ZHANG Enqi, LIU Xilong, LU Dan. Expression and clinical significance of mismatch repair proteins in endometrial carcinomaJ. Journal of Clinical Medicine in Practice, 2026, 30(4): 19-23, 29. DOI: 10.7619/jcmp.20257083
Citation: ZHANG Enqi, LIU Xilong, LU Dan. Expression and clinical significance of mismatch repair proteins in endometrial carcinomaJ. Journal of Clinical Medicine in Practice, 2026, 30(4): 19-23, 29. DOI: 10.7619/jcmp.20257083

Expression and clinical significance of mismatch repair proteins in endometrial carcinoma

  • Objective To investigate the association between the deficiency of mismatch repair (MMR) proteins and the clinicopathological characteristics of endometrial carcinoma (EC).
    Methods Immunohistochemistry was employed to detect the expression of MMR proteins in surgical specimens from patients with EC, and to analyze whether there were statistical differences in clinicopathological characteristics and recurrence rates between patients with normal expression and those with deficient expression of MMR proteins.
    Results A total of 217 patients with EC were included, with normal and deficient expression rates of MMR proteins being 74.65% and 25.35%, respectively. The deficiency rates of individual MLH1, MSH2, MSH6 and PMS2 were 0.46%, 0.46%, 1.38% and 7.83%, respectively. The co-deficiency rates of MLH1/PMS2, MSH2/MSH6, and MLH1/MSH2/PMS2 were 12.44%, 2.30% and 0.46%, respectively. There were no statistically significant differences in patient age, menopausal status, tumor type, degree of differentiation, tumor stage, myometrial invasion, lymph node metastasis, vascular invasion and recurrence rate between patients with normal MMR protein expression (microsatellite stable group) and those with deficient expression (microsatellite unstable group) (P>0.05).
    Conclusion The impact of MMR protein deficiency on the clinical behavior of endometrial carcinoma may not be directly reflected through traditional pathological and morphological indicators, but is influenced by a combination of tumor mutational burden, immune microenvironment, or other yet-to-be-determined molecular mechanisms.
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