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Production of novel-shaped microneedles to beat the actual disadvantages associated with solid microneedles for that transdermal shipping involving insulin.
Extranodal NK/T cell lymphoma, nasal type, is a rare type of non-Hodgkin's lymphoma (NHL), and the aetiology is not fully understood. Although the clinical outcome of anthracycline-based chemotherapy was dismal because of multidrug resistance (MDR). Novel therapeutic strategies including L-asparaginase-containing regimens, radiotherapy, sequential chemotherapy and radiotherapy, and concurrent chemoradiotherapy (CCRT) have remarkably improved outcomes. However, the overall survival (OS) rate of advanced stage patients is not satisfactory compared with patients with non-advanced-stage disease. Immunotherapy is a promising treatment for ENKTCL. Indeed, it has been proven that targeted therapies such as anti-CD30 antibodies and naked anti-CD38 antibodies are effective. In addition to these therapies that target cell surface antigens, therapies targeting intracellular signalling pathways and the microenvironment are considerably beneficial. EBV-driven overexpression of latent membrane proteins [LMP1 and LMP2] activates the pro-proliferation NF-κB/MAPK signalling pathway and leads to high PD-L1 expression. Binding of PD-L1 to PD-1 expressing cytotoxic T cells causes apoptosis and inactivation of T lymphocytes, achieving immune escape. On the basis of this mechanism, a variety of small molecular inhibitors, such as anti-PD-1 antibodies, NF-κB inhibitors, EBV antigens, and LMP1 and LMP2 antigens, can be applied. Via another signalling pathway the JAK/STAT pathway, upregulation and activation and mutation of genes promotes proliferation and ENKTCL lymphomagenesis, and JAK inhibitors have thus been applied. This article reviews recent advances in ENKTCL immunotherapy as a promising treatment for this fatal disease.Exosomes are a subtype of extracellular vesicles. They contain bioactive molecules, including nucleic acids, proteins and lipids. Among the currently described exosomes, a majority are potential candidates for the diagnosis and treatment of necrotizing enterocolitis (NEC). In this work, we reviewed existing literature reports on exosomes and explored their roles in NEC. Exosomes derived from intestinal epithelial cells (IECs) participates in the development of intestinal diseases, thus can potentially be utilized as biomarkers for NEC. Besides, exosomes of human milk have been demonstrated to protect IECs from oxidative stress, stimulate intestinal stem cells activity, improve the proliferation and migration of IECs, and lower the incidence and severity of experimental NEC. Further, exosomes produced by stem cells can reduce the severity of experimental NEC and protect the intestinal barrier function during NEC. Conclusively, exosomes have been shown to influence the pathogenesis of NEC and exert a protective effect on NEC. However, additional investigations would be urgently necessary to comprehensively elucidate the underlying mechanisms of exosomes in NEC.Cancer-testis antigens (CTA) are tumor antigens, present in the germ cells of testes, ovaries and trophoblasts, which undergo deregulated expression in the tumor and malignant cells. CTA genes are either X-linked or autosomal, favourably expressed in spermatogonia and spermatocytes, respectively. CTAs trigger unprompted humoral immunity and immune responses in malignancies, altering tumor cell physiology and neoplastic behaviors. CTAs demonstrate varied expression profile, with increased abundance in malignant melanoma and prostate, lung, breast and epithelial cell cancers, and a relatively reduced prevalence in intestinal cancer, renal cell adenocarcinoma and malignancies of immune cells. A combination of epigenetic and non-epigenetic agents regulates CTA mRNA expression, with the key participation of CpG islands and CpG-rich promoters, histone methyltransferases, cytokines, tyrosine kinases and transcriptional activators and repressors. eFT226 CTA triggers gametogenesis, in association with mutated tumorigenic genes and tumor repressors. The CTAs function as potential biomarkers, particularly for prostate, cervical, breast, colorectal, gastric, urinary bladder, liver and lung carcinomas, characterized by alternate splicing and phenotypic heterogeneity in the cells. Additionally, CTAs are prospective targets for vaccine therapy, with the MAGE-A3 and NYESO-1 undergoing clinical trials for tumor regression in malignant melanoma. They have been deemed important for adaptive immunotherapy, marked by limited expression in normal somatic tissues and recurrent up-regulation in epithelial carcinoma. Overall, the current review delineates an up-dated understanding of the intricate processes of CTA expression and regulation in cancer. It further portrays the role of CTAs as biomarkers and probable candidates for tumor immunotherapy, with a future prospect in cancer treatment.Candida albicans is a major opportunistic fungal pathogen of humans, especially in the oral cavity it involves in precancerous lesions. Numerous transcriptional regulators and hypha-specific genes involved in the morphogenesis mechanisms have been identified. Its virulence is predominantly attributed to the potentiality of morphological switching from yeast and pseudohyphae to hyphal growth. Giving attention in farnesol for prevention or intervention of its virulence sense and possible etiologic role in some uncovered premalignant diseases, in addition, to be a quorum-sensing signal molecule and relationship with HOG pathway, although its morphological switching inhibiting function has attracted high attention and got great progress in being elucidated, their exact mode of action is not completely understood. This report provides a review of characteristic aspects of farnesol signaling and HOG pathway during hyphal development. It also includes other associated pathways, molecules, and novel drug development based on the latest researches over the last decade. Furthermore, farnesol as immunomodulatory to host is an important inferring.LncRNAs and miRNAs are emerging players in epithelial ovarian cancer (EOC). LncRNA MALAT-1 and miR-22 play vital roles in the onset and development of multiple cancers. Both of them are abnormally expressed in ovarian cancer, but the molecular basis for their involvement in EOC is unclear. In this study, we found MALAT-1 was up-regulated but miR-22 was down-regulated in EOC tissues and cell lines when compared to normal ovarian epithelial cell line IOSE80. Both of MALAT-1shRNA and miR-22 mimics inhibited ovarian cell proliferation, migration, and invasion, while simultaneously overexpressing MALAT-1 and miR-22 largely canceled out this inhibitory effect. Consistently, MALAT-1 silencing and miR-22 overexpression restrained tumor growth and metastasis to lungs in nude mice, which could be largely counteracted by co-overexpressing MALAT-1 and miR-22. Mechanistically, MALAT-1 targeted and sponged miR-22, counteracting its inhibitory effect on c-myc and c-myc-mediated epithelial-mesenchymal transition. Our findings for the first time demonstrated that MALAT-1 supports EOC progression through sponging miR-22, providing a novel insight into the role of MALAT-1 in ovarian cancer.
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