulation of cell cycle progression in neuroendocrine tissues such as pancreatic islets and pituitary glands of CDK4-null mice; we have shown that in this particular type of cell cycle, Cdk4 plays an indispensable and rate-limiting role
- CDC25A phosphatase, which activates CDK2 and CDK1, is an oncogene that plays a rate-limiting role in initiation and progression of various tumors, including breast cancer
We are currently investigating roles of the cell cycle machinery in differentiation, tumorigenesis and apoptosis, by combinations of mouse models and molecular analyses.
For lab information and more, see Dr. Kiyokawa’s faculty profile.
See Dr. Kiyokawa's publications on PubMed.
Contact Dr. Kiyokawa 312-503-0699.
Molecular biology of human papillomaviruses (HPV) and their association with cervical cancer
Our efforts are divided into two main categories:
- An examination of how the viral oncoproteins E6 and E7 contribute to the development of malignancy
- Studies on the mechanisms controlling the viral life cycle in differentiating epithelia
More than 100 distinct types of human papillomavirus have been identified and approximately one-third specifically target squamous epithelial cells in the genital tract. Of these genital papillomaviruses, a subset including types 16,18 and 31 have been shown to be the etiological agents of most cervical cancers.
One of our goals is to understand why infection by specific HPV types contributes to the development of malignancy. For these studies we have examined the interaction of the oncoproteins E6 and E7 with cellular proteins. In particular, E6 binds the p53 protein and facilitates its degradation by a ubiquitin-mediated pathway. It also activates telomerase as well as associates with PDZ-domain containing proteins. The interactions of the E6 and E7 proteins with these cellular proteins are being examined at both the biochemical and genetic level.
In examining the papillomavirus life cycle, we have used organotypic tissue culture systems to faithfully reproduce the differentiation program of epithelial cells in the laboratory. Using this system, the viral life cycle has been duplicated. We are studying the mechanisms that regulate viral DNA replication, cell entry, immune evasion and gene expression. These studies should provide insight into viral pathogenesis as well as the mechanisms regulating epithelial differentiation.
See Dr. Laimins' publications on PubMed.
Contact Dr. Laimins at 312-503-0648 or the lab at 312-503-0650.
Pediatric Fertility & Hormone Preservation & Restoration
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.
Mechanisms of ovarian cancer metastasis and novel therapeutics for ovarian cancer
My laboratory studies mechanisms of ovarian cancer metastasis and novel therapeutics for ovarian cancer. The general theme is translation between bench and clinic; with laboratory research forming the foundation for clinical experiments.
One direction of investigation relates to the interaction between cancer cells and the peritoneal stroma. We described the functions of tissue transglutaminase as an interacting partner of b-integrins and regulator of peritoneal metastasis. Based on new mechanistic insight into the roles of this enzyme in ovarian cancer, we discovered and began characterizing new small molecule inhibitors for the transglutaminase-fibronectin-integrin interaction that are being developed as anti-cancer agents. We are studying these new inhibitors in-vitro and in in-vivo models of ovarian cancer metastasis.
Another area of research focusses on the characteristics and therapeutic vulnerabilities of ovarian cancer stem cells. We used small molecule inhibitors that target ALDH1A1 to block the tumorigenic capacity of these cancer-initiating cells. We are studying how ALDH1A1 inhibitors alter stem cell specific signaling and how ALDH1A1 is involved in maintaining the cancer stem cell properties.
More recently we identified new metabolic alterations involving fatty acids desaturation in cancer stem cells. We have targeted lipid metabolism using small molecule inhibitors and are studying the mechanisms by which these metabolic changes contribute to the maintenance and tumorigenicity of cancer stem cells. Future goals are to refine the use of ALDH and fatty acid desaturases inhibitors to target cancer stem cells residual after chemotherapy and to eradicate the disease.
