Research Lab Results
-
Zack Wang Lab
The Wang lab focuses on the signals that direct the differentiation of pluripotent stem cells, such as induced-pluripotent stem (iPS) cells, into hematopoietic and cardiovascular cells. Pluripotent stem cells hold great potential for regenerative medicine. Defining the molecular links between differentiation outcomes will provide important information for designing rational methods of stem cell manipulation. -
William B. Isaacs Laboratory
Prostate cancer is the most commonly diagnosed malignancy in men in the United States, although our understanding of the molecular basis for this disease remains incomplete. We are interested in characterizing consistent alterations in the structure and expression of the genome of human prostate cancer cells as a means of identifying genes critical in the pathways of prostatic carcinogenesis. We are focusing on somatic genomic alterations occurring in sporadic prostate cancers, as well as germline variations which confer increases in prostate cancer risk. Both genome wide and candidate gene approaches are being pursued, and cancer associated changes in gene expression analyses of normal and malignant prostate cells are being cataloged as a complementary approach in these efforts. It is anticipated that this work will assist in providing more effective methodologies to identify men at high risk for this disease, in general, and in particular, to identify new markers of prognostic and therapeutic significance that could lead to more effective management of this common disease. -
William G. Nelson Laboratory
Normal and neoplastic cells respond to genome integrity threats in a variety of different ways. Furthermore, the nature of these responses are critical both for cancer pathogenesis and for cancer treatment. DNA damaging agents activate several signal transduction pathways in damaged cells which trigger cell fate decisions such as proliferation, genomic repair, differentiation, and cell death. For normal cells, failure of a DNA damaging agent (i.e., a carcinogen) to activate processes culminating in DNA repair or in cell death might promote neoplastic transformation. For cancer cells, failure of a DNA damaging agent (i.e., an antineoplastic drug) to promote differentiation or cell death might undermine cancer treatment. Our laboratory has discovered the most common known somatic genome alteration in human prostatic carcinoma cells. The DNA lesion, hypermethylation of deoxycytidine nucleotides in the promoter of a carcinogen-defense enzyme gene, appears to result in inactivation of the gene and a resultant increased vulnerability of prostatic cells to carcinogens. Studies underway in the laboratory have been directed at characterizing the genomic abnormality further, and at developing methods to restore expression of epigenetically silenced genes and/or to augment expression of other carcinogen-defense enzymes in prostate cells as prostate cancer prevention strategies. Another major interest pursued in the laboratory is the role of chronic or recurrent inflammation as a cause of prostate cancer. Genetic studies of familial prostate cancer have identified defects in genes regulating host inflammatory responses to infections. A newly described prostate lesion, proliferative inflammatory atrophy (PIA), appears to be an early prostate cancer precursor. Current experimental approaches feature induction of chronic prostate inflammation in laboratory mice and rats, and monitoring the consequences on the development of PIA and prostate cancer. -
Karen Reddy Laboratory
The focus of the research in the Reddy Laboratory is to begin to understand how the nuclear periphery and other subcompartments contribute to general nuclear architecture and to specific gene regulation. Our research goals can be broken down into three complementary areas of research: understanding how genes are regulated at the nuclear periphery, deciphering how genes are localized (or ""addressed"") to specific nuclear compartments and how these processes are utilized in development and corrupted in disease. -
HPTN (HIV Prevention Trials Network) Network Lab
HPTN (HIV Prevention Trials Network) Network Laboratory (NL) is responsible for collecting, testing and reporting results from biological samples; assisting in the development and quality assurance assessment of local laboratory capacity at the Clinical Trials Units (CTUs) participating in HPTN clinical trials (www.hptn.org); and identifying and implementing state-of-the-art assays and technologies to advance the scientific agenda of the Network. -
Mihail Zilbermint Lab
Research in the Mihail Zilbermint Lab focuses on diabetes, adrenal disease and thyroid disease. Recent areas of focus include pseudohypoaldosteronism type 1 related to novel variants of SCNN1B gene, genetic variance in the ARMC5 gene in primary macronodular adrenocortical hyperplasia and hyperaldosteronism due to de novo KCNJ5 mutation. -
Ruth Faden Lab
Research in the Ruth Faden Lab focuses on biomedical ethics and health policy. Our specific areas of interest include justice theory; national and global challenges in learning health care systems, health-system design and priority setting; access global investments benefits in biomedical research; and ethical challenges in biomedical science and women’s health. -
The Howard and Georgeanna Seegar Jones Reproductive Endocrinology Lab
Research in the Howard and Georgeanna Seegar Jones Reproductive Endocrinology Lab supports a broad interest in reproductive conditions, but has a particular focus on endometriosis, uterine fibroids, polycystic ovary syndrome (PCOS) and genes causing infertility. PCOS and uterine fibroids are among the most prevalent conditions leading to infertility and diseases in women, but both remain poorly understood. Studying these areas may lead to the development of new treatments or preventative therapies. -
Sean Taverna Laboratory
The Taverna Laboratory studies histone marks, such as lysine methylation and acetylation, and how they contribute to an epigenetic/histone code that dictates chromatin-templated functions like transcriptional activation and gene silencing. Our lab uses biochemistry and cell biology in a variety of model organisms to explore connections between gene regulation and proteins that write and read histone marks, many of which have clear links to human diseases like leukemia and other cancers. We also investigate links between small RNAs and histone marks involved in gene silencing. -
Shyam Sundar Biswal Lab
xResearch in the Shyam Biswal Lab focuses on therapeutic resistance of cancer due to a gain-of-function mutation in transcription factor Nrf2. Using patient-derived xenografts in humanized immunocompetent mice and GEM models, we aim to understand the mechanisms of oncogenic cooperation and metabolic adaptation in cancer cells. We’re also investigating the systemic and pulmonary effects of air pollution as well as the health effects of recent tobacco products, such as electronic cigarettes and water pipes.