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Rotation Projects: <p >Potential rotation projects My lab primarily investigates Plasmodium falciparum malaria-induced dysregulation of EBV-specific T cell immunity and its role in the etiology of endemic Burkitt lymphoma (eBL), the most prevalent pediatric cancer in Equatorial Africa. Within the context of our ongoing studies of healthy Kenyan children with divergent malaria exposure histories (chronic/repeated infections in a holoendemic area versus low infection rates in a nearby highland, malaria hypoendemic area) and by examining children diagnosed with eBL we have established a repository of samples that can be used to address this question. <p >1. One avenue of exploration involves homeostatic cytokine regulation of memory T cells. IL-15 and/or IL-7 responsiveness of EBV-specific memory T cells may be impaired in children with chronic malaria exposure and in children with endemic Burkitt lymphoma (eBL). We would like to investigate IL-15Ra and IL-7Ra surface expression, and CFSE proliferation of EBV-specific T cells in response to cognate antigen with and without IL-15 or IL-7 stimulation and compared children with divergent malaria exposure histories and children diagnosed with eBL. T cell responsiveness to IL-15 and IL-7 can be measured by STAT5 phosphorylation and the specificity of this effect for EBV-specific T cells can be evaluated by comparing IL-15Ra and IL-7Ra expression and responsiveness on other lymphocyte subsets and CMV-specific T cells. <p >2. Another putative mechanism by which malaria may interfere with the development of immunologic memory and influence EBV-specific T cell immunity is through the Programmed death-1 (PD-1) pathway. PD-1 is an immune inhibitory molecule that negatively regulates activated immune cells upon interacting with its ligands, programmed death ligand-1 (PD-L1) and programmed death ligand-2 (PD-L2) resulting in down-regulation of immune responses. Previous studies in murine and primate viral and parasitic diseases have reported the up-r…
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Woda, Bruce
first name: Bruce
last name: Woda
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person in primary position: Professor
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preferred title: Professor

Heneka, Michael
first name: Michael
last name: Heneka
full name: Michael Thomas Heneka MD
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latitude: 50.70274210000000
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Person ID: 3432
person in primary position: Adjunct Professor
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preferred title: Adjunct Professor

Behar, Samuel
first name: Samuel
last name: Behar
full name: Samuel M Behar MD, PhD
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Person ID: 3437
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Lab URL: https://www.umassmed.edu/maps/research-labs/behar/
Rotation Projects: LAB ROTATION PROJECTS AVAILABLE -- PLEASE CONTACT SAM BEHAR FOR MORE INFORMATION
Summary: Focus: We seek to understand how the causative agent of tuberculosis, namely the bacterium Mycobacterium tuberculosis evades host immunity, and how different components of the immune response work together to contain infection. Our ultimate goal is to inform vaccine development and the design of host directed therapy.
preferred title: Professor

Epstein, Mara
first name: Mara
last name: Epstein
full name: Mara Meyer Epstein ScD, ScM
has faculty rank: Associate Professor
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Person ID: 3469
person in primary position: Associate Professor
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preferred title: Associate Professor

Szabo, Gyongyi
first name: Gyongyi
last name: Szabo
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Post Docs: Immediate opening! Two postdoctoral positions are available immediately to study cellular andmolecular mechanisms resulting in immunosuppression after alcohol use. Thefocus of this research is the role of monocytes and dendritic cells indecreased antigen-specific T cell activation after alcohol use.Intracellular signalling mechanisms resulting in decreased NF-kBactivation and inflammatory cytokine induction after acute alcoholconsumption are being investigated. Please contact Dr. Szabo for details.
preferred title: Adjunct Professor

Braun, Barry
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person in primary position: Associate Professor
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Arcaro, Kathleen
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Person ID: 3726
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Rotello, Vincent
first name: Vincent
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Peyton, Shelly
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Person ID: 3819
person in primary position: Assistant Professor
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Wolf, Greg
first name: Greg
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Twitter: https://profiles.umassmed.edu/profile/28867023
full name: Greg Wolf
has faculty rank: Other
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person in primary position: Chief Information Officer
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webpage: https://profiles.umassmed.edu/profile/28866533

