Znaczenie prognostyczne VEGF i jego receptorów w raku endometrium typu endometrioidalnego

Abstract Background: Angiogenesis is of crucial importance for endometrial tumor growth and Vascular Endothelial Growth Factor (VEGF) is the key mediator of angiogenesis. Objective: The purpose of our study was to assess the prognostic value of VEGF and its receptors in relation to endometrioid endometrial carcinomas. Material and methods: In this study, we conducted an immunohistochemical evaluation of VEGF and VEGFRs expression in 84 tissue samples obtained from endometrioid endometrial cancer patients undergoing curative surgical treatment. Results: Out of 84 cancers, strong positive expression of VEGF was seen in 35 (42%) tumors. The overall strong positive rates were 33% for VEGFR-1 and for 15% for VEGFR-2. There was a significant correlation between clinical stage and VEGF and VEGFR-1 overexpression (p=0.027 and p=0.004, respectively). Additionally, there was a significant correlation between histological grade and VEGF and VEGFR-1 overexpression (pStreszczenie Wstęp: Angiogeneza ma istotne znaczenie we wzroście raka endometrium. Naczyniowo-śródbłonkowy czynnik wzrostu (VEGF) jest kluczowym mediatorem angiogenezy. Cel pracy: W pracy oceniono wartość prognostyczną VEGF i jego receptorów w endometrioidalnym raku endometrium. Materiał i metody: Przeprowadzono immunohistochemiczną ocenę ekspresji VEGF i VEGFR w 84 preparatach uzyskanych od chorych leczonych operacyjnie. Wyniki: Wśród 84 raków intensywnie dodatnią ekspresję VEGF obserwowano w 35 (42%) przypadków. Intensywnie dodatnią ekspresję VEGFR-1 stwierdzono w 33% a VEGFR-2 w 15% przypadków. Wykazano istotny statystycznie związek pomiędzy stopniem zaawansowania klinicznego a nadekspresją VEGF i VEGFR-1 (p=0,027 i p=0,004 ). Ponadto, stwierdzono znamienny statystycznie związek pomiędzy nadekspresją VEGF i VEGFR-1 a zróżnicowaniem histologicznym (

Mapping chromatin accessibility and active regulatory elements reveals pathological mechanisms in human gliomas

Chromatin structure and accessibility, and combinatorial binding of transcription factors to regulatory elements in genomic DNA control transcription. Genetic variations in genes encoding histones, epigenetics-related enzymes or modifiers affect chromatin structure/dynamics and result in alterations in gene expression contributing to cancer development or progression. Gliomas are brain tumors frequently associated with epigenetics-related gene deregulation. We perform whole-genome mapping of chromatin accessibility, histone modifications, DNA methylation patterns and transcriptome analysis simultaneously in multiple tumor samples to unravel epigenetic dysfunctions driving gliomagenesis. Based on the results of the integrative analysis of the acquired profiles, we create an atlas of active enhancers and promoters in benign and malignant gliomas. We explore these elements and intersect with Hi-C data to uncover molecular mechanisms instructing gene expression in gliomas. Gliomas are tumors often associated with epigenetics-related gene deregulation. Here the authors reveal an atlas of active enhancers and promoters in benign and malignant gliomas by performing whole-genome mapping of chromatin accessibility, histone modifications, DNA methylation patterns and transcriptome analysis simultaneously in multiple tumor samples