Investigation of TRPM7 activity in endometrial tissue in treatment-resistant atype-free endometrial hyperplasia

Endometrial hyperplasia (EH) is an irregular proliferation of endonmetrial glands that has the potential to progress to endometrial cancer. Progestins are widely used in the conservative treatment of EH and early stage endometrial cancer (EEC). However, despite progesterone treatment, endometrial hyperplasia does not regress in some cases and may progress to endometrial cancer. It is essential for migration, adhesion, prolifcation and angiogenesis, tumor growth and metastasis, as it is an important regulator of transient receptor potential (TRP) channels. Calcium, whose intracellular concentrations are adjusted by ion channel activations, is an important regulator of these steps. Mg2 + takes part in every step of cell proliferation, with tumor cell growth where unregulated proliferation exerts its most detrimental effect. TRPM7 is associated with a predominant Mg2 + uptake mechanism in mammalian cells and has been shown to be a regulator of cell proliferation. If TRPM7 is blocked, the cell cycle is paused. Due to the relationship between proliferation and TRPM7, we also investigated TRPM7 activity in resistant endometrial hyperplasia. In this retrospective study, we reviewed the pathology reports of patients diagnosed with endometrial hyperplasia. We reviewed the endometrial biopsy reports of 6 months after 6 months of progesterone treatment with a diagnosis of endometrial hyperplasia without atypia. Randomly selected proliferative endometrium cases were formed as the control group (n = 20). The endometrial biopsy results of each of the 40 patients who were diagnosed with endometrial hyperplasia without atypia were analyzed before the treatment. In these cases, 5 µm thick sections were taken from paraffin sections and TRPM7 immunohistochemical staining was performed. Pre-treatment and post-treatment immunohistochemistry scores of each patient were calculated by evaluating the preparations under a light microscope and statistical comparison was made between the groups. As a result of our study, we found that TRPM7 imminreactivity increased significantly in all groups of endometrial hyperplasia compared to the proliferative endometrium group. At the end of six months of treatment, we found that the TRPM7 immunreactivity score decreased significantly in the recovered endometrial hyperplasia group compared to the score of 6 months ago, and was similar to the score in the proliferative endometrin group. In our group which did not improve after six months of treatment and persisted, the TRPM7 immunoreactivity score was similar to the score of 6 months ago. It was higher than the proliferative group and the TRPM7 imminreactivity score in the recovered endometrium group. In conclusion, if there is no significant decrease in the TRPM7 imumiinreactivity score in the second biopsies of endometrial hyperplasia cases receiving progesterone treatment, it can be expected that these cases are included in the refractory hyperplasia group and may have more malignancy and progression potential. Further studies can be conducted with a large number of cases on this subject