ArticleCancer2017
RNA sequencing of esophageal adenocarcinomas identifies novel fusion transcripts, including NPC1-MELK, arising from a complex chromosomal rearrangement.
Article in Cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- NPC1 promotes the progression of hepatocellular carcinoma by mediating the accumulation of neutrophils into the tumor microenvironment.FEBS open bio · 2025Article
- Diagnostic and Therapeutic Advances of RNAs in Precision Medicine of Gastrointestinal Tumors.Biomedicines · 2024Review
- Inhibition of NPC1 suppresses cell proliferation and β-catenin signaling activation of liver cancer.Journal of cancer research and clinical oncology · 2024Article
- Transcriptomic changes and gene fusions during the progression from Barrett's esophagus to esophageal adenocarcinoma.Biomarker research · 2024Article
- Article
- Aneuploidy and complex genomic rearrangements in cancer evolution.Nature cancer · 2024Review
- Roles of the CCR4-Not complex in translation and dynamics of co-translation events.Wiley interdisciplinary reviews. RNA · 2023Review
- Linking Late Endosomal Cholesterol with Cancer Progression and Anticancer Drug Resistance.International journal of molecular sciences · 2022Review
- Comprehensive RNA dataset of tissue and plasma from patients with esophageal cancer or precursor lesions.Scientific data · 2022Article
- Connecting Cholesterol Efflux Factors to Lung Cancer Biology and Therapeutics.International journal of molecular sciences · 2021Review
- The dysregulated expression and functional effect of CaMK2 in cancer.Cancer cell international · 2021Review
- Article
- MKL1/miR-5100/CAAP1 loop regulates autophagy and apoptosis in gastric cancer cells.Neoplasia (New York, N.Y.) · 2020Article
- Identification of potential key genes in esophageal adenocarcinoma using bioinformatics.Experimental and therapeutic medicine · 2019Article
- Cancer Cytogenetics: Deep Roots, New Branches in the Age of Omics.Cancer genomics & proteomicsReview
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundStudies of chromosomal rearrangements and fusion transcripts have elucidated mechanisms of tumorigenesis and led to targeted cancer therapies. This study was aimed at identifying novel fusion transcripts in esophageal adenocarcinoma (EAC).
methodsTo identify new fusion transcripts associated with EAC, targeted RNA sequencing and polymerase chain reaction (PCR) verification were performed in 40 EACs and matched nonmalignant specimens from the same patients. Genomic PCR and Sanger sequencing were performed to find the breakpoint of fusion genes.
resultsFive novel in-frame fusion transcripts were identified and verified in 40 EACs and in a validation cohort of 15 additional EACs (55 patients in all): fibroblast growth factor receptor 2 (FGFR2)-GRB2-associated binding protein 2 (GAB2) in 2 of 55 or 3.6%, Niemann-Pick C1 (NPC1)-maternal embryonic leucine zipper kinase (MELK) in 2 of 55 or 3.6%, ubiquitin-specific peptidase 54 (USP54)-calcium/calmodulin dependent protein kinase II γ (CAMK2G) in 2 of 55 or 3.6%, megakaryoblastic leukemia (translocation) 1 (MKL1)-fibulin 1 (FBLN1) in 1 of 55 or 1.8%, and CCR4-NOT transcription complex subunit 2 (CNOT2)-chromosome 12 open reading frame 49 (C12orf49) in 1 of 55 or 1.8%. A genomic analysis indicated that NPC1-MELK arose from a complex interchromosomal translocation event involving chromosomes 18, 3, and 9 with 3 rearrangement points, and this was consistent with chromoplexy.
conclusionsThese data indicate that fusion transcripts occur at a stable frequency in EAC. Furthermore, our results indicate that chromoplexy is an underlying mechanism that generates fusion transcripts in EAC. These and other fusion transcripts merit further study as diagnostic markers and potential therapeutic targets in EAC. Cancer 2017;123:3916-24. © 2017 American Cancer Society.
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