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Somatic Activating ESR1 Mutation in an Aggressive Prolactinoma.

Ticiana Paes1, Jacobo Buelvas Mebarak1, John C Magnotto1

  • 1Division of Endocrinology, Diabetes and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.

The Journal of Clinical Endocrinology and Metabolism
|September 6, 2024
PubMed
Summary
This summary is machine-generated.

A specific genetic mutation, ESR1Y537S, was found in an aggressive prolactinoma. This estrogen receptor signaling pathway discovery led to successful targeted therapy with elacestrant, controlling tumor growth and reducing prolactin levels.

Keywords:
ESR1OncoPanelbreast cancercell-free DNAprolactinomarecurrent

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Area of Science:

  • Endocrinology
  • Oncology
  • Genetics

Background:

  • Prolactinomas, pituitary tumors secreting prolactin, have a poorly understood genetic basis.
  • Estrogen receptor signaling is implicated in various cancers, but its role in prolactinomas is unclear.

Purpose of the Study:

  • To identify somatic genetic alterations in prolactinomas.
  • To investigate the role of estrogen receptor alpha (ESR1) mutations in aggressive prolactinoma.

Main Methods:

  • Massively parallel sequencing (OncoPanel) was used to analyze the genetic profile of prolactinomas.
  • Somatic mutations and copy number variations were assessed in a cohort of 20 patients.

Main Results:

  • An activating ESR1Y537S mutation was identified in one aggressive prolactinoma.
  • This prolactinoma exhibited a high number of copy number variations (233 events).
  • Treatment with elacestrant and radiotherapy controlled tumor growth and reduced prolactin levels in the patient with the ESR1 mutation.

Conclusions:

  • The ESR1Y537S mutation may contribute to prolactinoma aggressiveness.
  • Estrogen receptor signaling is significant in prolactinoma development and progression.
  • Targeted therapy with elacestrant offers a potential treatment strategy for aggressive prolactinomas with ESR1 mutations.