Directory - Jane Coffin Childs Memorial Fund

Status

Year Appointed

Institution

Name

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Andrew Taussig Jane Coffin Childs Fellow

McGill-Montreal General Hospital Research Institute

Appointed in 1961

C.P.S. Taylor Jane Coffin Childs Fellow

University of Cambridge, England

Appointed in 1960

John M. Taylor Jane Coffin Childs Fellow

Stanford University

Appointed in 1972

Kenneth A. Taylor Jane Coffin Childs Fellow

MRC Center, University Medical School, England

Appointed in 1976

John L. Teem Jane Coffin Childs Fellow

Whitehead Institute for Biomedical Research

Appointed in 1983

Gary F. Temple Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1972

Mabel Tettey, Ph.D. Jane Coffin Childs Fellow

National Institute of Allergy and Infectious Diseases

Appointed in 2023

In disease-causing organisms, hybridization allows for the transfer of traits such as virulence and drug resistance. Dr. Mabel Tettey will investigate how hybridization impacts African trypanosomiasis outbreaks caused by the parasite Trypanosoma brucei. Dr. Tettey will assess the degree of hybridization occurring in African trypanosome endemic areas, explore the impact of hybridization on virulence, and identify the key molecules involved in this process. She will conduct these experiments in Dr. Michael Grigg’s lab at the National Institute of Allergy and Infectious Diseases. These studies may enable the development of effective disease control strategies against African trypanosomes.

As a graduate student in Dr. Keith Matthews’ lab at the University of Edinburgh, Tettey examined the function of released peptidases in the transmission of African trypanosomes. Specifically, Dr. Tettey identified the genes that dominate quorum sensing signal in African trypanosomes. With her extensive background in trypanosome biology, Dr. Tettey will now examine the role of hybridization in trypanosome virulence.

Sheila Teves Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 2014

Cellular memory can be defined as the ability of a cell to transmit all its identifying functions to daughter cells during cell division. This ability to ¬ëremember¬í identity is crucial to the development of multicellular organisms, as evidenced when cells lose their identity and degenerate or become cancerous. Conversely, our ability to alter cell state, such as the generation of induced pluripotent stem (iPS) cells from differentiated cells, has become a promising therapeutic tool. Therefore, understanding how cells establish, maintain, and change identity will further our understanding of processes central to cellular development, disease progression, and therapy production. One mechanism for cellular memory is the ability to re-establish the transcriptional program following mitosis, which may function through bookmarking, the process of DNA-binding factors marking genes on condensed mitotic chromosomes to facilitate gene expression following mitosis. The main objective of this proposal is to analyze the mechanisms of bookmarking. I outline three independent approaches to characterize quantitatively the mechanisms of bookmarking. Using these approaches, I will test the hypothesis that histone variants and pluripotency factors function as bookmarkers to maintain the stem cell state. Lastly, I will perform an unbiased screen to identify putative bookmarking factors specific to embryonic stem cells.

Marla Tharp, Ph.D. Jane Coffin Childs - HHMI Fellow

Whitehead Institute for Biomedical Research

Appointed in 2021

Cancer affects men and women differently. For example, glioblastoma, the most aggressive form of brain cancer, has a male-biased incidence rate and poorer response to standard treatments in men versus women. My research investigates the genetic and molecular basis of sex differences in glioblastoma from the perspective of microglia, the resident immune cells of the brain. Microglia are a major player in the brain tumor microenvironment and promote tumor growth and metastasis. Using XX and XY human microglia isolated from healthy brain regions and brain tumors, I am identifying sex-biased genes and biological pathways that are responsible for establishing sexually dimorphic brain tumor microenvironments. Further, I am testing how possessing an XX or XY sex chromosome complement drives the observed genome-wide sex-biased gene expression patterns in microglia, in particular, through X-linked genes that aberrantly escape X chromosome inactivation or homologous X-Y gene pairs with imbalanced expression or function. I anticipate that my research will lay the groundwork for more effective and sex-specific treatments for glioblastoma.

