[Lani]

progress is being made im studies in mice so far, but now also using human immune cells removed from the body--next step, take these cells and replace them into the person they were taken from after treating them outiside the body...Something similar has been done with melanoma and other tumors at the NIH and the patients have gone from metastasis-riddled to NED and the results have been long-lasting 7,8,9 yrs etc. The technique is known as adoptive cell therapy.

So far it has been expensive and labor-intesive so only small trials done, but each year at AACR meetings more and more papers are given on this technique and how to make it better, cheaper, simpler-- this is tehe first paper I have seen utilizing it specifically against her2+bc even if it is in a mouse model

Breast Cancer Res Treat. 2013 Nov;142(1):45-57. doi: 10.1007/s10549-013-2733-5. Epub 2013 Oct 25.
Peripheral blood mononuclear cells of patients with breast cancer can be reprogrammed to enhance anti-HER-2/neu reactivity and overcome myeloid-derived suppressor cells.
Payne KK, Zoon CK, Wan W, Marlar K, Keim RC, Kenari MN, Kazim AL, Bear HD, Manjili MH.
Source
Department of Microbiology and Immunology, Virginia Commonwealth University, Massey Cancer Center, Box 980035, 401 College Street, Richmond, VA, 23298, USA.
Abstract
Two major barriers in the immunotherapy of breast cancer include tumor-induced immune suppression and the establishment of long-lasting immune responses against the tumor. Recently, we demonstrated in an animal model of breast carcinoma that expanding and reprogramming tumor-sensitized lymphocytes, ex vivo, yielded T memory (Tm) cells as well as activated CD25+ NKT cells and NK cells. The presence of activated CD25+ NKT and NK cells rendered reprogrammed T cells resistant to MDSC-mediated suppression, and adoptive cellular therapy (ACT) of reprogrammed lymphocytes protected the host from tumor development and relapse. Here, we performed a pilot study to determine the clinical applicability of our protocol using peripheral blood mononuclear cells (PBMCs) of breast cancer patients, ex vivo. We show that bryostatin 1 and ionomycin combined with IL-2, IL-7, and IL-15 can expand and reprogram tumor-sensitized PBMCs. Reprogrammed lymphocytes contained activated CD25+ NKT and NK cells as well as Tm cells and displayed enhanced reactivity against HER-2/neu in the presence of MDSCs. The presence of activated NKT cells was highly correlated with the rescue of anti-HER-2/neu immune responses from MDSC suppression. Ex vivo blockade experiments suggest that the NKG2D pathway may play an important role in overcoming MDSC suppression. Our results show the feasibility of reprogramming tumor-sensitized immune cells, ex vivo, and provide rationale for ACT of breast cancer patients.
PMID: 24197563