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. 2020 Oct 17;9(10):2312.
doi: 10.3390/cells9102312.

Anti-Müllerian Hormone Type II Receptor Expression in Endometrial Cancer Tissue

Marek Gowkielewicz  1 , Aleksandra Lipka  1 , Marta Majewska  2 , Aleksandra Piotrowska  3 , Marta Szadurska-Noga  4 , Jacek J Nowakowski  5 , Marta Wiszpolska  2 , Piotr Dzięgiel  3   6 , Tomasz Wasniewski  1 , Mariusz Krzysztof Majewski  2 , Marcin Jozwik  1
Affiliations

Anti-Müllerian Hormone Type II Receptor Expression in Endometrial Cancer Tissue

Marek Gowkielewicz et al. Cells. .

Abstract

Anti-Müllerian hormone (AMH) is responsible for the Müllerian ducts' regression in male fetuses. In cells of cancers with AMH receptors (AMHRII), AMH induces cell cycle arrest or apoptosis. As AMH occurs naturally and does not exhibit significant side effects while reducing neoplastic cell colonies, it can be considered as a potential therapeutic agent for cancer treatment. The purpose of this study was to assess the AMHRII expression in endometrial cancer (EC) in correlation to various demographic data and clinical conditions. Immunohistochemical analysis was used to assess AMHRII expression in EC tissue samples retrieved from 230 women with pre-cancerous state of endometrium (PCS) and EC. AMHRII was detected in 100% of samples. No statistical difference was observed for AMHRII expression depending on the histopathological type of EC, cancer staging, body mass index, and age, as well as the number of years of menstruation, births and miscarriages, and average and total breastfeeding time. Diabetes mellitus type 2 is the only factor that has an impact on AMHRII expression in EC tissue. Thus, this study supports the idea of theoretical use of AMH in EC treatment because all histopathological types of EC at all stages of advancement present receptors for AMH.

Keywords: AMH; AMHRII; endometrial cancer; expression; tissue microarray.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
A representative example (20 × magnification) of the weak (a), moderate (b, c), and strong (d) AMHRII immunohistochemistry (IHC) reaction within endometrioid adenocarcinoma G1 (a) and G2 (b–d) grade.
Figure 2
Figure 2
Mean AMHRII expression in: (a) different types of endometrial lesion (description of histopathological groups: NH, AH, G1, G2, G3, SA, CCA, MA in Table 1) (Kruskal–Wallis test, H(7, N = 230) = 11.438, p = 0.121); (b) in different clinical stages of endometrial cancer according to FIGO (Kruskal–Wallis test, H(8, N = 230) = 8.928, p = 0.348); (c) group of patients without and with diabetes mellitus type 2 (Mann–Whitney U test, AMHRII: Z = 2.275, p = 0.023); (d) group of patients that used hormone replacement therapy (Wald–Wolfowitz runs test, Z = 0.122, p = 0.923).
Figure 3
Figure 3
Mean AMHRII expression: (a) due to years of hormonal activity (rs = 0.053, n = 230, p = 0.426); (b) in a group of patients without and with arterial hypertension (Mann–Whitney U test: Z = 0.227, p = 0.821); (c) due to hormonal status: premenopausal (p), perimenopausal (o), and postmenopausal (m) women (Kruskal–Wallis test: H(2, N = 230) = 1.248, p = 0.536); (d) depending on the number of birth (rs = 0.033, n = 230, p = 0.624).
Figure 4
Figure 4
Mean AMHRII expression due to: (a) number of miscarriages (rγ = −0.127, n = 230, p = 0.123); (b) average weight of newborn (s) (rs = 0.102, n = 206, p = 0.146); (c) age of the patient (rs = −0.002, n = 230, p = 0.980); (d) BMI (rs = −0.088, n = 230, p = 0.183).
Figure 5
Figure 5
Mean AMHRII expression due to: (a) average breastfeeding time (rs = −0.049, n = 227, p = 0.459); (b) total breastfeeding time (rs = −0.030, n = 227, p = 0.650).
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