Sulconazole inhibits PD-1 expression in immune cells and cancer cells malignant phenotype through NF-κB and calcium activity repression.

The overexpression of the immunoinhibitory receptor programmed death-1 (PD1) on T-cells is involved in immune evasion in cancer. The use of anti-PD-1/PDL-1 strategy has deeply changed the therapies of cancers and patient survival. However, their efficacy diverges greatly along with tumor type and patient populations.

[Mechanisms of cancer drug resistance].

Despite decades of research into the molecular mechanisms of cancer and the development of new treatments, drug resistance persists as a major problem. This is in part due to the heterogeneity of cancer, including the diversity of tumor cell lineage and cell plasticity, the spectrum of somatic mutations, the complexity of microenvironments, and immunosuppressive characteristic, then necessitating the use of many different therapeutic approaches. We summarize here the biological causes of resistance, thus offering new perspectives for tackle drug resistance.

Integrative analysis of genomic and transcriptomic alterations of and in cancer.

The and genes have been shown by numerous groups to be functionally associated with adenocarcinoma progression and metastasis. In this paper, we explore the data available in databases concerning genomic and transcriptomic features of these two genes: the NCBI dbSNP database was used to explore the presence and roles of constitutional SNPs, and the NCI, Cancer Cell Line Encyclopedia (CCLE) and TCGA databases were used to explore somatic mutations and copy number variations (CNVs), as well as mRNA expression of these genes in human cancer cell lines and tumours. Relationships of / expression with whole-genome mRNA expression and cancer features (i.