Renal carcinogenesis--insights into signaling pathways

Rom J Morphol Embryol. 2015;56(1):15-9.

Abstract

Renal cancer represents about 3% of all human malignancies, 96% of cases being sporadic forms and only 4% hereditary. Research in renal tumor pathogenesis is currently oriented on the genetic and proteins framework of the renal cell carcinoma, with the aim to translate the level of knowledge on tumor subtypes from histological to molecular issues, simultaneously with the deciphering of the manner in which the signaling pathways intervene in the pathogenic mechanism. Alterations identified in proto-oncogenes and tumor suppressor genes lead to abnormal and deficient transmission of signal in the signaling pathways, and initiate the carcinogenesis mechanism by increased proliferation of tumor cells. Although it seems obvious that the classic sequence of carcinogenesis is respected at the renal site, unfortunately, the manner in which signaling pathways are involved, in the specific context of renal tumors, is not extensively investigated. This paper assembles recent data in the mainstream regarding the dialogue opened between the molecules in Wnt÷β-catenin, PI3K÷AKT÷mTOR, and HGF÷cMET signaling pathways. The review is also justified by the fact that these molecules may represent potential prognosis markers and÷or therapeutic targets.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Carcinogenesis / metabolism*
  • Carcinoma, Renal Cell / metabolism*
  • Cell Line, Tumor
  • Cytoplasm / metabolism
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Kidney / metabolism
  • Kidney Neoplasms / metabolism*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction*
  • Wnt Proteins / metabolism
  • beta Catenin / metabolism

Substances

  • Wnt Proteins
  • beta Catenin
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt