Dr. Kinzler’s laboratory has focused on the genetics of human cancer. They have identified a variety of genetic mutations that underlie cancer, including mutations of the APC pathway that appear to initiate the majority of colorectal cancers and IDH1/2 mutations that underlying many gliomas. In addition, they have developed a variety of powerful tools for analysis of expression and genetic alterations in cancer. Most recently, they have pioneered integrated whole genome analyses of human cancers through expression, copy number, and mutational analyses of all the coding genes in several human cancer types including colorectal, breast, pancreatic and brain. The identification of genetic differences between normal and tumor tissues provide new therapeutic targets, new opportunities for the early diagnosis of cancer, and important insights into the neoplastic process.

Research in the Kimberly Gudzune Lab examines how obesity affects patient-provider relationships and how physical and social environments impact body weight. We recently conducted a cohort study of married couples and found that having a spouse who become obese nearly doubles one's risk of becoming obese.

The King-Wai Yau Laboratory is interested in the area of sensory transduction. Specifically, we study visual transduction, the process by which the sense of vision is initiated. In our eyes, we have two primary photoreceptors-rods and cones-to absorb light and convert light into electrical signal, which is then transmitted to the brain for image formation. Rods are extremely sensitive and responsible for night vision, but cones are about 100-fold less sensitivity and responsible for daylight vision. We are studying the cellular and molecular details underlying rod and cone phototransduction, aiming to understand the mechanism of rod-cone difference. Our ultimate goal is to convert rods into cones, or cones into rods to rescue human vision loss.

Malfunction and malformation of blood vessels are associated with a broad range of medical conditions, including cancer, cardiovascular diseases, and neurological disorders. The ultimate goal of the Komatsu lab is to find a way to reverse the process of abnormal vessel formation and restore normal function to these vessels. In cancer, normalization of tumor blood vessels facilitates lymphocyte infiltration, potentiating anti-tumor immunity, and enhances the efficacy of immunotherapies as well as conventional cancer treatments. Normalization of regenerating blood vessels is also necessary for reestablishing blood flow to ischemic hearts and limbs, and preventing blindness caused by diabetic retinopathy or macular degeneration. Komatsu lab’s research is uncovering key molecular pathways important for the normalization of pathological vasculature.

The Konig Lab focuses on chimeric T cell- and antibody-based strategies for the treatment of autoimmune rheumatic diseases and cancer. A primary goal of the translational research program is the development of antigen-specific and personalized immunotherapies for autoimmune diseases, with the intent to achieve sustained disease remission and functional cure. The lab further aims to establish precision T cell-targeting therapies for the treatment of various autoimmune diseases. Applying these tools to immuno-oncology, the lab utilizes cellular engineering strategies to augment the cytotoxic killing of solid cancers by the immune system.

Work in the Kristin Riekert Lab focuses on methods for improving health care quality and delivery, particularly among underserved and disadvantaged populations. Our research covers a range of important topics, including health beliefs, treatment adherence, doctor-patient communication, self-management interventions, mobile health initiatives, health disparities and patient-reported outcome methodology. We also work with the National Institutes of Health on multiple intervention trials focused on improving adherence and health outcomes in asthma, chronic kidney disease, cystic fibrosis (CF), sickle cell disease and secondhand smoke reduction.

The Kristina Nielsen Laboratory investigates neural circuits in the visual cortex that are responsible for encoding objects to understand how the visual system performs object recognition. We aim to reveal the fine-scale organization of neural circuits, with an emphasis on higher-level visual areas. We use two-photon microscopy to perform high-resolution functional imaging of visual areas in the non-human primate. We also investigate how the function of higher visual areas changes over the course of brain development in ferrets, by measuring the activity of single neurons in these areas, as well as determining the animal's visual capabilities at various developmental stages. In both types of investigations, we also rely on detailed anatomical techniques to precisely observe how the function of neuronal circuits is related to their structure.

