Abstract
Uterine fibroids (UF; aka leiomyoma, myomas) are the most common benign tumors of
female reproductive tract. They are highly prevalent, with 70 to 80% of women burdened
by the end of their reproductive years. Fibroids are a leading cause of pelvic pain,
abnormal vaginal bleeding, pelvic bulk symptoms, miscarriage, and infertility. They
are the leading indication for hysterectomy, and costs exceed 34 billion dollars annually
in the United States alone. Recently, somatic mutations in exons 1 and 2 of Med12
gene emerged as common UF driver mutations. Unfortunately, the detailed etiology of
UF is not fully realized. Particularly, very little is known about possible dysregulation
of inflammatory and immune processes and their possible contribution to UF pathogenesis.
The notion on possible impact of altered estrogen and progesterone signaling in UF
on inflammatory responses and DNA repair machinery that can conceivably lead to tumor-specific
somatic mutation is indeed an intriguing concept which has some foundation in available
observation in other hormonally responsive tissues. This review highlights and summarizes
our current knowledge on the convergence of such pathways and their relevance for
UF pathogenesis.
Keywords
inflammation - progesterone - cytokines - immune cells - Estrogen - Med12