Brehm, Michael
first name: Michael
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Endowed Chair Honorary Title: Harvey A. Shultz Chair in Diabetes
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Harris, John
first name: John
last name: Harris
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Endowed Chair Honorary Title: Lambi and Sarah Adams Chair in Genetic Research
Rotation Projects: Rotations: Targeting the IFN-?-chemokine axis for treatment of vitiligo: We are using our newly developed mouse model and human tissues from patients with vitiligo to identify the cytokines and chemokines that are expressed within the depigmenting skin and which skin cells produce them. We are using genetically modified mouse strains (knockouts, conditional knockouts, fluorescent reporter strains), and cytokine and chemokine neutralizing antibodies to identify the key proteins required for disease. This data will permit us to rationally develop and test new therapeutic agents. Understanding the proinflammatory signals generated by melanocytes under cellular stress. Melanocytes from vitiligo patients have intrinsic abnormalities, including cellular stress evidenced by increased production of reactive oxygen species (ROS) and activation of the unfolded protein response (UPR). The immune system has evolved to recognize this stress as damage-associated molecular patterns (DAMPs), which activate innate immunity. We are using human cells and tissues to determine how cellular stress, innate immunity, and adaptive immunity cooperate to initiate and perpetuate depigmentation in vitiligo. Developing a humanized mouse model of immune-skin interactions to serve as a pre-clinical bridge to clinical studies: We are developing a humanized mouse model of skin disease that consists of an immunodeficient mouse strain as a host for an autologous human skin graft and immune reconstitution in order to study mechanisms of inflammation in the skin, including allergic contact dermatitis, response to infection, tumor immunotherapy, and autoimmunity, all within a fully human environment. This model system will act as a pre-clinical bridge between mouse models and human clinical trials, providing an opportunity to test new treatments on human cells and tissues prior to initiating trials on patients. Tracking real-time autoreactive T cell migration and interactions within the skin: We are usin…
Rotation Projects: Rotations: Targeting the IFN-g-chemokine axis for treatment of vitiligo: We are using our newly developed mouse model and human tissues from patients with vitiligo to identify the cytokines and chemokines that are expressed within the depigmenting skin and which skin cells produce them. We are using genetically modified mouse strains (knockouts, conditional knockouts, fluorescent reporter strains), and cytokine and chemokine neutralizing antibodies to identify the key proteins required for disease. This data will permit us to rationally develop and test new therapeutic agents. Understanding the proinflammatory signals generated by melanocytes under cellular stress. Melanocytes from vitiligo patients have intrinsic abnormalities, including cellular stress evidenced by increased production of reactive oxygen species (ROS) and activation of the unfolded protein response (UPR). The immune system has evolved to recognize this stress as damage-associated molecular patterns (DAMPs), which activate innate immunity. We are using human cells and tissues to determine how cellular stress, innate immunity, and adaptive immunity cooperate to initiate and perpetuate depigmentation in vitiligo. Developing a humanized mouse model of immune-skin interactions to serve as a pre-clinical bridge to clinical studies: We are developing a humanized mouse model of skin disease that consists of an immunodeficient mouse strain as a host for an autologous human skin graft and immune reconstitution in order to study mechanisms of inflammation in the skin, including allergic contact dermatitis, response to infection, tumor immunotherapy, and autoimmunity, all within a fully human environment. This model system will act as a pre-clinical bridge between mouse models and human clinical trials, providing an opportunity to test new treatments on human cells and tissues prior to initiating trials on patients. Tracking autoreactive T cell interactions within the skin: We are using fluorescently tagged C…
Summary: Interests: Vitiligo, autoimmunity, immunology, translational research
preferred title: Adjunct Professor

