title: Human biofield therapy does not affect tumor size but modulates immune responses in a mouse model for breast cancer.
abstract: OBJECTIVE
  To assess the effect of human biofield therapy, an integrative medicine modality, on the development of tumors and metastasis, and immune function in a mouse breast cancer model.
  
  
  METHODS
  Mice were injected with 66cl4 mammary carcinoma cells. In study one, mice received biofield therapy after cell injection. In study two, mice were treated by the biofield practitioner only prior to cell injection. Both studies had two control groups of mock biofield treatments and phosphate-buffered saline injection. Mice were weighed and tumor volume was determined. Blood samples were collected and 32 serum cytokine/chemokine markers were measured. Spleens/popliteal lymph nodes were isolated and dissociated for fluorescent-activated cell sorting (FACS) analysis of immune cells or metastasis assays in cell culture.
  
  
  RESULTS
  No significant differences were found in weight, tumor size or metastasis. Significant effects were found in the immune responses in study one but no additional effects were found in study two. In study one, human biofield treatment significantly reduced percentage of CD4(+)CD44loCD25(+) and percentage of CD8(+) cells, elevated by cancer in the lymph nodes, to control levels determined by FACS analysis. In the spleen, only CD11b(+) macrophages were increased with cancer, and human biofield therapy significantly reduced them. Of 11 cytokines elevated by cancer, only interferon-γ, interleukin-1, monokine induced by interfer-γ, interleukin-2 and macrophage inflammatory protein-2 were significantly reduced to control levels with human biofield therapy.
  
  
  CONCLUSIONS
  Human biofield therapy had no significant effect on tumor size or metastasis but produced significant effects on immune responses apparent in the down-regulation of specific lymphocytes and serum cytokines in a mouse breast cancer model.
authors.affiliation: Department of Surgery, University of Connecticut Health Center, Farmington, CT 06030, USA.
authors.forename: Gloria
authors.initials: G
authors.lastname: Gronowicz
authors.affiliation: Department of Immunology, University of Connecticut Health Center, Farmington, CT 06030, USA.|Hartford Healthcare, Hartford Hospital, Hartford, CT 06102-5037, USA.
authors.forename: Eric R
authors.initials: ER
authors.lastname: Secor
authors.affiliation: Department of Surgery, University of Connecticut Health Center, Farmington, CT 06030, USA.
authors.forename: John R
authors.initials: JR
authors.lastname: Flynn
authors.affiliation: Department of Reconstructive Sciences, University of Connecticut Health Center, Farmington, CT 06030, USA.
authors.forename: Liisa T
authors.initials: LT
authors.lastname: Kuhn
mesh_terms: D000818:Animals; D001943:Breast Neoplasms / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D016207:Cytokines / Q000097:blood; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D055048:Integrative Medicine; D008214:Lymphocytes / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D012107:Research Design; D047368:Tumor Burden; D023041:Xenograft Model Antitumor Assays
chemical_list: D016207:Cytokines