Adoptive immunotherapy of mucin1 expressing adenocarcinomas with mucin1 stimulated human peripheral blood mononuclear cells

• Published in: International journal of molecular medicine Vol. 9; no. 4; p. 401
• Main Authors: Wright, Stephen E, Rewers-Felkins, Kathleen A, Quinlin, Imelda S, Eldridge, Paul W, Zorsky, Paul E, Klug, Panpit P, Phillips, Catherine A, Philip, Ramila
• Format: Journal Article
• Language: English
• Published: Greece 01-04-2002
• Subjects: Adenocarcinoma - immunology; Adenocarcinoma - pathology; Adenocarcinoma - therapy; Animals; Breast Neoplasms - immunology; Breast Neoplasms - pathology; Breast Neoplasms - therapy; Cytokines - secretion; Female; Humans; Immunotherapy, Adoptive; Leukocytes, Mononuclear - immunology; Leukocytes, Mononuclear - transplantation; Mice; Mice, Inbred NOD; Mice, SCID; Mucin-1 - immunology; Mucin-1 - therapeutic use; Neoplasm Transplantation; Neoplasm, Residual - immunology; Neoplasm, Residual - therapy
• ISSN: 1107-3756
• DOI: 10.3892/ijmm.9.4.401

Mucin1 stimulated hematopoietic mononuclear cells (M1SHMC) from patients with breast cancer, adoptively transferred to non-obese diabetic, severe combined immunodeficient (NOD SCID) mice, extended survival in a therapy model of gross adenocarcinoma and prevented tumor growth in a model of minimal disease. M1SHMC exhibited specific lysis of a human breast adenocarcinoma cell line expressing mucin1, MCF-7 and produced interferon gamma. M1SHMC were injected intraperitoneally (IP) in NOD SCID mice after gross, palpable tumors appeared after MCF-7 were injected subcutaneously (SC). Survival was increased as compared to no M1SHMC controls. However tumors eventually regrew in all mice. To determine whether minimal disease (MD) could be controlled, NOD SCID were injected with MCF-7 cells, and on the same day, injected IP with M1SHMC. The M1SHMC injected mice were protected from tumor growth. These results imply that M1SHMC can prolong survival, but not cure NOD SCID mice bearing gross palpable adenocarcinomas. However in a minimal disease model tumor growth was prevented.