Pathologic Characteristics of Pregnancy-Related Meningiomas

Abstract

Meningiomas are the most common intracranial tumor. During pregnancy, explosive growth of a known meningioma occasionally occurs, but the underlying reasons remain unknown. Prolactin has been suggested as a possible key contributor to pregnancy-related meningioma growth. This study sets out to investigate prolactin and prolactin receptor status in 29 patients with pregnancy-related meningiomas in Denmark, from January 1972 to December 2016, as compared to 68 controls aged 20–45 years, also undergoing resection of a meningioma. Furthermore, we investigated potential differences in the progesterone and estrogen receptor statuses, WHO grade, Ki-67 labeling indices, and locations of the resected meningiomas between the cases and controls. Immunohistochemical analyses were performed, and histopathology and intracranial location were assessed with the investigator blinded for the case–control status. None of the samples stained positive for prolactin and very few samples stained positive for prolactin receptors, equally distributed among cases and controls. Estrogen and progesterone receptors generally followed the same distributional pattern between groups, whereas above cut-point Ki-67 labeling indices for both groups were observed. In conclusion, our results did not support the notion of prolactin as a key contributor to pregnancy-related meningioma growth. Rather, the similarities between the cases and controls suggest that meningiomas early in life may comprise a distinct biological entity.

Optic nerve sheath meningioma presenting as progressive visual disturbance during pregnancy: A case report

“…However, it is controversial whether the growth of meningiomas during pregnancy is only due to the expression of PR. A study of the pathology of meningiomas during pregnancy found that the frequency of PR positivity during pregnancy was similar with the control group (6,10). Meningioma growth during pregnancy have the possibility to be affected by not only hormone receptor expression but also tumor location (6,11).…”

Matched Paired Primary and Recurrent Meningiomas Points to Cell-Death Program Contributions to Genomic and Epigenomic Instability along Tumor Progression

“…From them, losses on TIMP3 (22q) have been suggested to take part in reduced apoptosis [ 30 , 31 ] or angiogenesis [ 32 ], and our finding supports the extensive belief that additional genes located on 22q should contribute to MN tumorigenesis [ 3 , 4 ]. The influence of estrogens in MN has been widely discussed on MN, with many discrepancies in the literature but little has been described at the genetic level [ 33 , 34 ]. Both ESR1 and PARK2 are located in a frequently altered chromosomal region in MN (6q), and both display effects over the Wtn/b-catenin pathway [ 35 , 36 , 37 , 38 , 39 ].…”

Malignant meningioma

“…33,34 Recently, a dose-dependent relationship between the growth of a subgroup of meningiomas and treatment with cyproterone acetate has been detected. 35 Reproductive factors and risk of meningioma development are not thoroughly elucidated, [36][37][38] and hormonal therapies in meningioma have not shown substantial effect. 39,40 The WHO classification system-meningiomas then and now…”