ArticleBioinformatics and biology insights2013
Molecular Insights on Post-chemotherapy Retinoblastoma by Microarray Gene Expression Analysis.
Article in Bioinformatics and biology insights, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
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- Evaluation of secretome biomarkers in glioblastoma cancer stem cells: A bioinformatics analysis.Cancer reports (Hoboken, N.J.) · 2024Article
- UBE2T/STAT3 Signaling Promotes the Proliferation and Tumorigenesis in Retinoblastoma.Investigative ophthalmology & visual science · 2022Article
- Molecular pathways in glioblastoma-derived stem cells to identify effective drug agents: A bioinformatics study.Journal of family medicine and primary care · 2022Article
- Centromere protein E as a novel biomarker and potential therapeutic target for retinoblastoma.Bioengineered · 2021Article
- TRIM59 Promotes Retinoblastoma Progression by Activating the p38-MAPK Signaling Pathway.Investigative ophthalmology & visual science · 2020Article
- Identification of pathogenic genes of pterygium based on the Gene Expression Omnibus database.International journal of ophthalmology · 2019Article
- Oncogenic role of epithelial cell transforming sequence 2 in lung adenocarcinoma cells.Experimental and therapeutic medicine · 2016Article
- Multiple Differential Networks Strategy Reveals Carboplatin and Melphalan-Induced Dynamic Module Changes in Retinoblastoma.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Activation of IFN/STAT1 signalling predicts response to chemotherapy in oestrogen receptor-negative breast cancer.British journal of cancer · 2016Article
- Characterization and pharmacologic targeting of EZH2, a fetal retinal protein and epigenetic regulator, in human retinoblastoma.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- Small interfering RNA-induced inhibition of epithelial cell transforming sequence 2 suppresses the proliferation, migration and invasion of osteosarcoma cells.Experimental and therapeutic medicine · 2015Article
- Integrated Analysis of Dysregulated miRNA-gene Expression in HMGA2-silenced Retinoblastoma Cells.Bioinformatics and biology insights · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeManagement of Retinoblastoma (RB), a pediatric ocular cancer is limited by drug-resistance and drug-dosage related side effects during chemotherapy. Molecular de-regulation in post-chemotherapy RB tumors was investigated. MATERIALS AND
methodscDNA microarray analysis of two post-chemotherapy and one pre-chemotherapy RB tumor tissues was performed, followed by Principle Component Analysis, Gene ontology, Pathway Enrichment analysis and Biological Analysis Network (BAN) modeling. The drug modulation role of two significantly up-regulated genes (p≤0.05) - Ect2 (Epithelial-cell-transforming-sequence-2), and PRAME (preferentially-expressed-Antigen-in-Melanoma) was assessed by qRT-PCR, immunohistochemistry and cell viability assays.
resultsDifferential up-regulation of 1672 genes and down-regulation of 2538 genes was observed in RB tissues (relative to normal adult retina), while 1419 genes were commonly de-regulated between pre-chemotherapy and post- chemotherapy RB. Twenty one key gene ontology categories, pathways, biomarkers and phenotype groups harboring 250 differentially expressed genes were dys-regulated (EZH2, NCoR1, MYBL2, RB1, STAMN1, SYK, JAK1/2, STAT1/2, PLK2/4, BIRC5, LAMN1, Ect2, PRAME and ABCC4). Differential molecular expressions of PRAME and Ect2 in RB tumors with and without chemotherapy were analyzed. There was neither up- regulation of MRP1, nor any significant shift in chemotherapeutic IC50, in PRAME over-expressed versus non-transfected RB cells.
conclusionCell cycle regulatory genes were dys-regulated post-chemotherapy. Ect2 gene was expressed in response to chemotherapy-induced stress. PRAME does not contribute to drug resistance in RB, yet its nuclear localization and BAN information, points to its possible regulatory role in RB.
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