期刊论文详细信息
Frontiers in Oncology
Low miR-214-5p Expression Correlates With Aggressive Subtypes of Pediatric ALCL With Non-Common Histology
Stefania Bortoluzzi1  Luca Lo Nigro2  Enrico Gaffo3  Rossella Mura4  Marta Pillon5  Elisa Carraro5  Federica Lovisa6  Piero Di Battista6  Carlotta C. Damanti6  Alessandra Biffi6  Lara Mussolin6  Lavinia Ferrone6  Ilaria Gallingani6  Anna Garbin6  Vincenza Guzzardo7  Marco Pizzi7  Angelo Paolo Dei Tos7 
[1] CRIBI Interdepartmental Research Center for Innovative Biotechnologies (CRIBI), University of Padova, Padova, Italy;Center of Pediatric Hematology Oncology, Azienda Policlinico G. Rodolico – San Marco, Catania, Italy;Department of Molecular Medicine, University of Padova, Padova, Italy;Department of Paediatric Haematology-Oncology, Ospedale Pediatrico Microcitemico, Cagliari, Italy;Division of Pediatric Hematology, Oncology and Stem Cell Transplant, Maternal and Child Health Department, University of Padova, Padova, Italy;Istituto di Ricerca Pediatrica Città della Speranza, Padova, Italy;Surgical Pathology and Cytopathology Unit, Department of Medicine - DIMED, University of Padova, Padova, Italy;
关键词: ALCL;    childhood;    miRNA;    prognosis;    biomarker;    RNA-seq;   
DOI  :  10.3389/fonc.2021.663221
来源: DOAJ
【 摘 要 】

The unsatisfactory cure rate of relapsing ALK-positive Anaplastic Large-Cell Lymphoma (ALCL) of childhood calls for the identification of new prognostic markers. Here, the small RNA landscape of pediatric ALK-positive ALCL was defined by RNA sequencing. Overall, 121 miRNAs were significantly dysregulated in ALCL compared to non-neoplastic lymph nodes. The most up-regulated miRNA was miR-21-5p, whereas miR-19a-3p and miR-214-5p were reduced in ALCL. Characterization of miRNA expression in cases that relapsed after first line therapy disclosed a significant association between miR-214-5p down-regulation and aggressive non-common histology. Our results suggest that miR-214-5p level may help to refine the prognostic stratification of pediatric ALK-positive ALCL.

【 授权许可】

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