Abbreviations (no more than 10): CT = Computed Tomography CXR = Chest radiograph RT-PCR = Reverse Transcription Polymerase Chain Reaction SARS = Severe acute respiratory syndrome Key Results: 1. Chest radiograph and CT findings of 21 patients with confirmed 2019 novel coronavirus infection in Shenzhen and Hong Kong are described and compared 2. A literature review and tabulation of the radiographic features in original publications are presented 3. One asymptomatic patient had evidence of consolidation on chest CT Abstract: Background: COVID-19 (formerly known as the 2019 novel coronavirus [2019-nCoV]) has rapidly spread in mainland China and into multiple countries worldwide. The radiographic profile of this infection continues to evolve as more cases present beyond the epicenter of Wuhan, China. Purpose: We present 21 COVID-19 cases from two Chinese centers with CT and chest radiograph (CXR) findings, as well as follow-up imaging in 5 cases. Materials and Methods: Retrospective study in Shenzhen and Hong Kong. Patients with COVID-19 infection were included. A systematic review of the published literature on COVID-19 infection's radiological features. Results: The predominant imaging pattern is of ground-glass opacification with occasional consolidation in the peripheries. Pleural effusions and lymphadenopathy were absent in all cases. Patients demonstrate evolution of the ground-glass opacities into consolidation, and subsequent resolution of the airspaces changes. Ground-glass and consolidative opacities visible on CT are sometimes undetectable on chest radiographs, suggesting that CT is a more sensitive imaging modality for investigation. The systematic review identified 4 other studies confirming the findings of bilateral and peripheral ground glass with or without consolidation as the predominant finding on CT chest examinations. Conclusion: The COVID-19 infection pulmonary manifestation is predominantly characterized by ground-glass opacification with occasional consolidation on CT. Radiographic findings in patients presenting in Shenzhen and Hong Kong are in keeping with 4 previous publications from other sites.

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In the tumour microenvironment (TME), immunogenic cell death (ICD) plays a major role in stimulating the dysfunctional antitumour immune system. Chronic exposure of damage‐associated molecular patterns (DAMPs) attracts receptors and ligands on dendritic cells (DCs) and activates immature DCs to transition to a mature phenotype, which promotes the processing of phagocytic cargo in DCs and accelerates the engulfment of antigenic components by DCs. Consequently, via antigen presentation, DCs stimulate specific T cell responses that kill more cancer cells. The induction of ICD eventually results in long‐lasting protective antitumour immunity. Through the exploration of ICD inducers, recent studies have shown that there are many novel modalities with the ability to induce immunogenic cancer cell death. In this review, we mainly discussed and summarized the emerging methods for inducing immunogenic cancer cell death. Concepts and molecular mechanisms relevant to antitumour effects of ICD are also briefly discussed.

Contact with food animals was associated with SARS-CoV infection in the People’s Republic of China.

Objectives Although myeloid-derived suppressive cells (MDSCs) have been linked to T-cell tolerance, their role in autoimmune rheumatoid arthritis (RA) remains elusive. Here we investigate the potential association of MDSCs with the disease pathogenesis using a preclinical model of RA and specimen collected from RA patients. Methods The frequency of MDSCs in blood, lymphoid tissues, inflamed paws, or synovial fluid and their association with disease severity, tissue inflammation, and the levels of pathogenic T-helper (Th) 17 cells was examined in arthritic mice or in patients with RA (n=35) and osteoarthritis (OA, n=15). The MDSCs in arthritic mice were also characterized for their phenotype, inflammation status, T-cell suppressive activity, and their capacity of pro-Th17 cell differentiation. The involvement of MDSCs in the disease pathology and a Th17 response was examined by adoptive transfer or antibody depletion of MDSCs in arthritic mice or by co-culturing mouse or human MDSCs with naïve CD4+ T cells under Th17-polarizing conditions. Results MDSCs significantly expanded in arthritic mice and in RA patients, which correlated positively with disease severity and an inflammatory Th17 response. While displaying T-cell suppressive activity, MDSCs from arthritic mice produced high levels of inflammatory cytokines (e.g., IL-1β, TNF-α). Both mouse and human MDSCs promoted Th17 cell polarization ex vivo. Transfer of MDSCs facilitated disease progression, whereas their elimination in arthritic mice ameliorates disease symptoms concomitant with reduction of IL-17A/Th17 cells. Conclusions Our studies suggest that proinflammatory MDSCs with their capacity to drive Th17 cell differentiation may be a critical pathogenic factor in autoimmune arthritis.

Carcinoma cells undergo epithelial-mesenchymal transition (EMT); however, contributions of EMT heterogeneity to disease progression remain a matter of debate. Here, we addressed the EMT status of ex vivo cultured circulating and disseminated tumor cells (CTCs/DTCs) in a syngeneic mouse model of metastatic breast cancer (MBC). Epithelial-type CTCs with a restricted mesenchymal transition had the strongest lung metastases formation ability, whereas mesenchymal-type CTCs showed limited metastatic ability. EpCAM expression served as a surrogate marker to evaluate the EMT heterogeneity of clinical samples from MBC, including metastases, CTCs, and DTCs. The proportion of epithelial-type CTCs, and especially DTCs, correlated with distant metastases and poorer outcome of patients with MBC. This study fosters our understanding of EMT in metastasis and underpins heterogeneous EMT phenotypes as important parameters for tumor prognosis and treatment. We further suggest that EpCAM-dependent CTC isolation systems will underestimate CTC numbers but will quantify clinically relevant metastatic cells.

Asplatin, a fusion of aspirin and cisplatin, exhibits significant cytotoxicity in tumor cells and almost fully overcomes the drug resistance of cisplatin resistant cells. Asplatin is highly accumulated in cancer cells and is activated upon the reduction by ascorbic acid.

Cancer stem cells (CSCs) represent a major source of treatment resistance and tumor progression. However, regulation of CSCs stemness is not entirely understood. Here, we report that TSPAN8 expression is upregulated in breast CSCs, promotes the expression of the stemness gene NANOG, OCT4, and ALDHA1, and correlates with therapeutic resistance. Mechanistically, TSPAN8 interacts with PTCH1 and inhibits the degradation of the SHH/PTCH1 complex through recruitment of deubiquitinating enzyme ATXN3. This results in the translocation of SMO to cilia, downstream gene expression, resistance of CSCs to chemotherapeutic agents, and enhances tumor formation in mice. Accordingly, expression levels of TSPAN8, PTCH1, SHH, and ATXN3 are positively correlated in human breast cancer specimens, and high TSPAN8 and ATXN3 expression levels correlate with poor prognosis. These findings reveal a molecular basis of TSPAN8-enhanced Sonic Hedgehog signaling and highlight a role for TSPAN8 in promoting cancer stemness.