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Tumorigenesis has traditionally been considered as a multi-step process involving the activation of oncogenes as well as the inactivation of tumor suppressor genes. However, the mechanisms driving cancer initiation and progression are not restricted to molecular alterations and instead should be viewed as a complex process that interfaces with the entire organism. This didactic review provides an integrated and global view of the key fundamental principles of cancer development., (Copyright © 2020 Société Française du Cancer. Published by Elsevier Masson SAS. All rights reserved.)

Acute kidney injury (AKI) is characterized by acute tubular necrosis (ATN) which involves mainly proximal tubules. Past AKI is associated with higher risk of chronic kidney disease (CKD). The MUC1 mucin is a large glycoprotein responsible for epithelial protection and locates to convoluted distal tubules and collecting ducts. Since MUC1 activates the epithelial-mesenchymal transition (EMT) in carcinoma cells, we hypothesized that MUC1 could be involved in epithelial tubular cell plasticity, a process that not only accompanies epithelial repair, but also participates into kidney fibrosis, histological substratum of CKD. In cultured human proximal cells and in human kidney allograft biopsies, we observed MUC1 induction in proximal tubules displaying ATN. Transient MUC1 induction localized with mesenchymal and stem-cell markers and was associated in vitro with reduced anoikis. In a mouse ischemia-reperfusion (IR) model, Muc1 expression mitigates severe tubular injury, as WT displayed less ATN than Muc1 KO mice. But, WT mice displayed more severe kidney fibrosis than Muc1 KO 28days after ischemia. Besides, sustained Muc1 expression in WT was associated with less kidney M2 macrophages. Human kidney biopsies performed within the first week (W1) of transplantation in the context of IR showed MUC1 W1 induction associated with EMT markers. Protocol biopsies performed 3months after demonstrated sustained abnormal MUC1 induction in atrophic tubules within kidney fibrosis. Altogether these data showed that sustained abnormal MUC1 induction accompanies failing epithelial repair, chronic inflammation and kidney fibrosis. In conclusion, MUC1 exerts opposite effects during kidney response to IR: first protective and then harmful., (Copyright © 2017 Elsevier B.V. All rights reserved.)

In mammalian cells, hypoxia, or inadequate oxygen availability, regulates the expression of a specific set of MicroRNAs (MiRNAs), termed "hypoxamiRs." Over the past 10 years, the appreciation of the importance of hypoxamiRs in regulating the cellular adaptation to hypoxia has grown dramatically. At the cellular level, each hypoxamiR, including the master hypoxamiR MiR-210, can simultaneously regulate expression of multiple target genes in order to fine-tune the adaptive response of cells to hypoxia. This review addresses the complex molecular regulation of MiRNAs in both physiological and pathological conditions of low oxygen adaptation and the multiple functions of hypoxamiRs in various hypoxia-associated biological processes, including apoptosis, survival, proliferation, angiogenesis, inflammation, and metabolism. From a clinical perspective, we also discuss the potential use of hypoxamiRs as new biomarkers and/or therapeutic targets in cancer and aging-associated diseases including cardiovascular and fibroproliferative disorders., (© 2017 Elsevier Inc. All rights reserved.)

Type 1 xanthinuria is a rare cause of urolithiasis due to xanthine dehydrogenase deficiency. Pediatric cases are exceptional. Through the genetic analysis of two cases, we discovered three mutations responsible for a loss of enzyme activity. The first one had a C.3536T>C missense mutation in the XDH gene and the other one was heterozygous for two mutations c.700+1G>T and c.31778_82delTCAT. We review the diagnostic methods, possible complications, and preventive measures for stone formation., (Copyright © 2015 Elsevier Masson SAS. All rights reserved.)