Unopposed estrogen stimulation is hypothesized to cause endometrial hyperplasia, which precedes malignant development in type 1 endometrial cancer. While aldehyde dehydrogenase 1 (ALDH1) has been proposed as a possible cancer stem cell marker in various cancer types, its clinical and predictive relevance in endometrial cancer remains debatable. For this study, the researchers wanted to look at the clinical significance of ALDH1 expression in endometrial hyperplasia and its capacity to predict progression to endometrial cancer.
An examination of the TCGA database found that numerous isoforms were upregulated in endometrial cancer, with the ALDH1 isoforms being the biggest group. To translate its expression, a tissue microarray with a diverse sample of normal and malignant endometrial tissues was previously developed. The array includes a metachronous cohort of samples from people who had endometrial cancer or did not have it. The intensity and frequency of ALDH1 expression were measured by immunohistochemical staining.
While ALDH1 was found in extremely low levels in benign proliferative and secretory endometrium, it was found at slightly higher levels in the stratum basalis. Endometrial hyperplasia, atypical hyperplasia, and endometrial cancer were all associated with an increase in cytoplasmic ALDH1 expression. ALDH1 was also found to be an early predictor of EC development, indicating that it might be used as an independent prognostic indicator of patients with endometrial hyperplasia with or without atypia who progressed to carcinoma (p = 0.012).
Reference:www.nature.com/articles/s41598-021-90570-3
