Prophylactic vaccination against infectious diseases is one of the most successful public health measures of our lifetime. More recently, therapeutic vaccination against established diseases such as cancer has proven to be more challenging. In the host, cancer cells evade immunologic regulation by multiple means, including altering the antigens expressed on their cell surface or recruiting inflammatory cells that repress immune surveillance. Nevertheless, recent clinical data suggest that two classes of antigens show efficacy for the development of anticancer vaccines: tumor-associated antigens and neoantigens. In addition, many different vaccines derived from antigens based on cellular, peptide/protein, and genomic components are in development to establish their efficacy in cancer therapy. Some vaccines have shown promising results, which may lead to favorable outcomes when combined with standard therapeutic approaches. This review provides an overview of the innate and adaptive immune systems, their interactions with cancer cells, and the development of various different vaccines for use in anticancer therapeutics.
Long noncoding RNAs (lncRNAs) have been identified to play a role in the progression of many different types of cancer. Some biological processes that are involved with lncRNA include but are not limited to chromatin organization, transcriptional and post-transcriptional gene expression, and protein and transcript trafficking. When lncRNAs are aberrantly expressed, disruption in the biological processes can cause tumor proliferation and progression leading to cancers. Studies have shown the role of lncRNAs in association with breast cancers. While estrogen receptor alpha positive (ERα+) breast cancer responds well to anti-estrogen treatment, the cancer can become refractory. With breast cancer as one of the leading causes of mortality in women, deeper understanding of lncRNAs can establish it as a potential therapeutic target. It will be determined the functional mechanisms by which lncRNAs, specifically lncRNA161, drives hormone-resistance in breast cancer. LncRNA161 was selected from a comprehensive list of lncRNAs due to it being expressed in reproductive tissue, being tamoxifen resistant, being robustly regulated by estrogen, and its association with the chromatin. It was determined that lncRNA161 was upregulated in breast cancers. When lncRNA161 was treated with estrogen, there was transcriptional activation and localization to the chromatin. Subsequent knockdown of lncRNA161 affected other genes in the estrogen signaling pathway. Overexpression of lncRNA161 demonstrated increased proliferation, and knockdown showed decreased proliferation indicating a role of lncRNA161 in tumor proliferation and progression in breast cancer. Altogether, the results suggest lncRNA161’s involvement in the estrogen signaling pathway and establish it as a potential therapeutic target in hormone-refractory breast cancer. Supported by grant from the Cancer Prevention and Research Institute of Texas to S.S.G.
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