Recent advancements in the molecular biology of pituitary adenomas.
Autor: | Zheng AC; Department of Neurosurgery; University of California at San Francisco (UCSF) San Francisco, CA, USA., Wang EJ; Department of Neurosurgery; Warren Alpert Medical School of Brown University Providence, RI, USA., Aghi MK; Department of Neurosurgery; University of California at San Francisco (UCSF) San Francisco, CA, USA. |
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Jazyk: | angličtina |
Zdroj: | Expert review of endocrinology & metabolism [Expert Rev Endocrinol Metab] 2022 Jul; Vol. 17 (4), pp. 293-304. Date of Electronic Publication: 2022 Jun 14. |
DOI: | 10.1080/17446651.2022.2082942 |
Abstrakt: | Introduction: Pituitary adenomas are a common and diverse group of intracranial tumors arising from the anterior pituitary that are usually slow-growing and benign, but still pose a significant healthcare burden to patients. Additionally, they are increasing in both incidence and prevalence, leading to a need for better understanding of molecular changes in the development of these tumors. Areas Covered: A PubMed literature search was conducted using the terms 'pituitary adenoma' in combination with keywords related to secretory subtype: lactotroph, somatotroph, corticotroph, gonadotroph and null cell, in addition to their transcription factor expression: PIT1, TPIT, and SF-1. Articles resulting from this search were analyzed, as well as relevant articles cited as their references. In this review, we highlight recent advances in the genetic and epigenetic characterization of individual pituitary adenoma subtypes and the effect it may have on guiding future clinical treatment of these tumors. Expert Opinion: Understanding the molecular biology of pituitary adenomas is a fundamental step toward advancing the treatment of these tumors. Yet crucial knowledge gaps exist in our understanding of the underlying molecular biology of pituitary adenomas which can potentially be addressed by turning to differentially activated molecular pathways in tumor relative to normal gland. |
Databáze: | MEDLINE |
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