Estrogen Receptor, Progesterone Receptor, and HER2 Receptor Markers in Endometrial Cancer.

Background: Endometrial cancer (EC) is a major gynecologic adenocarcinoma that arises from the endometrium. While the incidence of EC is on the rise worldwide, survivorship and clinical advancement have considerably lagged compared to other cancers. Given the sensitive nature of the endometrium and its high expression of hormone receptors, hormonal therapy has become a favorable alternative treatment compared to highly toxic chemotherapeutics and radiation therapy. Methods: Clinical samples from patients diagnosed with EC were obtained. ER and PR staining were performed according to the S-P kit, and HER2 staining was carried out according to the UltrasensitiveTM S-P immunohistochemistry kit protocol. Chi-square analysis was conducted using the SPSS. P-values of less than 0.05 were taken as an a priori value for statistical significance. Results: Immunohistochemical (IHC) analysis showed the overall positive expression rates of ER, PR, and HER2 to be 59.8%, 75.0%, and 71.1%, respectively. Significant co-expression was found among all three receptors, suggesting a cooperative, synergistic effect. More importantly, we found that ER expression was correlated with FIGO staging and cervical invasion, whereas PR expression was associated with histologic type. No clinicopathologic features were correlated with HER2 expression, but HER2 positivity was inversely associated with the degree of HER2 overexpression. Conclusions: These results suggest that EC is a heterogeneous disease that may not conform to traditional, prototypically defined subtypes. The status of ER, PR, and HER2 receptors may have the potential to serve as prognostic indicators for EC, but further analysis is needed to ascertain their prognostic significance.

Lichen Sclerosus: An autoimmunopathogenic and genomic enigma with emerging genetic and immune targets.

Lichen sclerosus (LS) is an inflammatory dermatosis with a predilection for anogenital skin. Developing lesions lead to vulvar pain and sexual dysfunction, with a significant loss of structural anatomical architecture, sclerosis, and increased risk of malignancy. Onset may occur at any age in both sexes, but typically affects more females than males, presenting in a bimodal fashion among pre-pubertal children and middle-aged adults. A definitive cure remains elusive as the exact pathogenesis of LS remains unknown. A general review of LS, histologic challenges, along with amounting support for LS as an autoimmune disease with preference for a Th1 immune response against a genetic background is summarized. In addition to the classically referenced ECM1 (extracellular matrix protein 1), a following discussion of other immune and genetic targets more recently implicated as causative or accelerant agents of disease, particularly miR-155, downstream targets of ECM1, galectin-7, p53, and epigenetic modifications to CDKN2A, are addressed from the viewpoint of their involvement in three different, but interconnected aspects of LS pathology. Collectively, these emerging targets serve not only as inherently potential therapeutic targets for treatment, but may also provide further insight into this debilitating and cryptic disease.