Persistent Link:
http://hdl.handle.net/10150/291654
Title:
Growth of immunogenic skin tumors: Infiltrating leukocytes
Author:
Chen, HwuDauRw, 1958-
Issue Date:
1989
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
Subpopulations of tumor infiltrating leukocytes in immunogenic skin tumors were identified with monoclonal antibodies. The tumors studied included primary UV-induced tumors and JB/MS melanomas, which survive in the host by immunosuppression of the immune response. The proportions of nucleated cells in primary UV-induced tumor cell suspensions which reacted with monoclonal antibodies were: 52% Mac-1+, 21% Lyt-1+, 13% Lyt-2+, 7% L3T4+, and 8% IL-2R+. Thus there was a high proportion of cells of the macrophage lineage in the growing UV-induced tumors. In JB/MS melanoma cell suspensions the mean proportion of macrophages was 6.4%, and total T lymphocytes (Lyt-1) averaged only 5.5%. Thus, there was little leukocytes infiltration into JB/MS melanoma, suggesting that chemotaxis was defective. The high level of macrophages and T cells in the primary UV-induced tumors indicates that chemotaxis was intact. Therefore, either the tumorcidal capacities of the macrophages and Tc were insensitive to activated macrophages and to Tc cells.
Type:
text; Thesis-Reproduction (electronic)
Keywords:
Skin -- Tumors.; Radiation carcinogenesis.; Immunosuppression.; Leucocytes.
Degree Name:
M.S.
Degree Level:
masters
Degree Program:
Graduate College; Microbiology and Immunology
Degree Grantor:
University of Arizona
Advisor:
Bernstein, Harriss; Gensler, Helen

Full metadata record

DC FieldValue Language
dc.language.isoen_USen_US
dc.titleGrowth of immunogenic skin tumors: Infiltrating leukocytesen_US
dc.creatorChen, HwuDauRw, 1958-en_US
dc.contributor.authorChen, HwuDauRw, 1958-en_US
dc.date.issued1989en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractSubpopulations of tumor infiltrating leukocytes in immunogenic skin tumors were identified with monoclonal antibodies. The tumors studied included primary UV-induced tumors and JB/MS melanomas, which survive in the host by immunosuppression of the immune response. The proportions of nucleated cells in primary UV-induced tumor cell suspensions which reacted with monoclonal antibodies were: 52% Mac-1+, 21% Lyt-1+, 13% Lyt-2+, 7% L3T4+, and 8% IL-2R+. Thus there was a high proportion of cells of the macrophage lineage in the growing UV-induced tumors. In JB/MS melanoma cell suspensions the mean proportion of macrophages was 6.4%, and total T lymphocytes (Lyt-1) averaged only 5.5%. Thus, there was little leukocytes infiltration into JB/MS melanoma, suggesting that chemotaxis was defective. The high level of macrophages and T cells in the primary UV-induced tumors indicates that chemotaxis was intact. Therefore, either the tumorcidal capacities of the macrophages and Tc were insensitive to activated macrophages and to Tc cells.en_US
dc.typetexten_US
dc.typeThesis-Reproduction (electronic)en_US
dc.subjectSkin -- Tumors.en_US
dc.subjectRadiation carcinogenesis.en_US
dc.subjectImmunosuppression.en_US
dc.subjectLeucocytes.en_US
thesis.degree.nameM.S.en_US
thesis.degree.levelmastersen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplineMicrobiology and Immunologyen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorBernstein, Harrissen_US
dc.contributor.advisorGensler, Helenen_US
dc.identifier.proquest1338071en_US
dc.identifier.oclc24021895en_US
dc.identifier.bibrecord.b17721027en_US
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