Another important direction of investigation is epigenetic modulation as a method of resensitization to platinum in ovarian cancer. We successfully brought to the clinic the concept that epigenetic modulation re-sensitizes chemotherapy-resistant ovarian tumors to carboplatin. I led a randomized multi-institutional clinical trial testing the effects of DNA hypomethylating agents and carboplatin compared to standard chemotherapy. We are now analyzing the genome and epigenome of platinum resistant ovarian cancer using specimens from this trial. We have identified several pathways that are associated with platinum resistance and respond to hypomethylating agents. We have designed a new strategy to target pathway-specific DNA methylation and are testing the effects of this intervention on cell signaling and gene expression profiles in ovarian cancer cells.
View Dr. Matei's publications on PubMed
Phone 312 503-4853
Epigenetics of Stem Cells and the Stem Cell Niche
My lab focuses on how genetic and epigenetic modulators promote the development and maintenance of adult stem cells.
Microenvironments, or niches, support the maintenance of stem cells and facilitate the development of tumors through largely unknown mechanisms. Cell-autonomous genetic pathways and epigenetic networks have emerged as important determinants for the self-renewal and differentiation of stem cells in embryonic, juvenile and adult tissues. The importance of non-cell autonomous genetic and epigenetic factors is less well established. Our goal is to identify and characterize the genetic and epigenetic mechanisms utilized by both stem cells and their surrounding niche in supporting the stem cell program. For these studies, the developing mouse testis is used to examine interactions between male germline stem cells (GSCs) and their somatic niche.
Within the testis, differentiated germ cells are continually replenished by self-renewing GSCs to ensure the continuation of spermatogenesis throughout the lifetime of the male. GSCs are adult stem cells that develop after birth but which derive from embryonic primordial germ cells (PGCs). Under abnormal conditions, PGCs are thought to become pluripotent in vivo, develop into carcinoma in situ and form post-pubertal testicular germ cell tumors, the most common cancer in men aged 15-40. When GSC differentiation occurs at the expense of self-renewal, depletion of germ cells and infertility can result.
Several candidate factors influencing GSC self-renewal and differentiation are being studied: chromatin remodeling gene Sin3a, Polycomb group member Ezh2 and a chemokine ligand and its receptor, Cxcl12 and Cxcr4. Current research is examining the role of Sin3a in somatic Sertoli cells, which support GSCs and nurture all differentiating germ cells. Analysis of Ezh2 in GSCs as well as in testicular germ cell tumors is being conducted to determine whether an altered “Polycomb repression signature” promotes germ cell tumorigenesis. Characterization of Cxcl12, which is expressed in Sertoli cells, and Cxcr4, expressed in germ cells, is being performed to determine whether this chemokine signaling pathway is required to maintain GSCs in their niche and whether this mechanism involves non-coding microRNAs.
To achieve these aims, distinct testicular cell populations are separated by fluorescence- and magnetic-activated cell sorting and analyzed by transcriptional profiling. Potential SIN3A and EZH2 complex-bound target genes are identified by chromatin immunoprecipitation. Loss-of-function effects are examined by one of two methods: generation of conditional knockout mice or RNAi knockdown and transplantation of cultured GSCs into recipient testes. Future studies are aimed at understanding how the niche maintains stem cells and ensures proper organogenesis, with the possibility of tissue regeneration and cancer prevention as therapeutic applications.
For more information visit Dr. Payne's faculty profile page
View Dr. Payne's publications at PubMed
Studying benign prostate diseases, chronic prostatitis/chronic pelvic pain syndrome
The focus of research in the laboratory is to understand the pathogenesis of genitourinary diseases with emphasis on benign prostate disease in humans. Inflammation is a significant finding in a variety prostate diseases including prostatitis, BPH and prostate cancer. We study microbial and autoimmune mediated inflammation and innate and adaptive immune mechanisms in prostate disease. A particular area of interest is chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), a debilitating medical condition characterized by dysuria and pain. Projects in the lab use a combination of in vitro studies, animal models and clinical specimen assays to examine questions of interest such as the role of chemokines and T-cells in chronic pelvic pain.
