Rationale:Pancreatic acinar cell carcinoma (PACC) is a relatively rare malignancy of the exocrine pancreas. BRCA2, a cancer susceptibility gene, has been widely studied in breast and ovarian carcinomas as mutation carriers for this gene are at a high risk for cancer development. Olaparib, an oral poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitor, has been approved for the treatment of ovarian cancer with any BRCA 1/2 mutations. Herein, we report the first case of a germline BRCA2-mutated unresectable advanced PACC patient who responded well to olaparib treatment.Patient concerns:A 59-year-old male with a family history of cancer presented with a persistent epigastric dull pain for 3 months.Diagnosis:The patient was diagnosed with advanced PACC based on computed tomography (CT) scan, laparotomy, and pathology.Interventions:Exploratory laparotomy, intratumoral brachytherapy by radioiodine-125 seeds, modified FOLFIRINOX chemotherapy, and targeted therapy with olaparib were administered.Outcomes:The patient responded well to olaparib until the occurrence of severe adverse drug reactions, he died as a result of multiple organ failure with an overall survival period of 12 months.Lessons:As a PARP inhibitor, olaparib has remarkable curative effect not only on breast and ovarian cancers, but also on other malignancies with BRCA mutations. Patients with advanced cancer could benefit from active targeted therapy with improvement in overall survival and quality of life.

Objectives 18F-Fluorodeoxyglucose positron emission tomography (FDG-PET) has been an important modality for detecting malignancies. Recently, an increasing number of studies reported the utility of FDG-PET parameters in predicting clinical outcomes and treatment assessment in variety of cancers. We aimed at clarifying both the prognostic role and assessment value of FDG-PET in pancreatic carcinoma. Methods We systematically searched electronic databases of PubMed, Embase, Cochrane Library, and Web of Science to identify relevant studies to conduct this meta-analysis. Comparative analyses of the pooled hazard ratio (HR) for overall survival were performed to assess the utility of FDG-PET parameters in prognosis evaluation and treatment assessment by random-effect model. Results Twenty-three studies with 1762 patients met the inclusion criteria of this meta-analysis. The pooled results revealed that greater maximum standardized uptake value of the primary tumor was significantly correlated with poorer overall survival (HR, 1.31; 95% confidence interval, 1.15–1.50; P < 0.001). Besides, greater reduction of maximum standardized uptake value after treatments indicated significant better overall survival (HR, 0.68; 95% confidence interval, 0.47–0.98; P = 0.037). Conclusions 18F-Fluorodeoxyglucose positron emission tomography parameters might be helpful not only for predicting survival outcome but also for selecting potentially efficacious treatments in patients with pancreatic carcinoma.

The upregulation of cell division cycle associated protein 5 (CDCA5) has been observed in various cancer types. However, the prognostic value of CDCA5 and its underlying mechanism contributing to tumorigenesis in hepatocellular carcinoma (HCC) remain poorly understood. We used tissue microarray (TMA) to evaluate the prognosis of 304 HCC samples based on their CDCA5 expression, and analyzed the genomic features correlated with CDCA5 by using dataset from The Cancer Genome Atlas (TCGA). Compared with adjacent normal tissues, increased expression of CDCA5 was found in HCC tissues. Moreover, higher expression of CDCA5 was associated with inferior OS and DFS outcomes in HCC patients. The enrichment plots showed that the gene signatures in cell cycle, DNA replication and p53 pathways were enriched in patients with higher CDCA5 expression. Meanwhile, statistically higher mutations burdens in TP53 could also be observed in CDCA5-high patients. Integrative analysis based on miRNAseq and methylation data demonstrated a potential association between CDCA5 expression and epigenetic changes. In conclusion, our study provided the evidence of CDCA5 as an oncogenic promoter in HCC and the potential function of CDCA5 in affecting tumor microenvironment.

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