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Uterine fibroid tissue

Molecular classification: Other. Uterine fibroid tissue is a benign monoclonal smooth‑muscle neoplasm with extracellular matrix overproduction; it is not a molecular class like receptor/enzyme/ion channel.

Overview

Uterine fibroids (uterine leiomyomas) are benign, monoclonal smooth-muscle neoplasms of the uterine myometrium, highly prevalent in reproductive-age women, characterized by estrogen/progesterone-dependent growth and excessive extracellular matrix deposition.[3][6][2] They comprise genetically and molecularly distinct subclasses, most commonly driven by MED12 mutations or HMGA2 overexpression, which differ in clinical features and therapeutic response, including to the progesterone receptor modulator ulipristal acetate.[1][3] Current medical therapies act on hormonal pathways (PR modulation, GnRH axis suppression) rather than on a single fibroid-specific molecular target.[1]

Other names: Uterine fibroidUterine leiomyomaLeiomyomaMyoma

Mechanism of action

Progesterone receptor modulation (e.g., ulipristal reduces fibroid volume via PR signaling pathways; response varies by molecular subclass) Suppression of pituitary gonadotropins via GnRH analogs → decreased ovarian estrogen/progesterone → fibroid shrinkage, often with regrowth after cessation

Biological functions

Cell proliferation (hormone-responsive growth of smooth muscle cells)Extracellular matrix production and fibrosisAngiogenesis and inflammation (reported contributions in pathogenesis)Steroid hormone signaling dependence (estrogen and progesterone)

Disease associations

Other. Benign tumor of the uterus (gynecologic benign neoplasm) with significant morbidity (bleeding, pain, infertility) but not cancer.Rare differential with uterine leiomyosarcoma; overlap complicates diagnosis.

Safety considerations

Pharmacotherapy limitations: variable response; regrowth after GnRH therapy; PR modulator hepatotoxicity concerns have constrained use in some regions (regulatory context not specified in provided sources; general limitation noted).Diagnostic challenge distinguishing fibroids from leiomyosarcoma preoperatively; overlapping features can affect surgical planning.Heterogeneity within tumors (smooth muscle cells vs tumor-associated fibroblasts) and hormone response diversity complicate predictable outcomes.

Interacting drugs

Ulipristal acetate (selective progesterone receptor modulator)

1 more in the full profile.

Biomarkers

Molecular subclasses defined by driver alterations: MED12 mutations and HMGA2 overexpression; these subtypes show distinct biology and differential response to ulipristal (MED12-mutant fibroids more likely to shrink than HMGA2-driven).Additional drivers/markers reported in subsets: FH deficiency; COL4A5–COL4A6 rearrangements; emerging serum/urine oxidative stress markers (investigational, not established for clinical selection).Imaging-based assessment (ultrasound/MRI) remains standard for diagnosis and monitoring; no universally accepted blood biomarker yet.

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