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To evaluate the role of c-jun and c-myc proto-oncogenes in normal, hyperplastic and neoplastic endometrium in relation to estrogen receptor (ER) status and to investigate whether these genes can be related to other histopathological features of endometrial carcinoma, 32 endometrial carcinomas, 38 endometrial hyperplasias and 22 cyclic endometria (10 proliferative and 12 secretory) were evaluated histologically. Endometrial hyperplasia cases were classified as simple and complex hyperplasia without atypia, and atypical hyperplasia. Endometrial carcinoma cases were subtyped according to the International Society of Gynecological Pathologists. Modified FIGO system was used for both grading and staging. Immunohistochemical examination was performed using antibodies to ER-alpha, c-myc and c-jun with streptavidin-biotin-peroxidase technique. The mean percentage of ER-alpha positive cells changed cyclically during the menstrual cycle, and it was the highest (96%) and the lowest (31.6%) in proliferative and carcinomatous endometrium, respectively. There was a statistically significant difference between proliferative and secretory phases and proliferative and carcinomatous endometrium in relation to ER-alpha staining (p<0.05). There was also a statistically significant difference with respect to ERalpha reactivity between secretory phase and each hyperplastic group, as well as between the carcinoma group and each hyperplastic group (p<0.05). Although not significant, the mean percentage of c-myc expressing cells in the carcinoma group was higher (15.3%) than that of proliferative phase and hyperplastic groups. The mean percentage of c-jun positive cells in proliferative endometrium was slightly higher than in secretory endometrium, and it was the highest in atypical hyperplastic endometrium (28.3%), but there was no statistically significant difference between the groups. In carcinoma cases, a positive correlation was observed between c-jun positivity and tumor grade (p=0.027, r=0.3908), but such a correlation with c-myc was not found. A positive correlation was detected between ER-alpha and c-myc expression (p=0.038, r=0.3686). A progressive loss of ER seems to be correlated with increasing malignant transformation. C-myc expression might play a role in the development of endometrial carcinoma via ER. The association between c-jun and ER appears to be lost in endometrial carcinoma. The relationship between c-myc, c-jun and ER appears to be altered in endometrial carcinoma compared to that of menstrual endometrium.

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EGFR and KRAS mutation profile in non-small cell lung cancers (NSCLCs) shows wide variations due to geographic and ethnic background. We aimed to determine the frequency and types of EGFR and KRAS mutations in a sample group of Turkish NSCLC cases. The study included 14 adenocarcinomas (ACs), 11 squamous cell carcinoma (SCC) patients selected from archival material including small biopsy or surgical specimens. Their formalin fixed paraffin-embedded tumor tissues were used for genomic DNA extraction for EGFR exon 19 and 21, and KRAS exon 2 mutations. Eleven NSCLCs (44 %) had EGFR mutations. Exon 19 and 21 mutations were found in 8 (32 %) and 5 (20 %) cases. Two cases showed double EGFR mutations. In ACs, 5 (35.7 %) patients had EGFR gene mutation, 3 in exon 19 and 3 in exon 21. In SCCs, 6 (54.5 %) cases had EGFR mutation, 5 in exon 19 and 2 in exon 21. All exon 19 mutations were deletion-type mutations. For exon 21, 3 cases had L858R point mutation (CTG>CGG) and two cases showed deletion-type mutations. Six (24 %) NSCLCs showed KRAS mutations (three ACC, three SCC), 5 codon 12 mutations (G>T, T>C, G>A) and one codon 13 mutation (G>T). Three NSCLC cases showed both EGFR and KRAS mutations together. The profile of KRAS mutation in our AC cases was quite similar to those seen in the Western countries; however, frequency and clustering of EGFR mutations were similar to those seen in the Eastern countries.

Objectives: The aims of this study were to investigate the expression of CD10 in normal bladder tissue and urothelial bladder carcinomas and to clarify its association with histopathological variables. Materials and Methods: A total of 79 urothelial bladder carcinomas were selected from routine archival material. All cases were reevaluated histopathologically and graded according to the World Health Organization (WHO) 1973, WHO/ISUP 1998, and WHO 1999 systems. The TNM system was used for their pathological staging. CD10 immunohistochemical staining was performed in selected slides. Results: Tumoral cases consisted of 74 men (93.7%) and 5 women (6.3%). According to the pathological stage, 25 (31.6%), 33 (41.8%), and 21 (26.6%) cases had pTa, pT1, and pT2–3 carcinomas, respectively. 34 of 79 (43%) urothelial carcinomas and only 1 of 11 (9.1%) nontumoral cases showed positive CD10 immunostaining. It was a cytoplasmic diffuse or granular immunostaining pattern both in nontumoral and tumoral urothelia. There was no statistically significant difference between tumoral and nontumoral cases with respect to CD10 reactivity (p = 0.051), but there was a trend toward significance. In urothelial tumors, there was a significant inverse correlation between pathological stages and CD10 immunoreactivity (p = 0.036, r = –0,237). There was also a statistically significant difference between pTa and pT2–3 urothelial tumors in relation to the CD10 expression (p = 0.034). No association was detected between CD10 expression and grades according to all systems used (p > 0.05). Conclusions: According to our findings, the CD10 expression in noninvasive carcinomas showed a higher level than that in invasive carcinomas, and it is inversely correlated with the pathological stage. CD10 may play an important role in the progression of urothelial bladder carcinomas, and downregulation probably facilitates invasion, especially muscle invasion.