Author: Yang P1, Jiang Y1, Rhea PR1, Coway T1, Chen D1, Gagea M1, Harribance SL2, Cohen L1
11 The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
22 Sean Harribance Institute for Parapsychology, Inc., Sugarland, TX, USA.
Conference/Journal: Integr Cancer Ther.
Date published: 2019 Jan-Dec
Other: Volume ID: 18 , Pages: 1534735419840797 , Special Notes: doi: 10.1177/1534735419840797. , Word Count: 273
Biofield therapies have gained popularity and are being explored as possible treatments for cancer. In some cases, devices have been developed that mimic the electromagnetic fields that are emitted from people delivering biofield therapies. However, there is limited research examining if humans could potentially inhibit the proliferation of cancer cells and suppress tumor growth through modification of inflammation and the immune system. We found that human NSCLC A549 lung cancer cells exposed to Sean L. Harribance, a purported healer, showed reduced viability and downregulation of pAkt. We further observed that the experimental exposure slowed growth of mouse Lewis lung carcinoma evidenced by significantly smaller tumor volume in the experimental mice (274.3 ± 188.9 mm3) than that of control mice (740.5 ± 460.2 mm3; P < .05). Exposure to the experimental condition markedly reduced tumoral expression of pS6, a cytosolic marker of cell proliferation, by 45% compared with that of the control group. Results of reversed phase proteomic array suggested that the experimental exposure downregulated the PD-L1 expression in the tumor tissues. Similarly, the serum levels of cytokines, especially MCP-1, were significantly reduced in the experimental group ( P < .05). Furthermore, TILs profiling showed that CD8+/CD4- immune cell population was increased by almost 2-fold in the experimental condition whereas the number of intratumoral CD25+/CD4+ (T-reg cells) and CD68+ macrophages were 84% and 33%, respectively, lower than that of the control group. Together, these findings suggest that exposure to purported biofields from a human is capable of suppressing tumor growth, which might be in part mediated through modification of the tumor microenvironment, immune function, and anti-inflammatory activity in our mouse lung tumor model.
KEYWORDS: Lewis lung carcinoma; PD-L1; biofield; immune modulation
PMID: 30947564 DOI: 10.1177/1534735419840797