RESUMEN
BACKGROUND: Liver hepatocellular carcinoma (LIHC) is a lethal cancer. This study aimed to identify the N6 -methyladenosine (m6 A)-targeted long non-coding RNA (lncRNA) related to LIHC prognosis and to develop an m6 A-targeted lncRNA model for prognosis prediction in LIHC. METHODS: The expression matrix of mRNA and lncRNA was obtained, and differentially expressed (DE) mRNAs and lncRNAs between tumor and normal samples were identified. Univariate Cox and pathway enrichment analyses were performed on the m6 A-targeted lncRNAs and the LIHC prognosis-related m6 A-targeted lncRNAs. Prognostic analysis, immune infiltration, and gene DE analyses were performed on LIHC subgroups, which were obtained from unsupervised clustering analysis. Additionally, a multi-factor Cox analysis was used to construct a prognostic risk model based on the lncRNAs from the LASSO Cox model. Univariate and multivariate Cox analyses were used to assess prognostic independence. RESULTS: A total of 5031 significant DEmRNAs and 292 significant DElncRNAs were screened, and 72 LIHC-specific m6 A-targeted binding lncRNAs were screened. Moreover, a total of 29 LIHC prognosis-related m6 A-targeted lncRNAs were obtained and enriched in cytoskeletal, spliceosome, and cell cycle pathways. An 11-m6 A-lncRNA prognostic model was constructed and verified; the top 10 lncRNAs included LINC00152, RP6-65G23.3, RP11-620J15.3, RP11-290F5.1, RP11-147L13.13, RP11-923I11.6, AC092171.4, KB-1460A1.5, LINC00339, and RP11-119D9.1. Additionally, the two LIHC subgroups, Cluster 1 and Cluster 2, showed significant differences in the immune microenvironment, m6 A enzyme genes, and prognosis of LIHC. CONCLUSION: The m6 A-lncRNA prognostic model accurately and effectively predicted the prognostic survival of LIHC. Immune cells, immune checkpoints (ICs), and m6 A enzyme genes could act as novel therapeutic targets for LIHC.
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Adenosina/análogos & derivados , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/mortalidad , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/mortalidad , ARN Largo no Codificante/genética , Adenosina/genética , Anciano , Biomarcadores de Tumor/genética , Carcinoma Hepatocelular/inmunología , Femenino , Regulación Neoplásica de la Expresión Génica , Humanos , Estimación de Kaplan-Meier , Neoplasias Hepáticas/inmunología , Masculino , Persona de Mediana Edad , Pronóstico , Modelos de Riesgos Proporcionales , ARN Largo no Codificante/metabolismo , Microambiente Tumoral/genética , Microambiente Tumoral/inmunologíaRESUMEN
INTRODUCTION: Intrapancreatic accessory spleen is an uncommon congenital abnormality of the spleen with no indication for surgical intervention. Among the few cases reported, IPAS coexisted with a normal spleen. We here report the first case of IPAS arising a couple years after splenectomy with the appearance of an endocrine tumor of the pancreas. PRESENTATION OF CASE: A 62-year-old female presented with a one-week history of left upper quadrant discomfort. She had splenectomy for the treatment of hypersplenism caused by cirrhotic portal hypertension two years before this admission. Her physical examination was unremarkable and laboratory data was within the normal range. Both the ultrasonography and magnetic resonance image revealed a small oval-shaped mass in the tail of her pancreas with the diameter 2cm or less. A distal pancreatectomy was performed for the suspection of malignant neuroendocrine tumor of the pancreas. An intrapancreatic accessory spleen was confirmed by the pathologic examination. DISCUSSION: Intrapancreatic accessory spleen is one kind of congenital ectopic spleen without indication for operative intervention. We present the case to support that intrapancreatic accessory spleen may enlarge through a compensatory mechanism, and raise the awareness of this intrapacreatic entity to avoid unnecessary surgical operation. CONCLUSION: IPAS should be highly considered as a differential diagnosis while the lesion is no more than 2.5cm in diameter and/or other accessory spleens show around the splenic hilum.