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Expression data from rat urinary bladder and non-glandular stomach tissue samples

ABSTRACT: Seven novel and potent Raf small molecule kinase inhibitors were evaluated in 7-day oral repeat-dose rat toxicity studies. All compounds tested induced hyperplasia in multiple tissues. Microarrays were used to investigate transciptional changes associated by treatment with a single compound to gain insight into the cellular changes that may contribute to the tissue hyperplasia.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE26936 | GEO | 2011/07/19

SECONDARY ACCESSION(S): PRJNA136093

REPOSITORIES: GEO

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Expression data from rat urinary bladder and non-glandular stomach tissue samples

Project description:Seven novel and potent Raf small molecule kinase inhibitors were evaluated in 7-day oral repeat-dose rat toxicity studies. All compounds tested induced hyperplasia in multiple tissues. Microarrays were used to investigate transciptional changes associated by treatment with a single compound to gain insight into the cellular changes that may contribute to the tissue hyperplasia. Two groups (25 females/group) received oral daily dosing for 7 days of either Vehicle or compound C1 dosed at 100 mg/kg. Five animals from each group were euthanized on Days 1 (4-5 hrs post first dose; received 1 dose), 2 (received 1 dose), 3 (received 2 doses), 5 (received 4 doses) and 8 (received 7 doses). Bladder tissues were collected and profiled at all five time points. Stomach tissues were collected and profiled at the earliest two time points. A single day 3 animal was not available for genomic profiling; therefore, expression data was collected for a total of 49 bladder and 20 stomach samples.

2011-07-18 | E-GEOD-26936 | biostudies-arrayexpress

Comparative genomic profiling of glandular bladder tumours.

Project description:Primary glandular bladder tumours (bladder adenocarcinoma [BAC], urachal adenocarcinoma [UAC], urothelial carcinoma with glandular differentiation [UCg]) are rare malignancies with histological resemblance to colorectal adenocarcinoma (CORAD) in the majority of this subgroup. Definite case numbers are very low, molecular data are limited and the pathogenesis remains poorly understood. Therefore, this study was designed to complement current knowledge by in depth analysis of BAC (n = 12), UAC (n = 13), UCg (n = 11) and non-invasive glandular lesions (n = 19). In BAC, in addition to known alterations in TP53, Wnt, MAP kinase and MTOR pathway, mutations in SMAD4, ARID1A and BRAF were identified. Compared to published data on muscle invasive bladder cancer (BLCA) and CORAD, UCg exhibited frequent "urothelial" like alterations while BAC and UAC were characterised by a more "colorectal" like mutational pattern. Immunohistochemically, there was no evidence of DNA mismatch repair deficiency or PD-L1 tumour cell positivity in any sample. Depending on the used antibody 0-45% of BAC, 0-30% of UCg and 0% UAC cases exhibited PD-L1 expressing tumour associated immune cells. A single BAC (9%, 1/11) showed evidence of ARID1A protein loss, and two cases of UCg (20%, 2/10) showed loss of SMARCA1 and PBRM1, respectively. Taken together, our data suggest at least in part involvement of similar pathways driving tumourigenesis of adenocarcinomas like BAC, UAC and CORAD independent of their tissue origin. Alterations of TERT and FBXW7 in single cases of intestinal metaplasia further point towards a possible precancerous character in line with previous reports.

| S-EPMC7443184 | biostudies-literature

Life after urinary bladder removal and new bladder formation in urinary bladder cancer

Project description:Intervention1: Radical cystectomy: NIL Control Intervention1: Radical cystectomy: NIL Primary outcome(s): Quality of life and sexual functionTimepoint: Post-operatively at 1 month, 3 month, 6 month and thereafter yearly

| 2582039 | ecrin-mdr-crc

Expression data of tongue mucosa from normal mice and mice treated by the 4-NQO

Project description:A better understanding of molecular changes during oral tumorigenesis may help defining new personalized prevention strategies. In order to test this hypothesis, we analyzed whole-genome expression changes in a murine model of oral carcinogenesis, induced by an oral carcinogen (4-NQO) We generated genome-wide expression profiles of microdissected cells from murine tongue at each step of oral tumorigenesis: normal mucosa, hyperplasia, dysplasia and tumor.

2016-12-06 | GSE75421 | GEO

Trancriptional profiling of rat bladder after daily administration of Pioglitazone and Rosiglitazone in vivo (miRNA)

Project description:The purpose of the study was to investigate the nongenotoxic carcinogenic effect of Pioglitazone. Pioglitazone is a PPARgamma agonist and is known to cause bladder tumours in male rats and an increase in the incidence of bladder cancer in humans has been observed in patients treated with Pioglitazone. Pioglitazone is not considered genotoxic or carcinogenic in mice and tumours are only observed in male rats suggesting a nongenotoxic mechanism of tumorigenesis. A suggested hypothesis is urinary calculi formation and subsequent irritation, hyperplasia and metaplasia. Rosiglitazone was used as reference compound as this PPARgamma agonist does not cause changes in the bladder but cause lipoma/liposarcoma in rats.

