Evaluation of Microvascular Density in Glioblastomas in Relation to p53 and Ki67 Immunoexpression.

Glioblastoma is the most aggressive tumor in the central nervous system, with a survival rate of less than 15 months despite multimodal therapy. Tumor recurrence frequently occurs after removal. Tumoral angiogenesis, the formation of neovessels, has a positive impact on tumor progression and invasion, although there are controversial results in the specialized literature regarding its impact on survival. This study aims to correlate the immunoexpression of angiogenesis markers (CD34, CD105) with the proliferation index Ki67 and p53 in primary and secondary glioblastomas. This retrospective study included 54 patients diagnosed with glioblastoma at the Pathology Department of County Emergency Clinical Hospital Târgu Mureș. Microvascular density was determined using CD34 and CD105 antibodies, and the results were correlated with the immunoexpression of p53, IDH1, ATRX and Ki67. The number of neoformed blood vessels varied among cases, characterized by different shapes and calibers, with endothelial cells showing modified morphology and moderate to marked pleomorphism. Neovessels with a glomeruloid aspect, associated with intense positivity for CD34 or CD105 in endothelial cells, were observed, characteristic of glioblastomas. Mean microvascular density values were higher for the CD34 marker in all cases, though there were no statistically significant differences compared to CD105. Mutant IDH1 and ATRX glioblastomas, wild-type p53 glioblastomas, and those with a Ki67 index above 20% showed a more abundant microvascular density, with statistical correlations not reaching significance. This study highlighted a variety of percentage intervals of microvascular density in primary and secondary glioblastomas using immunohistochemical markers CD34 and CD105, respectively, with no statistically significant correlation between evaluated microvascular density and p53 or Ki67.

Changes in immunoexpression of p53, Ki-67, Ets-1, APAF-1 and PTEN in serrated and conventional colon adenomas.

UNLABELLED: The balance between apoptosis and proliferation is tipped towards a decrease of apoptosis as the colonocyte progresses in the adenoma to carcinoma sequence of colon carcinogenesis. According to literature data, proteins like p53, Ki-67, APAF-1, Ets-1, PTEN contribute to inhibition of apoptosis and stimulation of proliferation. AIM: Considering the complex interference among colorectal carcinogenetic mechanisms, our aim was to study the markers Ets-1 and APAF-1 relative to p53, Ki-67 and PTEN expression in colon adenomas/polyps (A/P). MATERIALS AND METHODS: We performed immunohistochemistry on 99 colon A/P cases from the material of the Department of Pathology, Emergency County Hospital of Tirgu Mures, Romania. Secondary EnVision Flex/HRP (Horseradish peroxidase) (20 minutes) was used for signal amplification. RESULTS: The majority of A/P show increased Ki-67, p53, Ets-1 expression, decreased APAF-1 expression and preserved PTEN expression. p53, Ki-67, Ets-1 and APAF-1 demonstrated statistically significant correlations with histological type and grade of dysplasia. We also observed that expression of these proteins in the intestinal crypts has a typical distribution according to histological type and grade of dysplasia. CONCLUSIONS: In case of hyperplastic polyps APAF-1 expression decreases as p53 and Ki-67 expression increases, followed by a decrease in PTEN expression in serrated adenomas, and an increase of Ets-1 expression in conventional adenomas.

Immunohistochemical study of Ki67, CD34 and p53 expression in human tooth buds.

AIM OF THE STUDY: Establishment of Ki67, p53 and CD34 expression in human tooth buds of different stages of odontogenetic development. MATERIALS AND METHODS: Tissue samples containing tooth buds were removed from the incisor areas of human fetuses in different stages of development (weeks 9-10, 12-13, 13-16, 21-24), and from the canine and molar areas of 21-24 weeks fetuses. The tissue fragments were fixed using formalin and were processed using common histological techniques with paraffin embedding. Immunostaining for Ki67, p53 and CD34 has been performed using the dextran method and moist heat antigen retrieval (except for CD34). The resulting slides were photographed and quantitatively evaluated. RESULTS: Ki67 immunoexpression decreases with advancement of the developmental stage of the tooth bud: in the inner enamel epithelium, between weeks 9 and 16 (IEE), in the preameloblasts (PB) between weeks 13 and 16, in the ameloblasts (AB) between weeks 21 and 24; outer enamel epithelium (OEE); stratum intermedium (SI); in the dental papilla: between weeks 9 and 10 in the dental papilla (DP), between weeks 13 and 16 in the outer layer of the dental papilla (DP1) and in the central layer of the dental papilla (DP2). Likewise, we noted Ki67 expression in the odontoblast layer (O) and pulp (P), between weeks 21 and 24. Concerning CD34 expression, we observed a decrease from weeks 9-10 until weeks 13-16, followed by an increase until weeks 21-24 of intrauterine life. From weeks 9-10, we observed a constant decrease of expression until weeks 13-16, followed by an increase during weeks 21-24. CONCLUSIONS: All Ki67, p53 and CD34 have been identified in the tooth bud. Ki67 expression gradually decreases with the embryonic development of the tooth, while p53 and CD34 expression decreases from weeks 9-10 to weeks 13-16 of intrauterine life, followed by an increase until weeks 21-24.