Helen P. Thompson Jane Coffin Childs Fellow

Rockefeller University

Appointed in 1948

Lynnmarie K. Thompson Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1989

Catherine C. Thompson Jane Coffin Childs Fellow

Carnegie Institute for Science

Appointed in 1990

Jeremy W. Thorner Jane Coffin Childs Fellow

Stanford University

Appointed in 1972

Clark J.B. Tibbetts Jane Coffin Childs Fellow

University of Uppsala, Sweden

Appointed in 1972

David C. Tiemeier Jane Coffin Childs Fellow

National Institutes of Health

Appointed in 1973

Alisa C. Tietz Jane Coffin Childs Fellow

New York University

Appointed in 1956

David P. Toczyski Jane Coffin Childs Fellow

University of Washington

Appointed in 1993

Joanne Topol Jane Coffin Childs Fellow

California Institute of Technology

Appointed in 1990

Margaret Torrence, Ph.D. Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 2022

Pancreatic cancer represents 3% of all new cancer cases in the United States, yet it has the worst 5-year survival rate of all cancer types. While many cancer types display durable responses to cancer immunotherapy, which harnesses the cytotoxic activity of the immune system to treat malignancies, immunotherapy has largely failed to treat pancreatic ductal adenocarcinoma (PDAC). The complex tumor microenvironment of PDAC likely underlies the refractory response of PDAC to immunotherapy, including immune checkpoint blockade (ICB). One example of a known mechanism that aids immune evasion by PDAC is the presence of desmoplastic stroma that hinders the infiltration of cytotoxic T cells. In addition to exclusion of immune infiltrate, the cytotoxic T cells that are present within the microenvironment are dysfunctional. Nutrient availability within the tumor environment likely impacts the function of cytotoxic T cells and research in immunometabolism is of growing interest. Understanding cell-specific metabolic changes within GEMMs has been hindered by a lack of mouse models that properly recapitulate the tumor microenvironment and lack of tools able to properly isolate cells in a way that preserves the integrity of the metabolites. My project will use a GEMM of PDAC, congenic markers, and cancer cell-specific surface tags in order to rapidly purify and perform metabolomics of both cancer cells and T-cells. Using this technique, I hope to identify metabolic pathways that are hindering immune cell proliferation and cytotoxic capabilities to reinvigorate the immune microenvironment for tumor control and in response to ICB.

Daniel E. Tracey Jane Coffin Childs Fellow

Karolinska Institutet, Stockholm

Appointed in 1973

Robert R. Traut Jane Coffin Childs Fellow

University Medical School, England

Appointed in 1962

Tatjana Trcek-Pulisic Jane Coffin Childs - HHMI Fellow

New York University

Appointed in 2012

Jessica E. Treisman Jane Coffin Childs Fellow

University of California, Berkeley

Appointed in 1991

John J. Trentin Jane Coffin Childs Fellow

Yale University

Appointed in 1948

E. Sergio Trombetta Jane Coffin Childs Fellow

Yale University

Appointed in 1995

Eirini D. Trompouki Jane Coffin Childs Fellow

Boston Children's Hospital

Appointed in 2007

Ian S. Trowbridge Jane Coffin Childs Fellow

Salk Institute for Biological Studies

Appointed in 1972

Heather L. True-Krob Jane Coffin Childs Fellow

University of Chicago

Appointed in 1998

Patricia A. Trumper Jane Coffin Childs Fellow

Sidney Farber Cancer Center

Appointed in 1977

Nancy J. Trun Jane Coffin Childs Fellow

National Cancer Institute

Appointed in 1988

Benes L. Trus Jane Coffin Childs Fellow

California Institute of Technology

Appointed in 1972

Kaloyan Tsanov Jane Coffin Childs Fellow

Memorial Sloan-Kettering Cancer Center

Appointed in 2018

Hemizygous deletions of ribosomal protein genes (RPGs) are recurrently found across human cancers, yet their role in tumorigenesis is poorly understood. Here, I propose to systematically investigate the function of RPG hemizygosity in cancer, using hepatocellular carcinoma (HCC) as a model, by exploring two specific hypotheses. First, based on genomic data from HCC and other tumors, and emerging biochemical evidence for mRNA-specific translational control by individual RPs, I hypothesize that RPGs act as haploinsufficient tumor suppressor genes by selectively altering the translation of oncogenic and/or tumor-suppressive mRNAs. I will assess the contribution of RPG hemizygosity to tumor initiation, progression and maintenance, and analyze its impact on mRNA translation. Second, given that RPG deletions are almost invariably hemizygous and strongly associate with loss of the p53 tumor suppressor gene, I hypothesize that RPG hemizygosity renders cancer cells more vulnerable to perturbations of ribosome homeostasis. I will examine the effects of p53 restoration and further RPG depletion in RPG hemizygous cells, and perform a ribosome homeostasis-focused screen for RPG hemizygosity-specific tumor dependencies. Together, the proposed studies may provide an explanation for the striking patterns of RPG loss in human cancer, with potential broad implications for both fundamental biology and cancer treatment.

