The CONSORT-EHEALTH checklist is intended for authors of randomized trials evaluating web-based and Internet-based applications/interventions, including mobile interventions, electronic games (incl multiplayer games), social media, certain telehealth applications, and other interactive and/or networked electronic applications. Some of the items (e.g. all subitems under item 5 -description of the intervention) may also be applicable for other study designs.The goal of the CONSORT EHEALTH checklist and guideline is to be a) a guide for reporting for authors of RCTs, b) to form a basis for appraisal of an ehealth trial (in terms of validity) CONSORT-EHEALTH items/subitems are MANDATORY reporting items for studies published in the Journal of Medical Internet Research and other journals / scientific societies endorsing the checklist.Items numbered 1., 2., 3., 4a., 4b etc are original CONSORT or CONSORT-NPT (nonpharmacologic treatment) items. Items with Roman numerals (i., ii, iii, iv etc.) are CONSORT-EHEALTH extensions/clarifications.As the CONSORT-EHEALTH checklist is still considered in a formative stage, we would ask that you also RATE ON A SCALE OF 1-5 how important/useful you feel each item is FOR THE PURPOSE OF THE CHECKLIST and reporting guideline (optional).

Aberrant expression of B7-H4 occurs across a broad spectrum of human cancers. The aim of this study was to investigate the key role of B7-H4 during tumorigenesis and metastasis of human lung cancer. Our data showed that the shRNA-mediated disruption of B7-H4 markedly inhibited tumor cell proliferation, invasion and migration, increased cell apoptosis and arrested cell cycle at G0/G1. These changes were accompanied by a marked increase in Bax and caspase-3/caspase-8, but a decrease in Bcl-2, cyclinD1 and activation of AKT. In addition, our shRNA-mediated disruption of B7-H4 led to a marked decrease in tumor growth in the immune-compromised mice. Importantly, B7-H4 was expressed in 53.33% of lung carcinomas from our patient cohort (n = 90), but not in any of adjacent non-cancerous tissues, according to our IHC analyses. In particular, B7-H4 expression appeared to be associated with lymph node metastasis (P = 0.008) and TNM stage (P = 0.012). Taken together, our study demonstrates a strong promoting role of B7-H4 in lung tumor growth, progression and metastasis, and supports its potential as a therapeutic target for the treatment of the disease.

microRNAs are small, non-coding RNAs that contribute into various biological processes during cancer progression. However, the potential role of miR-489 in the development of Non-Small Cell Lung Cancer (NSCLC) is not demonstrated. In present study, miR-489 was down-regulated both in tumor tissues and cells. Inhibition of miR-489 promoted cells invasion by using an invasion assay. Furthermore, miR-489 could regulate SUZ12 as shown by luciferase reporter and Western blot assays. Aberrant miR-489 expression could regulate the molecular changes (E-cadherin, N-cadherin, and Vimentin) of epithelial mesenchymal transition (EMT). In conclusion, our study revealed that miR-489 may play an essential role in the progression of NSCLC.

The genetic diversity of avian leukosis virus subgroup J (ALV-J) is determined not only by the env gene, but also by its 39 UTR and 39 LTR. They all play important roles in extending the host range and tumour development. In the present study, one ALV-J strain (ZB110604-6) from Black-Bone Silky Fowl (BSF) and three ALV-J strains (ZB110604-3/4/5) from grey partridge (GP), which bore multiple tumours and breed in one house of Farm A, were demonstrated extending their host to GP, while two other ALV-J strains (LC110515-3/4) from BSF of Farm B could not infect the embryo fibroblast of GP. The BSF is a unique species of chicken in China, while the GP is a close relative of the pheasant that previously demonstrated resistance to ALV-J. Histopathology showed that various tumours were induced by ALV-J in the two species. Phylogenetic tree analysis showed that the isolates from Farms A and B, rather than species, belong to two different clusters of ALV-J. Genetic mutations analysis revealed that the isolates obtained from Farm A showed a higher frequency of mutation in the hypervariable region 2 domain than in other variable regions of the gp85 gene. From the nucleotide alignment of the 39 UTR and 39 LTR gene, and the spectrum of tumours observed in this study, we speculate that the deletions or mutations in the redundant transmembrane region, E element and U3 (CAAT boxes, CArG box and Y box) might associate with tumour formation and development. The extension of the host range of ALV-J to the GP suggested that housing different species together provides more opportunities for ALV-J to evolve rapidly.