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. 2019 Mar 15;20(6):1325.
doi: 10.3390/ijms20061325.

Anti-Müllerian Hormone Expression in Endometrial Cancer Tissue

Marek Gowkielewicz  1 , Aleksandra Lipka  2 , Aleksandra Piotrowska  3 , Marta Szadurska-Noga  4 , Jacek J Nowakowski  5 , Piotr Dzięgiel  6   7 , Mariusz Krzysztof Majewski  8 , Marcin Jozwik  9 , Marta Majewska  10
Affiliations

Anti-Müllerian Hormone Expression in Endometrial Cancer Tissue

Marek Gowkielewicz et al. Int J Mol Sci. .

Abstract

Anti-Müllerian hormone (AMH) is a commonly known factor secreted by Sertoli cells, responsible for regression of the Müllerian ducts in male fetuses. AMH has also other functions in humans. In vivo and in vitro studies have shown that AMH inhibits cell cycle and induces apoptosis in cancers with AMH receptors. The aim of the study was to assess whether the tissue of pre-cancerous states of endometrium (PCS) and various histopathologic types of endometrial cancer (EC) exhibit the presence of AMH. We aimed to investigate whether the potential presence of the protein concerns menopausal women or those regularly menstruating, and whether is related to cancers with a good or a bad prognosis, as well as what other factors may influence AMH expression. The undertaken analysis was carried out on tissues retrieved from 232 women who underwent surgical treatment for PCS and EC. Tissues were prepared for immunohistochemical assessment with the use of a tissue microarrays method. AMH expression was confirmed in 23 patients with well differentiated endometrioid adenocarcinoma (G1), moderately differentiated endometrioid adenocarcinoma (G2), clear cell carcinoma (CCA) and nonatypical hyperplasia. AMH was not found in EC tissues in regularly menstruating women. An appropriately long mean period of breastfeeding in line with a prolonged period of hormonal activity had a positive effect on AMH expression. Our results may suggest that AMH is a factor which protects the organism against cancer, and should be further investigated as a potential prognosis marker and a therapeutic agent.

Keywords: AMH; endometrial cancer; endometrium.

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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 immunohistochemistry (IHC) reaction: (a) well-differentiated (G1) endometrioid carcinoma showing focal but intense positive, membranous staining with AMH; (b) clear cell carcinoma showing few scattered anti-Müllerian hormone (AMH) positive cells with low intensity of staining. (c) AMH negative staining of well-differentiated (G1) endometrioid carcinoma; (d) well differentiated (G1) endometrioid carcinoma showing few scattered AMH positive cells with moderate intensity of staining.
Figure 2
Figure 2
Mean AMH expression in: (a) different types of endometrial lesion (description of histopathological groups: NH—nonatypical hyperplasia, AH—atypical hyperplasia, G1—well differentiated endometroid adenocarcinoma, G2—moderately differentiated endometrioid adenocarcinoma, G3—poorly differentiated endometrioid adenocarcinoma, SA—serous adenocarcinoma, CCA—clear cell adenocarcioma, MA—mixed adenocarcinoma in Table 1) (Kruskal–Wallis ANOVA, H (7, N = 232) = 20.636, p = 0.004); (b) in different clinical stages of endometrial cancer according to FIGO (International Federation of Gynecology and Obstetrics) 0—carcinoma in situ, IA —carcinoma limited to the inner lining of the uterus, IB—invasion less than half of the myometrium, IC—invasion equal to or more than half of the myometrium, IIA—invasion of the cervical glands, IIB —invasion of the cervical stroma, IIIA—involvement of the serosa or adnexa or both, IIIB—vaginal and/or parametrial involvement, IIIC—pelvic and/or paraaortic lymph node involvement IVA—Tumor invades bladder mucosa and/or bowel mucosa, IVB—Distant metastases (Kruskal–Wallis ANOVA, H (9, N = 231) = 12.819, p = 0.171); (c) group of patients without and with diabetes mellitus type 2 (Mann–Whitney U test, AMH: Z = 0.019, p = 0.985); (d) group of patients that used hormone replacement therapy (Wald–Wolfowitz runs test, Z = 2.240, p = 0.025). IRS—immunoreactive score of Remmele and Stegner; c.l.—confident limits.
Figure 3
Figure 3
Mean AMH expression: (a) in premenopausal (p), perimenopausal (o) and postmenopausal (m) women (Kruskal–Wallis ANOVA: H (2, N = 231) = 3.117, p = 0.210); (b) in the group of women that menstruated less than 40 years or more than 40 years (Mann–Whitney U test: Z = 1.854, p = 0.064); (c) in the group of patients without and with arterial hypertension (Mann–Whitney U test: Z = 1.880, p = 0.06); (d) depending on the number of births (rs = 0.021, n = 232, p = 0.077).
Figure 4
Figure 4
Mean AMH expression due to: (a) the weight of newborn (s) (rs = −0.054, n = 207, p = 0.440); (b) age of the patient (rs = −0.116, n = 232, p = 0.077); (c) mean breastfeeding time (rs = −0.163, n = 229, p = 0.014); (d) total breastfeeding time (rs = −0.134, n = 229, p = 0.042).
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