Stathmin 1 (Phospho-Ser62) ELISA Kit

Various drug-sensitivity markers are potentially responsible for tumor progression and chemotherapy resistance in cancer patients with both epithelial and sarcomatous components; however, the clinicopathological significance of drug-sensitivity markers in patients with pulmonary pleomorphic carcinoma (PPC) remains unknown. Here, we clarified the prognostic impact of these drug-sensitivity markers in PPC by performing immunohistochemical and clinicopathologic analyses of samples from 105 patients with surgically resected PPC in order to evaluate levels of vascular endothelial growth factor 2 (VEGFR2), stathmin 1 (STMN1), tubulin beta 3 class III (TUBB3), thymidylate synthetase (TS), topoisomerase II (Topo-II), glucose-regulated protein, and 78 kDa (GRP78)/binding immunoglobulin protein (BiP). We observed the rates of high expression for VEGFR2, STMN1, TUBB3, TS, Topo-II, and GRP78/BiP were 33% (39/105), 35% (37/105), 61% (64/105), 51% (53/105), 31% (33/105), and 51% (53/105) of the samples, respectively. Moreover, multivariate analysis identified VEGFR2 and GRP78/BiP as significant independent markers for predicting worse prognosis. These findings suggested elevated VEGFR2 and decreased GRP78/BiP levels as independent factors for predicting poor outcomes following surgical resection in patients with PPC.

Endometrial carcinomas are known to have the potential for recurrences that are distinctly discordant at the morphologic and immunophenotypic levels from their antecedent primary tumors. This report describes 3 patients with stage I, low or intermediate grade, conventional endometrioid carcinomas that recurred at the vaginal apex as notably clear cell-rich, higher grade, histotypically ambiguous neoplasms. Comparative immunohistochemical analyses were performed on all cases on both the original and the recurrent tumors using a panel of 8 biomarkers, including estrogen receptor, progesterone receptor, vimentin, p53, p16, hepatocyte nuclear factor 1 beta, BAF250a (ARID1A), and stathmin or oncoprotein-18 (STMN1). Notable immunophenotypic differences (relative to the original tumor) in case 1 included the relative loss of vimentin and estrogen receptor and the acquisition of p53, p16, and STMN1 expression in the recurrence. In case 2, significant p16 and STMN1 expression were identified only in the recurrence. In case 3, there were no significant immunophenotypic differences between the original tumor and the recurrence. In all 3 cases, the recurrent and original tumors showed no significant differences in BAF250a, hepatocyte nuclear factor 1 beta, and progesterone receptor expression. In summary, our cases confirm that endometrioid carcinomas can recur as clear cell-rich tumors. The relative acquisition of STMN1 expression in 2 of the 3 recurrences and p53 overexpression in 1 of 3 recurrences suggests that this phenomenon represents a form of tumor evolution, and this may be a potential contributor to tumor progression in these patients. (C) 2013 Elsevier Inc. All rights reserved.