English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Breast cancer represents a major health problem in women, with more than 1,000,000 new cases and 370,000 deaths yearly worldwide [1]. Perhaps more worrisome is an apparently increasing incidence of breast cancer among younger women under 40 years of age recently reported in many countries worldwide [2-4]. The lethality of breast cancer is largely due to metastasis, preferentially to the lymph nodes, lungs and bones [5]; in order to delay the progression of breast cancer and prolong patient life, more effective chemopreventive and antimetastatic treatments and less toxic chemotherapeutic agents are desperately required. Vascular endothelial growth factor-C (VEGF-C) is expressed in a variety of malignant tumors including mammary cancer [6] and over-expression of VEGF-C has been reported to be associated with lymph node metastasis and poor prognosis in breast cancer patients [7,8]. A number of animal studies using cell lines [9-11] and transgenic mice[12] have been conducted in an attempt to demonstrate that VEGF-C over-expression is able to promote cancer metastasis. Using a ‘RNA interference’ approach with an immunocompetent mouse mammary cancer model, we previously demonstrated that inhibition of VEGF-C or VEGF-A by gene silencing using vectors expressing short interfering RNA (siRNA) leads to suppression of lymphatic and/or hematogenous metastasis [13]. The cytokine interleukin-12 (IL-12), a heterodimer composed of p35 and p40 subunits, is produced primarily by dendritic cells, macrophages/monocytes, and neutrophils and functions in enhancing the activity of cytotoxic T lymphocytes and NK cells. Both subunits are necessary to exert biological activity [14]. IL-12 plays an important role in the induction of a cell-mediated immune response [15]. This cytokine is also involved in the differentiation of native T cells to the Th1 subset, and induces production of interferon- (IFN) in both T and NK cells. In addition, IL-12 has been shown to exert a potent anti-neoplastic effect in a

Inhibition of Tumor Growth and Metastasis by a Combination of Anti-VEGF-C and Enhanced IL-12 Therapy in an Immunocompetent Mouse Mammary Cancer Model