Project description:We used RNA-SEQ technique to detect lncRNAs expression differences in 53 pairs of tumor and adjacent normal tissues of renal papillary cell carcinoma
Project description:Clear cell papillary renal cell carcinoma (CCPRCC) is a low-grade renal neoplasm with morphological characteristics mimicking both clear cell renal cell carcinoma (CCRCC) and papillary renal cell carcinoma (PRCC). However, despite some overlapping features, their morphological, immunohistochemical, and molecular profiles are distinct. To better understand the biology of this tumor, we analyze the miRNA expression profiles of a set of CCPRCC by microarrays.
Project description:The proteome of clinical tissue samples diagnosed with clear cell renal cell carcinoma (ccRCC) and papillary renal cell carcinoma (pRCC) were evaluated analyzed along with the dataset identifier PXD022018 to establish a potential discriminative biomarker panel of proteins for these tumors subtypes.
Project description:Renal cell carcinoma is the most common neoplasm of the adult kidney. A few subtypes of RCC include papillary RCC (pRCC), chromophobe RCC (chRCC) and the benign oncocytoma tumor. In some cases, distinguishing between the RCC subyptes is difficult. We performed a mircroRNA (miRNA) microarray to determine differential miRNA expression between pRCC, chRCC, and oncocytoma. We performed a miRNA microarray on 10 tumor samples of each papillary renal cell carcinoma (pRCC), chromophobe renal cell carcinoma (chRCC), and oncocytoma.
Project description:Between 80% and 90% of renal carcinomas are either clear cell renal cell carcinoma or papillary RCC although there are at least 20 other distinct forms of RCC recognised by the World Health Organization (WHO). Emerging or provisional entities have been considered as variants of PRCC, including papillary renal neoplasm with reversed polarity (PRNRP). However, the molecular basis of PRNRP, and miRNA expression profile, is unknown. We used microarray analysis to elucidate the non-coding RNA (ncRNA) profiles of 10 PRNRP cases and compared them with other renal neoplasms. Cases were only considered for this study after fulfilment of strict inclusive histological and immunohistochemical criteria. We used Affymetrix miRNA v.4.0 arrays to elucidate the expression of these samples.
Project description:Fumarate hydratase (FH) mutation causes hereditary type 2 papillary renal cell carcinoma (HLRCC, Hereditary Leiomyomatosis and Renal Cell Cancer (MM ID # 605839)). The main effect of FH mutation is fumarate accumulation. The current paradigm posits that the main consequence of fumarate accumulation is HIF-a stabilization. Paradoxically, FH mutation differs from other HIF-a stabilizing mutations, such as VHL and SDH mutations, in its associated tumor types. We identified that fumarate can directly up-regulate antioxidant response element (ARE)-controlled genes. We demonstrated that AKR1B10 is an ARE-controlled gene and is up-regulated upon FH knockdown as well as in FH-null cell lines. AKR1B10 overexpression is also a prominent feature in both hereditary and sporadic PRCC2. This phenotype better explains the similarities between hereditary and sporadic PRCC2. Expression profiling renal normal and tumor tissue
Project description:Papillary renal cell carcinoma (pRCC) is a malignant kidney cancer with a prevalence of 7-20% of all renal cell tumors. Proteome and metabolome profiles of 19 pRCC and patient-matched healthy kidney controls and transcriptome data derived from TCGA were used to elucidate the regulation of metabolic pathways and underlying molecular mechanisms. Glutathione (GSH), a main reactive oxygen species (ROS) scavenger, was tremendously increased in pRCC type I, II, and metastatic type II and can be regarded as a new hallmark in this malignancy. Isotope tracing revealed an increased de novo synthesis rate of GSH and a glutamine addiction in pRCC derived cell lines. Furthermore, a rewiring of the main pathways involved in ATP and glucose synthesis was observed on the protein level: the abundance of enzymes involved in gluconeogenesis and of the respiratory chain was found to be significantly reduced in pRCC. In contrast, transcripts encoding for the respiratory chain were not regulated, which prompts for non-genetic profiling. The main molecular characteristics of pRCC are the increased GSH synthesis to cope with ROS stress, the deficient anabolic glucose synthesis, and the compromised oxidative phosphorylation, which could be exploited in novel anti-cancer strategies.