The Glunde lab is within the Division of Cancer Imaging Research in the Department of Radiology and Radiological Science. The lab is developing mass spectrometry imaging as part of multimodal molecular imaging workflows to image and elucidate hypoxia-driven signaling pathways in breast cancer. They are working to further unravel the molecular basis of the aberrant choline phospholipid metabolism in cancer. The Glunde lab is developing novel optical imaging agents for multi-scale molecular imaging of lysosomes in breast tumors and discovering structural changes in Collagen I matrices and their role in breast cancer and metastasis.

The Krummey Lab is a part of the Department of Pathology at the Johns Hopkins School of Medicine.

Our research prioritizes understanding the cellular mechanisms of alloimmunity, with a concentration on manipulating various cosignaling receptors and antigen recognition pathways to restrain the key lymphocytes principally involved in graft rejection. With the use of MHC tetramers, transgenic mouse models, and high-dimensional flow cytometry, we focus on mouse- and human-graft specific CD8+ T cells, CD4+ T cells, and B cells.

Transplantation is a life-saving procedure against a variety of diseases. Despite technical advances vastly improving early outcomes after transplant, long-term survival of transplanted organs has remained stagnant for the better part of three decades. A major cause of graft loss is immune-mediated rejection, which traditionally has be classified as acute or chronic based on its occurrence early or late after transplantation. Recently, this consensus has shifted to defining a graft rejection by its immunologic characteristics, either antibody-mediated or T cell-mediated (cellular rejection). This is because modern discoveries have identified the true major contributor to graft failures that occur many years after transplantation: not chronic rejection, but rather the cumulative impact of T cell-mediated acute rejection as a risk factor for later graft loss. Thus, original approaches to specifically prohibit and/or treat T cell-mediated acute rejection are of major significance for improving post-transplant outcomes.

HLA compatibility has also proven to be paramount for graft rejection. Originally, this was believed to be at the cellular level, then the single HLA protein level, and now at the epitope or molecular mismatch level. Specifically, HLA class II epitope-level mismatch has been identified as a risk factor for graft rejection, and multiple studies have identified specific epitopes within HLA class II peptides that are thought to be highly pathogenic. Few techniques directly measure antibody responses against specific regions of HLA proteins, but such measurements could provide both new information about the strength and character of alloimmunity and serve as an important new tool to study allogeneic B cells and antibody-secreting cells.

The Kunisaki lab is a NIH-funded regenerative medicine group within the Division of General Pediatric Surgery at Johns Hopkins that works at the interface of stem cells, mechanobiology, and materials science. We seek to understand how biomaterials and mechanical forces affect developing tissues relevant to pediatric surgical disorders. To accomplish these aims, we take a developmental biology approach using induced pluripotent stem cells and other progenitor cell populations to understand the cellular and molecular mechanisms by which fetal organs develop in disease.

Our lab projects can be broadly divided into three major areas: 1) fetal spinal cord regeneration 2) fetal lung development 3) esophageal regeneration

Lab members: Juan Biancotti, PhD (Instructor/lab manager); Annie Sescleifer, MD (postdoc surgical resident); Kyra Halbert-Elliott (med student), Ciaran Bubb (undergrad)

Recent publications:
Kunisaki SM, Jiang G, Biancotti JC, Ho KKY, Dye BR, Liu AP, Spence JR. Human induced pluripotent stem cell-derived lung organoids in an ex vivo model of congenital diaphragmatic hernia fetal lung. Stem Cells Translational Medicine 2021, PMID: 32949227

Biancotti JC, Walker KA, Jiang G, Di Bernardo J, Shea LD, Kunisaki SM. Hydrogel and neural progenitor cell delivery supports organotypic fetal spinal cord development in an ex vivo model of prenatal spina bifida repair. Journal of Tissue Engineering 2020, PMID: 32782773.

Kunisaki SM. Amniotic fluid stem cells for the treatment of surgical disorders in the fetus and neonate. Stem Cells Translational Medicine 2018, 7:767-773