Angiogenesis is the mechanism by which new blood vessels are formed by tumours to provide them with the nutrients to continue developing. Antiangiogenic drugs obstruct this mechanism precisely. Typically, this form of treatment has positive short-term effects, reducing tumour development. Interestingly, some studies show that these therapies improve tumour invasiveness and facilitate more aggressive behaviour, leading to poor prognosis.

Several studies show that in some cases, antiangiogenic drugs improve the aggressiveness of tumours, and in others, they remain unaffected. These findings confirm the heterogeneous effects of antiangiogenic therapy and how these can have a significant influence on normal tumour development and cause malignancy. The study employed multiple bioinformatics tools that pointed to the presence of a cell signalling pathway for genetic and molecular analyses, specifically the ALDH1A3 gene, in the divergent response to antiangiogenic therapy.

Several models were created to study the tumor behavior with the antiangiogenic treatment, and determine the existing interpatient variation. These models consist of the implantation of renal tumour biopsies in patients in the same mouse tissue, which replicate the heterogeneity between patients and recognise essential aspects of tumour evolution. It is a preclinical method with great potential. The study of genes expressed by kidney tumours after antiangiogenic therapy and their association with subsequent tumour response has allowed the discovery of biomarkers that can differentiate between invasive and non-invasive tumours.

Journal of Clinical & Experimental Nephrology focuses on the dissemination of the latest  advancements on the current knowledge on all the aspects of Nephrology such as Peritoneal Dialysis, Kidney Diseases, Acute Renal Replacement Therapy, Chronic Kidney Disease, End-Stage Renal Diseases, Lupus Nephritis and Renal Transplantation.

Regards,

Calvin Parker
Journal of Clinical & Experimental Nephrology
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