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Cathy S. Madsen

Researcher at Mayo Clinic

Publications -  20
Citations -  867

Cathy S. Madsen is an academic researcher from Mayo Clinic. The author has contributed to research in topics: MUC1 & Antigen. The author has an hindex of 13, co-authored 18 publications receiving 805 citations. Previous affiliations of Cathy S. Madsen include University of Pittsburgh.

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Journal ArticleDOI

Immune recognition of tumor-associated mucin MUC1 is achieved by a fully synthetic aberrantly glycosylated MUC1 tripartite vaccine

TL;DR: The minimum requirements to consistently induce CTLs and ADCC-mediating antibodies specific for the tumor form of MUC1 are identified resulting in a therapeutic response in a mouse model of mammary cancer.
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Mice with Spontaneous Pancreatic Cancer Naturally Develop MUC-1-Specific CTLs That Eradicate Tumors When Adoptively Transferred

TL;DR: The MET mice appropriately mimic the human condition and are an excellent model with which to elucidate the native immune responses that develop during tumor progression and to develop effective antitumor vaccine strategies.
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Mucin 1-specific immunotherapy in a mouse model of spontaneous breast cancer.

TL;DR: Using an injectable breast cancer model, the authors show that targeting a single tumor antigen may not be an effective antitumor treatment, but that immunization with dendritic cells fed with whole tumor lysate is effective in breaking tolerance and protecting mice from subsequent tumor challenge.
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Mucin mRNA expression in normal and vasomotor inferior turbinates

TL;DR: Understanding the expression patterns in normal turbinates will serve as the foundation for further study of these mucins in disease states, and the variety of mucins expressed and the diversity of their expression patterns may have significance in terms of the rheologic and particle clearance properties of nasal secretions.
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MUC1-specific CTLs are non-functional within a pancreatic tumor microenvironment.

TL;DR: It is demonstrated that the CTL tolerance could be reversed at least in vitro with the use of anti-CD40 co-stimulation, which indicates theuse of several immune evasion mechanisms by tumor cells to evade CTL killing.