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M-HIFU inhibits tumor growth, suppresses STAT3 activity and enhances tumor specific immunity in a transplant tumor model of prostate cancer.

dc.contributor.author Huang, X
dc.contributor.author Liang, Meihua
dc.contributor.author Lo, Hui-Wen
dc.contributor.author Robertson, Cary Nobles
dc.contributor.author Shinohara, Mari L
dc.contributor.author Yuan, F
dc.contributor.author Zhong, Pei
dc.coverage.spatial United States
dc.date.accessioned 2017-05-01T15:02:14Z
dc.date.available 2017-05-01T15:02:14Z
dc.date.issued 2012
dc.identifier https://www.ncbi.nlm.nih.gov/pubmed/22911830
dc.identifier PONE-D-12-05711
dc.identifier.uri http://hdl.handle.net/10161/14230
dc.description.abstract OBJECTIVE: In this study, we explored the use of mechanical high intensity focused ultrasound (M-HIFU) as a neo-adjuvant therapy prior to surgical resection of the primary tumor. We also investigated the role of signal transducer and activator of transcription 3 (STAT3) in M-HIFU elicited anti-tumor immune response using a transplant tumor model of prostate cancer. METHODS: RM-9, a mouse prostate cancer cell line with constitutively activated STAT3, was inoculated subcutaneously in C57BL/6J mice. The tumor-bearing mice (with a maximum tumor diameter of 5∼6 mm) were treated by M-HIFU or sham exposure two days before surgical resection of the primary tumor. Following recovery, if no tumor recurrence was observed in 30 days, tumor rechallenge was performed. The growth of the rechallenged tumor, survival rate and anti-tumor immune response of the animal were evaluated. RESULTS: No tumor recurrence and distant metastasis were observed in both treatment groups employing M-HIFU + surgery and surgery alone. However, compared to surgery alone, M-HIFU combined with surgery were found to significantly inhibit the growth of rechallenged tumors, down-regulate intra-tumoral STAT3 activities, increase cytotoxic T cells in spleens and tumor draining lymph nodes (TDLNs), and improve the host survival. Furthermore, M-HIFU combined with surgery was found to significantly decrease the level of immunosuppression with concomitantly increased number and activities of dendritic cells, compared to surgery alone. CONCLUSION: Our results demonstrate that M-HIFU can inhibit STAT3 activities, and when combined synergistically with surgery, may provide a novel and promising strategy for the treatment of prostate cancers.
dc.language eng
dc.relation.ispartof PLoS One
dc.relation.isversionof 10.1371/journal.pone.0041632
dc.subject Animals
dc.subject Cell Line, Tumor
dc.subject Cell Proliferation
dc.subject Cytotoxicity, Immunologic
dc.subject Dendritic Cells
dc.subject Disease Models, Animal
dc.subject High-Intensity Focused Ultrasound Ablation
dc.subject Humans
dc.subject Immunity
dc.subject Lymph Nodes
dc.subject Lymphocyte Count
dc.subject Male
dc.subject Mice
dc.subject Mice, Inbred C57BL
dc.subject Neoplasm Transplantation
dc.subject Phosphorylation
dc.subject Prostatic Neoplasms
dc.subject STAT3 Transcription Factor
dc.subject Spleen
dc.subject Survival Analysis
dc.subject T-Lymphocytes, Cytotoxic
dc.subject T-Lymphocytes, Regulatory
dc.title M-HIFU inhibits tumor growth, suppresses STAT3 activity and enhances tumor specific immunity in a transplant tumor model of prostate cancer.
dc.type Journal article
pubs.author-url https://www.ncbi.nlm.nih.gov/pubmed/22911830
pubs.begin-page e41632
pubs.issue 7
pubs.organisational-group Basic Science Departments
pubs.organisational-group Biomedical Engineering
pubs.organisational-group Clinical Science Departments
pubs.organisational-group Duke
pubs.organisational-group Duke Cancer Institute
pubs.organisational-group Immunology
pubs.organisational-group Institutes and Centers
pubs.organisational-group Mechanical Engineering and Materials Science
pubs.organisational-group Molecular Genetics and Microbiology
pubs.organisational-group Pratt School of Engineering
pubs.organisational-group School of Medicine
pubs.organisational-group Surgery
pubs.organisational-group Surgery, Surgical Sciences
pubs.organisational-group Surgery, Urology
pubs.publication-status Published
pubs.volume 7
dc.identifier.eissn 1932-6203


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