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Stathmin-1 false negative in high grade squamous intraepithelial lesion. The three photomicrographs are obtained from a case of high grade squamous intraepithelial lesion (Case# 13, Supplemental Table 1). A Stathmin-1 shows negative staining of the dysplastic squamous epithelium. B HSP27 shows cytoplasmic staining of the dysplastic squamous cells. C p16 positive immunostain shows diffuse nuclear and cytoplasmic staining of the high grade squamous intraepithelial lesion/cervical intraepithelial lesion grade III. (Objective 40x)

Stathmin-1 false negative in high grade squamous intraepithelial lesion. The three photomicrographs are obtained from a case of high grade squamous intraepithelial lesion (Case# 13, Supplemental Table 1). A Stathmin-1 shows negative staining of the dysplastic squamous epithelium. B HSP27 shows cytoplasmic staining of the dysplastic squamous cells. C p16 positive immunostain shows diffuse nuclear and cytoplasmic staining of the high grade squamous intraepithelial lesion/cervical intraepithelial lesion grade III. (Objective 40x)

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Background The aim of this study was to determine how Stathmin-1 and Heat Shock Protein 27 (HSP27) can be used as adjunctive biomarkers to differentiate high-grade dysplasia from benign/reactive lesions in cervical tissues. In addition, we aimed to see if any of these markers can differentiate endometrial from endocervical adenocarcinomas. Methods...

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Cervical cancer is caused by a persistent infection with high-risk types of HPV and an accumulation of (epi)genetic alterations in host cell. Acquisition of anchorage-independent growth represents a critical hallmark during HPV-induced carcinogenesis, thereby yielding the most valuable biomarkers for early diagnosis and therapeutic targets. In a previous study, we found that miR-193a-3p and miR-193b-3p were involved in anchorage-independent growth. This study aimed to delineate the role of miR-193a/b-3p in HPV-induced carcinogenesis and to identify their target genes related to anchorage-independent growth. Cell viability and colony formation were assessed in SiHa cancer cells and HPV-16 and -18 immortalized keratinocytes upon miR-193a/b-3p overexpression. Both miRNAs reduced cell growth of all three cell lines in low-attachment conditions and showed a minor effect in adherent conditions. Online target predicting programs and publicly available expression data were used to find candidate mRNAs targets of miR-193a/b-3p. Seven targets showed reduced mRNA expression upon miR-193a/b-3p overexpression. For 3 targets Western blot analysis was also performed, all showing a reduced protein expression. A direct interaction was confirmed using luciferase assays for 6 genes: LAMC1, PTK2, STMN1, KRAS, SOS2, and PPP2R5C, which are PIK3/AKT regulators. All 6 targets were overexpressed in cervical cancers and/or precursor lesions. Together with an oberserved downregulation of phosphorylated-AKT upon miR-193a/b-3p overexpression, this underlines the biological relevance of miR-193a/b-3p downregulation during HPV-induced cervical carcinogenesis. In conclusion, downregulation of miR-193a-3p and miR-193b-3p is functionally involved in the acquisition of HPV-induced anchorage independence by targeting regulators of the PIK3/AKT pathway. This article is protected by copyright. All rights reserved.
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Studies on the relationship between stathmin 1 (STMN1) and cutaneous squamous cell carcinoma (cSCC) are limited. We aimed to evaluate the relationship between clinicopathological factors and STMN1 and p53 expressions in cSCC and compare them with those in the precursor lesions of cSCC and normal tissue. A total of 195 patients, followed between January 2014 and December 2021, with diagnoses of primary cSCC (n = 129), in situ cSCC (n = 20), or actinic keratosis (n = 46), as well as 29 histopathologically normal tissue samples, were included in the study. Immunohistochemical staining for STMN1 and p53 was performed. In the cSCC group, STMN1 scores were higher in poorly differentiated (P = 0.001) and ulcerated (P < 0.001) tumors. A linear relationship between STMN1 score and tumor area, tumor thickness, and mitosis was found (P = 0.001, P = 0.003, and P < 0.001, respectively). There was no statistically significant correlation between STMN1 and p53 scores. Our results support the previous view that STMN1 may be associated with some adverse clinicopathological and high-risk features of cSCC. To the best of our knowledge, this is the first and largest study to investigate STMN1 expression in cSCC, precancerous lesions of cSCC, and normal tissues.