2018-05-05 | GSE68604 | GEO

Trancriptional profiling of rat bladder after daily administration of Pioglitazone and Rosiglitazone in vivo (mRNA)

2018-05-05 | GSE68592 | GEO

Extranodal marginal zone B cell lymphoma of MALT type involving the mucosa of both the urinary bladder and stomach.

Project description:Primary lymphoma of the urinary bladder is a very rare tumour. A bladder tumour was found in a 57 year old man with obstructive dysuria. It was found by histological and immunohistohistochemical investigation to be an extranodal marginal zone B cell lymphoma. Lymphoepithelial lesions were absent, but were found in a clinically silent gastric lymphoma discovered four weeks later during staging investigations; this gastric lymphoma was negative for Helicobacter pylori by breath test and molecular biological analysis. Sequencing of the clonal immunoglobulin heavy chain gene in both tumours indicated the same precursor cell, of follicular or post follicular origin. In synopsis, the data suggested that this was a case of primary lymphoma of the bladder with involvement of the stomach. The application of a chromosome 3 specific alpha satellite probe revealed trisomy 3. A tumour with these characteristics arising as a lymphoma of the bladder with a metachronous involvement of the gastric mucosa has not been described previously.

| S-EPMC1769687 | biostudies-literature

Urinary bladder post-spinal cord injury: time-points

Project description:Previously, we demonstrated using a rat model of spinal cord injury (SCI) that bladder wall tissue compliance significantly increased within the first 2 weeks following injury. In order to explore the potential molecular-level mechanisms of this event, the present study quantified molecules pertinent to bladder tissue remodeling and changes in mechanical properties. An initial gene array analysis followed by real-time qPCR revealed that the message levels for tropoelastin and lysyl oxidase were as high as 8-fold in SCI rats compared to normal. Furthermore, both the message and protein levels of TGF-beta1 and IGF-1, known stimulators of elastin synthesis, in SCI rat bladders were significantly higher compared to those of normal rats. Taken together, it can be speculated that functional changes of the bladder associated with SCI induce release of select growth factors, which, in turn, stimulate elastogenesis that lead to alteration of biomechanical properties of the wall tissue.

2008-12-25 | GSE14096 | GEO

GATA4 Controls Epithelial Morphogenesis in the Developing Stomach to Promote Establishment of Glandular Columnar Epithelium.

Project description:Background & aimsThe transcription factor GATA4 is broadly expressed in nascent foregut endoderm. As development progresses, GATA4 is lost in the domain giving rise to the stratified squamous epithelium of the esophagus and forestomach (FS), while it is maintained in the domain giving rise to the simple columnar epithelium of the hindstomach (HS). Differential GATA4 expression within these domains coincides with the onset of distinct tissue morphogenetic events, suggesting a role for GATA4 in diversifying foregut endoderm into discrete esophageal/FS and HS epithelial tissues. The goal of this study was to determine how GATA4 regulates differential morphogenesis of the mouse gastric epithelium.MethodsWe used a Gata4 conditional knockout mouse line to eliminate GATA4 in the developing HS and a Gata4 conditional knock-in mouse line to express GATA4 in the developing FS.ResultsWe found that GATA4-deficient HS epithelium adopted a FS-like fate, and conversely, that GATA4-expressing FS epithelium adopted a HS-like fate. Underlying structural changes in these epithelia were broad changes in gene expression networks attributable to GATA4 directly activating or repressing expression of HS or FS defining transcripts. Our study implicates GATA4 as having a primary role in suppressing an esophageal/FS transcription factor network during HS development to promote columnar epithelium. Moreover, GATA4-dependent phenotypes in developmental mutants reflected changes in gene expression associated with Barrett's esophagus.ConclusionsThis study demonstrates that GATA4 is necessary and sufficient to activate the development of simple columnar epithelium, rather than stratified squamous epithelium, in the embryonic stomach. Moreover, similarities between mutants and Barrett's esophagus suggest that developmental biology can provide insight into human disease mechanisms.

| S-EPMC8479485 | biostudies-literature

Gene expression profile associated with the PDZ ligand-motif of HPV16-E6 oncoprotin in the skin of transgenic mice models

Project description:The K14E6 transgenic mice developskin hyperplasia,benign tumors and skin cancer. The tumor formation capacity diminishes when E6 lacks its PDZ ligand-motif. This study aims to compare the transciptional profiles of transgenic K14E6 mice with K14E6 Δ146-151 (lacking the PDZ domain) in order to explore the role of PDZ in early skin carcinogenesis.

2010-07-27 | GSE22417 | GEO

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