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Hypoxanthine phosphoribosyl transferase 1 is upregulated, predicts clinical outcome and controls gene expression in breast cancer

ABSTRACT: Hypoxanthine phosphoribosyl transferase 1 is upregulated, predicts clinical outcome and controls gene expression in breast cancer

PROVIDER: PRJNA630075 | ENA |

REPOSITORIES: ENA

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Hypoxanthine phosphoribosyl transferase 1 is upregulated, predicts clinical outcome and controls gene expression in breast cancer

Project description:Hypoxanthine phosphoribosyl transferase 1 (HPRT1) is traditionally believed to be a housekeeping gene; however, recent reports suggest that it is upregulated in several cancers and associates with clinical outcome. Like several cancer testis (CT) genes, HPRT1 is found on chromosome X, and encodes the HPRT enzyme, which functions in recycling nucleotides to supply for DNA and RNA synthesis in actively dividing cells. Here, we have used genome wide expression to interrogate its expression across all known cancer types and elucidated its functional role in breast cancer. We observed elevated HPRT1 RNA levels in malignant tissues when compared to normal controls, indicating its potential as a diagnostic and prognostic marker. Further, in breast cancer, subtype specific analysis showed that its expression was highest in basal and triple-negative breast cancer, and HPRT1 knockdown in breast cancer cells suggested that HPRT1 positively regulates genes specific to cellular and DNA repair pathways. Collectively, our results essentially highlight the importance and change the way HPRT1’s function is studied in biology, and warrants careful examination of its role in cancer.

2020-07-15 | GSE149768 | GEO

Hypoxanthine Phosphoribosyl Transferase 1 Is Upregulated, Predicts Clinical Outcome and Controls Gene Expression in Breast Cancer.

Project description: Not available

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A novel six-CpGs signature predicts clinical outcome in glioblastomas

Project description:We aimed to identify a clinically useful biomarker using DNA methylation-based information to optimize the management of glioblastoma (GBM) patients. We identified a novel six-CpGs signature that predicts the clinical outcome in GBM. The methylation profiling of 79 GBM patients has been used as a validation cohort to demonstrate the performance and the robustness of the identified six-CpGs signature. The status of the âMGMTâ biomarker, traditionally used by clinicians to predict survival in GBM, is also indicated per sample.

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Distinct SOX signature determines neuroblastoma origin and predicts clinical outcome

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Gene expression signature from tumor initiating population predicts clinical outcome in undifferentiated pleomorphic sarcoma (UPS)

Project description:Undifferentiated pleomorphic sarcomas (UPS) are thought to harbor a small population of cells with unique capability of tumor initiation and maintenance. These tumor initiating cells (TICs) are regarded as the drivers of cancer progression. However, the evidence for this tumor initiating cell (TIC) concept is based on the xenotransplantation assays in mice and the clinical relevance of the TIC concept remains unclear in UPS. We hypothesized that the distinct properties of the TICs would be reflected in the clinical outcome if the TIC concept is relevant in UPS. Here we performed global gene expression profiling of TIC-enriched side population (SP) fractions and non-SP fractions sorted from 15 UPS primary samples. Ninety-three genes were differentially expressed in between SP fractions and non-SP fractions. The UPS TIC gene expression signature score summarizing expression of these genes was calculated for a gene expression data and was correlated with clinical outcome. In the 15 samples used to generate the signature, patients with high scores in the SP fractions were associated with worse survival. We then tested the two independent published datasets with gene expression data on bulk unsorted samples, assuming that the TIC gene expression would persist in the non-TICs. Patients with high scores had significantly worse metastasis-free survival in both datasets. The significance of the score remained significant even considering for the known prognostic factor of UPS. Thus, gene expression signature derived from UPS TICs predicts clinical outcome, suggesting the clinical relevance of the TIC concept in UPS.

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MicroRNA expression profiling predicts clinical outcome of chronic hepatitis C by interferon administration

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Down modulation of miR-99a/let-7c/miR-125b miRNA cluster predicts clinical outcome in patients with unresected malignant pleural mesothelioma

Project description:Malignant pleural mesothelioma (MPM) is an aggressive tumor with a dismal overall survival (OS) and to date few molecular markers are available to guide patient management. This study aimed to identify a prognostic miRNA signature in MPM patients who did not undergo tumor resection. Whole miRNA profiling using a microarray platform was performed on 26 unresected MPM with distinct clinical outcome: 15 patients had aggressive disease (OS<12 months) and 11 patients indolent disease (OS>36 months). Three prognostic miRNAs (mir-99a, let-7c and miR-125b) encoded at the same cluster (21q21) were selected for further validation and tested on publicly available miRNA sequencing data (TCGA) from 72 MPM patients with survival data. A risk model was built based on these 3 miRNAs that was validated by quantitative PCR in an independent set of 30 MPM patients. High risk patients had shorter median OS (7.6 months) as compared with low-risk patients (median not reached). In the multivariate Cox model, a high risk score was an independently associated with shorter OS (HR=3.14; 95% CI, 1.18–8.34; P=0.022). Our study identified that the downregulation of the miR-99a/let-7/miR-125b miRNA cluster predicts poor outcome in unresected MPM.

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MicroRNA expression profiling predicts clinical outcome of chronic hepatitis C by interferon administration

Project description:We attempt to catalog the microRNA (miRNA) expression profile according to the response of combination therapy in order to predict the outcome of drug-response before administration and clarify the relationship between aberrant expression of miRNAs and chronic liver disease. We quantified expression profile of 474 mature miRNAs by microarray in the liver biopsy specimen from 99 CH patients without history of anti-viral therapy.

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Distinct SOX signature determines neuroblastoma origin and predicts clinical outcome

Project description:Multimodality treatment of high-risk neuroblastoma can be effective, but up to 50% of children experience recurrent disease with fatal outcome. Extensive genetic intratumoral heterogeneity and diverse clinical outcomes pose therapeutic challenges in treating children affected by this aggressive disease. Several hypotheses have been proposed to explain the heterogeneity of neuroblastoma, including a possible origin from multipotent neural crest stem cells (NCSCs). Utilizing an in vivo mouse genetics approach, we demonstrate that lineage-restricted sympathoadrenal (SA) progenitors and not NCSCs are the cellular origin of neuroblastoma. Human neuroblastoma tissue is composed of two spatially juxtaposed cell types, neuroblasts and Schwann cells, both cell types derive from neural crest (NC) lineage. This composition mimics the architecture of sympathetic ganglions (SG) as well as of adrenal medulla at the late stage of neural crest (NC) development. Similarly to SG, SOX10 is restricted to Schwannian cells and is not present in tumorigenic neuroblasts. Transcriptional landscape of Sox genes can serve as paradigmatic model for stage identification along NC lineage development. While early multipotent NCSCs are characterized by the expression of Sox9/Sox10 transcription factors (TF), committed SA progenitor identity is defined by the presence of Sox4/Sox11 TFs. Molecularly, we show that the core transcriptional network that orchestrate neuroblastoma maintenance is highly reminiscent of the SA progenitors. Taken together, the data presented here show that neuroblastoma cells functionally resemble the committed SA progenitors, while lacking specific stem cell program.

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