Greiner, Dale
first name: Dale
last name: Greiner
full name: Dale L Greiner PhD
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Person ID: 612
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Endowed Chair Honorary Title: Herman G. Berkman Chair in Diabetes Care Innovation
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Stern, Lawrence
first name: Lawrence
last name: Stern
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Person ID: 730
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Rotation Projects: Potential Rotation Projects Several rotation projects are available in structural biology of immune receptors, antigen presentation pathways, T-cell activation, and development of novel T-cell detection reagents. Please see Prof. Stern for details.
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Kornfeld, Hardy
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Cerny, Jan
first name: Jan
last name: Cerny
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Person ID: 777
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Goldberg, Robert
first name: Robert
last name: Goldberg
full name: Robert Joel Goldberg PhD
has faculty rank: Professor Emeritus
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Cantor, Sharon
first name: Sharon
last name: Cantor
full name: Sharon B Cantor PhD
has faculty rank: Professor
latitude: 42.27985300000000
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Person ID: 828
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Endowed Chair Honorary Title: Gladys Smith Martin Chair in Oncology
Post Docs: A post-doctoral position is available immediately to study the role of genes found in a genome-wide RNAi screen to regulate the cellular response to the chemotherapy agent, cisplatin. The goal is to determine whether these genes function as tumor suppressor and/or regulate the mechanism of DNA repair processing. The laboratory is interested in understanding the role of hereditary cancer genes of the BRCA-Fanconi anemia pathway in DNA damage repair and tumor suppression. We seek motivated candidates with a PhD and background in cancer cell biology. Experience in mouse cancer models is desirable. The exceptional training environment within the Department of Cancer Biology at UMASS Medical School offers a rigorous and interactive research environment covering several aspects of tumor biology. Applicants should have excellent communication skills, and ability to conduct research independently and as a team. To apply, please send your CV with bibliography, a brief description of research experience and contact information for at least two references via email.
Rotation Projects: The laboratory is interested in a range of DNA replication/repair-related topics including (i) Defining biomarkers of “BRCAness” that signifies deficiency in the hereditary breast/ovarian cancer genes, BRCA1 or BRCA2, (ii) Targeting BRCAness as a replication gap vulnerability, (iii) Defining why replication proficiency requires the FANCJ helicase disengage mismatch repair proteins, (iv) Determining if suppressing gaps improves the health of Fanconi anemia patient cells, (v) Hunting down the cancer vulnerability that defines curability, (vi) performing functional genomic screens to uncover mechanisms regulating chemotherapy resistance.
preferred title: Professor

Shaw, Leslie
first name: Leslie
last name: Shaw
full name: Leslie M Shaw PhD
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Mercurio, Arthur
first name: Arthur
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full name: Arthur M Mercurio PhD
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Person ID: 901
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Rotation Projects: <p >Rotation Projects <p >Rotation projects are designed to expose students to the molecular cell biology of solid tumors and to provide them with an appreciation for translational cancer research. Specific rotation projects, which are focused on the major themes of the lab, include: <p >Function and Regulation of Integrins (Cell Adhesion Receptors) in Cancer Epigenetic mechanisms that regulate integrin gene expression in human cancers Regulation of integrin expression and function during the EMT Role of specfic microRNAs (miRs) in regulating integrin function and signaling Contribution of integrins to carcinoma progression using mouse models of breast carcinoma <p >Vascular Endothelial Growth Factor (VEGF) Signaling, EMT and Carcinoma Progression Function and expression of VEGF receptors in carcinoma cells Regulation of VEGF transcription in response to EMT stimuli Role of miRs in regulating VEGF receptors and signaling Contribution of VEGF signaling to the behavior of aggressive, de-differentiated carcinomas <p >Nuclear Hormone Receptors and EMT Role of estrogen receptors in regulating the EMT Regulation of VEGF transcription by estrogen receptors
preferred title: Professor

McManus, David
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Endowed Chair Honorary Title: Richard M. Haidack Professor in Medicine
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UMass Chan – Baystate Regional Campus
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Dunn, Steven
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Dermatology
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Lindenauer, Peter
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Schneider, Sallie
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Berrett-Abebe, Julie
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Lou, Feiran
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Usmani, Saad
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Population and Quantitative Health Sciences
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Patel, Shyam
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Bankier, Alexander
first name: Alexander
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Ruscetti, Marcus
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Nason, Katie
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Sayej, Wael
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Mulvaney, Patrick
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Anesthesiology at UMass Chan - Baystate
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Associate Professor
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Chief Information Officer
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Weiss, Glen
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Singhal, Amit
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Professor Emeritus
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Associate Professor
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Whelan, Anna
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Laus, Ana
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Shin, Dong-Soo
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