The involvement of the MAPK pathway in pilocytic astrocytomas

Pathol Res Pract. 2022 Apr:232:153821. doi: 10.1016/j.prp.2022.153821. Epub 2022 Feb 25.

Abstract

Pilocytic astrocytomas are the primary tumors most found in the first two decades of life, accounting for around 15% of all brain tumors. Research at the molecular level of pilocytic astrocytoma makes possible to compose an overview of what is known about the origin and development of the tumor. It is known that there are alterations in the Mitogen Activated Protein Kinase (MAPK) signaling pathway that are important auxiliary markers in diagnosis. This study seeks to list the main points about the involvement of this pathway in tumor formation in pilocytic astrocytoma. A review was conducted in search of published studies available in NCBI, PubMed, MEDLINE, Scielo and Google Scholar. The most frequent alteration is the gene fusion between BRAF and KIAA1549 genes, found in approximately 90% of pediatric cases. The second most common event is the BRAFV600E mutation, also often found in children than in adult cases. The molecular origin of pilocytic astrocytomas is related to alterations in the MAPK pathway, which acts with several functions in the brain such as memory formation, pain perception, induction of cortical neurogenesis, and midbrain and cerebellum development. Alterations in this pathway can be therapeutic targets in the treatment of patients with pilocytic astrocytoma. The MAPK pathway is extremely important and knowledge about its involvement in astrocytic tumors is essential for a better approach to the patient.

Keywords: Fusion; MAPK; Molecular; Mutation; Pilocytic astrocytoma; Therapy.

Publication types

  • Review

MeSH terms

  • Adult
  • Astrocytoma* / pathology
  • Brain Neoplasms* / diagnosis
  • Brain Neoplasms* / genetics
  • Child
  • Humans
  • Mitogen-Activated Protein Kinases / genetics
  • Mitogen-Activated Protein Kinases / metabolism
  • Mutation
  • Proto-Oncogene Proteins B-raf / genetics
  • Proto-Oncogene Proteins B-raf / metabolism
  • Signal Transduction / genetics

Substances

  • Proto-Oncogene Proteins B-raf
  • Mitogen-Activated Protein Kinases