Claire C. Tseng Jane Coffin Childs Fellow

Whitehead Institute for Biomedical Research

Appointed in 2004

Christopher A. Tsu Jane Coffin Childs Fellow

University of Colorado, Boulder

Appointed in 1995

Rocky S. Tuan Jane Coffin Childs Fellow

Massachusetts General Hospital

Appointed in 1977

Gregory E. Tullis Jane Coffin Childs Fellow

Princeton University

Appointed in 1993

Glenn C. Turner Jane Coffin Childs Fellow

California Institute of Technology

Appointed in 2002

Gregory E. Turnick Jane Coffin Childs Fellow

Cornell University

Appointed in 1966

Geoffrey Turnock Jane Coffin Childs Fellow

Cornell University

Appointed in 1966

Claudia Turro Jane Coffin Childs Fellow

Columbia University

Appointed in 1992

Jonathan M. Tyler Jane Coffin Childs Fellow

University of Alberta, Canada

Appointed in 1980

Jayant B. Udgaonkar Jane Coffin Childs Fellow

Stanford University

Appointed in 1986

Jay N. Umbreit Jane Coffin Childs Fellow

Johns Hopkins University

Appointed in 1972

Elçin Unal Jane Coffin Childs - HHMI Fellow

Massachusetts Institute of Technology

Appointed in 2008

Jay C. Unkeless Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1974

Wilfred A. Van der Donk Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1994

Susan S. Van Rheenen Jane Coffin Childs Fellow

Tufts University School of Medicine

Appointed in 2000

Petra Vande Zande, Ph.D. Jane Coffin Childs Fellow

University of Minnesota

Appointed in 2023

The human pathogen Candida albicans’ genome varies substantially between clinical isolates, yet it is currently unknown how this variation affects infection. Since many genetic variants are located in gene regulatory sequences, Dr. Petra Vande Zande predicts that there is substantial divergence in gene-regulatory networks between different C. albicans isolates that modifies their fitness. Dr. Vande Zande will use gene expression data from different isolates to model gene regulatory networks and identify key differences that impact fitness. Vande Zande will conduct these experiments in Dr. Anna Selmecki’s lab at the University of Minnesota. This research will provide direct insight into genetic differences that impact C. albicans infections. It may also provide clues into other genetically diverse systems with differences in gene-regulatory networks, including human cancers.

As a graduate student in Dr. Patricia Wittkopp’s lab at the University of Michigan, Vande Zande studied gene expression in the context of adaptive evolution. In particular, Dr. Vande Zande discovered that mutations affecting a gene’s expression from a distance are more pleiotropic and more detrimental to fitness than mutations occurring proximally to the gene of interest. With her experience in the evolution of gene expression, Dr. Vande Zande is now interested in understanding divergence in gene-regulatory networks between different clinical isolates of yeast infections.

Christopher D. Vanderwal Jane Coffin Childs Fellow

Harvard University

Appointed in 2003

Frederick Varn Jane Coffin Childs - Merck Fellow

Jackson Laboratory

Appointed in 2019

Diffuse glioma is the most common primary brain tumor in adults and is characterized by a poor prognosis and near universal recurrence following therapy. Given the poor response rate to the current standard-of-care, there is an active interest in applying immunotherapy to treat this disease. However, progress on this front has been limited, due in part to limited knowledge of how the immune system interacts with glioma to influence the tumor‚Äôs evolution. My work focuses on how cells of the immune system and accompanying microenvironment interact with malignant cells to influence the developmental trajectory of diffuse glioma. By integrating multi-omic bulk and single-cell datasets from pre- and post-treatment tumors, I aim to develop a better understanding of how gliomas evade the immune response and how the standard-of-care alters these processes. Results from this work can provide insights into how to shape disease progression and enable the sensitization of the gliomas to subsequent treatment approaches.

Inder M. Verma Jane Coffin Childs Fellow

Massachusetts Institute of Technology

Appointed in 1971