For more information, see the faculty profile of Praveen Thumbikat, PhD.
View Dr. Thumbikat's publications at PubMed
Larry Y Wong, Kenny Roman, Stephen F Murphy
Joseph D Done
Susceptibility genes for complex diseases
Dr. Urbanek’s research focuses on the identification of susceptibility genes for complex diseases. Her approach to this research is to use family-based gene-mapping techniques and population-based association studies in conjunction with molecular techniques to identify and verify genes and pathways contributing to the pathogenesis of genetically complex diseases. Specifically, she is carrying out studies to identify susceptibility genes for polycystic ovary syndrome (PCOS) that map to Chr19p3.13. She has previously shown that this region shows linkage and association with PCOS in a large set of families. Other projects focus on identifying candidate genes for gestational diabetes and glycemic control during pregnancy and identifying genetic variation contributing to extreme obesity
Identification of sequence variants in PCOS candidate genes
Identification of candidate genes for contributing glycemic control during pregnancy and to gestational diabetes
Genetic variation contributing to extreme obesity
Linkage and family-based association studies
Genome-wide association studies
For more information, visit Dr. Urbanek's faculty profile page.
View Dr. Urbanek's publications at PubMed.
Understand the development of the ovarian follicle, identify markers and determinants of egg quality and discover how this basic biology can be applied to patients.
Welcome to the Woodruff Lab, a team of research faculty, post-doctoral professionals, graduate students and lab technicians devoted to the study of ovarian health and development. We are working in three main areas. The first is ovarian follicle development, the study of the formation and maturation of the ovarian follicle, which is the basic functional unit of the ovary. The follicle includes somatic cells (which make hormones like estrogen and inhibin) and the oocyte (or egg). We are attempting to isolate the factors that regulate follicle and oocyte maturation and to understand the mechanisms of follicle and oocyte survival and death. The second focus of the Woodruff Lab is to develop in vitro follicle culture systems that can mimic the normal in vivo patterns of follicle development. The end goal of this research is to allow us to successfully remove healthy ovarian tissue from a cancer patient, safely store it until the patient has completed their treatment and then either harvest follicles from the tissue in an effort to grow them or surgically transplant the tissue to restore natural ovulation. Our third area of study is on the endocrine hormones inhibin and activin, which govern the reproductive cycle. Work on these hormones is essential to an understanding of healthy reproductive cyclicity and on the treatment of infertility.
View publications on PubMed.
Contact the Woodruff Lab via email.
Research Assistant Professor:
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.
Kim J, Lee Y, Lu X, Song B, Fong KW, Cao Q, Licht JD, Zhao JC, Yu J. Polycomb- and Methylation-Independent Roles of EZH2 as a Transcription Activator. Cell Reports. 2018 Dec 04. PMID: 30517868
Fong KW, Zhao JC, Song B, Zheng B, Yu J. TRIM28 protects TRIM24 from SPOP-mediated degradation and promotes prostate cancer progression. Nat Commun. 2018 Nov 27. PMID: 30479348
Fong KW, Zhao JC, Kim J, Li S, Yang YA, Song B, Rittie L, Hu M, Yang X, Perbal B, Yu J. Polycomb-mediated disruption of an androgen receptor feedback loop drives castration-resistant prostate cancer. CancerRes. 2016 Nov 4. PMID: 27815387
View all lab publications via PubMed.
Contact Dr. Yu at 312-503-2980 or the Yu Lab at 312-503-3041.
Will Ka-Wing Fong
Research Assistant Professor
Jonathan Zhao, MD, MS
Research Associate Professor
Nathan Damaschke, PhD
Yongik Lee, PhD
Xiaodong Lu, PhD
Gang Zhen, PhD
Xiaoyan Zhu, PhD