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Connie L. Sivinski
Researcher at University of Nebraska Medical Center
Publications - 5
Citations - 88
Connie L. Sivinski is an academic researcher from University of Nebraska Medical Center. The author has contributed to research in topics: Immune system & CD28. The author has an hindex of 4, co-authored 5 publications receiving 88 citations. Previous affiliations of Connie L. Sivinski include Eppley Institute for Research in Cancer and Allied Diseases.
Papers
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Journal ArticleDOI
Organ-specific pancreatic tumor growth properties and tumor immunity
Keita Morikane,Richard M. Tempero,Connie L. Sivinski,Mitsuharu Nomoto,Michelle L. Van Lith,Tetsuichiro Muto,Michael A. Hollingsworth +6 more
TL;DR: The results show that the growth properties and immunological rejection of pancreatic tumors is affected by the organ site at which the tumor grows.
Journal ArticleDOI
Influence of organ site and tumor cell type on MUC1-specific tumor immunity.
Keita Morikane,Richard M. Tempero,Connie L. Sivinski,Shimichi Kitajima,Sandra J. Gendler,Michael A. Hollingsworth +5 more
TL;DR: It is shown that it is more difficult to produce immune responses to tumors growing at the pancreatic site than the s.c.C.Tg mice, and immune responses evoked by presentation of MUC1 in wild-type mice were effective in rejecting tumor cells in the pancreas of both wild- type and M UC1.
Journal ArticleDOI
MUC1‐specific anti‐tumor responses: molecular requirements for CD4‐mediated responses
Michelle L. VanLith,Karl G. Kohlgraf,Connie L. Sivinski,Richard M. Tempero,Michael A. Hollingsworth +4 more
TL;DR: It is demonstrated that the immune response generated against MUC1 does not fit the type 1 or 2 model described for many immune responses, and multiple cytolytic mechanisms are required for B16.MUC1 rejection.
Journal ArticleDOI
Molecular requirements for CD8-mediated rejection of a MUC1-expressing pancreatic carcinoma: Implications for tumor vaccines
Connie L. Sivinski,Karl G. Kohlgraf,Michelle L. VanLith,Keita Morikane,Richard M. Tempero,Michael A. Hollingsworth +5 more
TL;DR: B16.MUC1 immunity clearly demonstrate that different effector cells and cytolytic mechanisms are required to eliminate MUC1-expressing tumors derived from different organ sites, and provide insight into the immune components required to eliminated tumors expressing the same antigen butderived from different tissues.
Book ChapterDOI
Paraneoplastic Autoimmune Reactions
TL;DR: In some cases, it is believed that inflammatory and autoimmune reactions result from interactions between substances and cells of the immune responses that are directed against tumor cells but cross react with normal tissues.