Literature DB >> 27689616

Glypican-3 and KRT19 are markers associating with metastasis and poor prognosis of pancreatic ductal adenocarcinoma.

Hongliang Yao1, Zhulin Yang2, Ziru Liu2, Xiongying Miao2, Leping Yang2, Daiqiang Li3, Qiong Zou4, Yuan Yuan4.   

Abstract

OBJECTIVE: Pancreatic ductal adenocarcinoma (PDAC) is a highly malignant tumor with metastasis in most patients at diagnosis. The molecular mechanisms associated with its high malignancy have not been fully elucidated. This study investigated the clinicopathological significances of GPC3 and KRT19 expression in PDAC.
METHODS: GPC3, KRT19, and CA19-9 protein expression were measured by immunohistochemistry.
RESULTS: GPC3 and KRT19 protein levels were overexpressed in PDAC tumors compared to normal pancreatic tissues, benign pancreatic tissues, and peritumoral tissues (P< 0.01). The percentage of positive GPC3 and KRT19 expression were significantly higher in PDAC patients with larger tumor size, poorly differentiated tumor, lymph node metastasis, invasion, and TNM stage III/IV disease than in patients with small tumor size, well-differentiated tumor, no lymph node metastasis and invasion, as well as TNM stage I/II stage disease (P< 0.05 or P< 0.01). Benign pancreatic lesions with positive GPC3 and KRT19 protein expression exhibited dysplasia or intraepithelial neoplasia. Kaplan-Meier survival analysis showed that PDAC patients with positive GPC3 and KRT19 expression survived significantly shorter than patients with negative GPC3 and KRT19 expression (P < 0.05 or P< 0.001). Cox multivariate analysis revealed that positive GPC3 and KRT19 expression were independent poor prognosis factors in PDAC patients.
CONCLUSIONS: GPC3 and KRT19 overexpression are associated with carcinogenesis, progression, and poor prognosis in patients with PDAC and a valuable biomarker for diagnosis of PDAC.

Entities:  

Keywords:  CA19-9; GPC3; KRT19; Pancreatic ductal adenocarcinoma; dysplasia; immunohistochemistry; pancreatic intraepithelial neoplasia

Mesh:

Substances:

Year:  2016        PMID: 27689616     DOI: 10.3233/CBM-160655

Source DB:  PubMed          Journal:  Cancer Biomark        ISSN: 1574-0153            Impact factor:   4.388


  16 in total

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Journal:  Cancers (Basel)       Date:  2019-11-29       Impact factor: 6.639

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