• Title/Summary/Keyword: Pancreatic cancer surgery

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Chronic Hepatitis B Virus Infection and Risk of Pancreatic Cancer: A Meta-analysis

  • Li, Lei;Wu, Bo;Yang, Li-Bo;Yin, Guan-Cheng;Liu, Ji-Yong
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.1
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    • pp.275-279
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    • 2013
  • Objectives: A number of studies have shown that chronic hepatitis B virus infection is implicated in susceptibility to pancreatic cancer. However, the results are still controversial. This meta-analysis aimed to quantitatively assess the relationship between chronic hepatitis B virus infection and incidence of pancreatic cancer of cohort and case-control studies. Methods: A literature search was performed for entries from 1990 to 2012 using PUBMED and EMBASE. Studies were included if they reported odds ratios (ORs) and corresponding 95% CIs of pancreatic cancer with respect to the infection of hepatitis B virus. Results: Eight studies met the inclusion criteria, which included five case-control studies and three cohort studies. Compared with individuals who have not infection of hepatitis B virus, the pooled OR of pancreatic cancer was 1.403 (95%CI: 1.139-1.729, P=0.001) for patients with hepatitis B virus infection. Sub-group analysis by study design showed that the summary OR was 1.43 (95%CI: 1.06-1.94, P=0.021) when pooling case-control studies and 1.31 (95%CI: 1.00-1.72, P=0.05) when pooling cohort studies. Conclusion: Findings from this meta-analysis suggest that chronic hepatitis B virus infection may increase the risk of pancreatic cancer. This relationship needs to be confirmed by further follow-up studies.

Practice guidelines for managing extrahepatic biliary tract cancers

  • Hyung Sun Kim;Mee Joo Kang;Jingu Kang;Kyubo Kim;Bohyun Kim;Seong-Hun Kim;Soo Jin Kim;Yong-Il Kim;Joo Young Kim;Jin Sil Kim;Haeryoung Kim;Hyo Jung Kim;Ji Hae Nahm;Won Suk Park;Eunkyu Park;Joo Kyung Park;Jin Myung Park;Byeong Jun Song;Yong Chan Shin;Keun Soo Ahn;Sang Myung Woo;Jeong Il Yu;Changhoon Yoo;Kyoungbun Lee;Dong Ho Lee;Myung Ah Lee;Seung Eun Lee;Ik Jae Lee;Huisong Lee;Jung Ho Im;Kee-Taek Jang;Hye Young Jang;Sun-Young Jun;Hong Jae Chon;Min Kyu Jung;Yong Eun Chung;Jae Uk Chong;Eunae Cho;Eui Kyu Chie;Sae Byeol Choi;Seo-Yeon Choi;Seong Ji Choi;Joon Young Choi;Hye-Jeong Choi;Seung-Mo Hong;Ji Hyung Hong;Tae Ho Hong;Shin Hye Hwang;In Gyu Hwang;Joon Seong Park
    • Annals of Hepato-Biliary-Pancreatic Surgery
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    • v.28 no.2
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    • pp.161-202
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    • 2024
  • Backgrounds/Aims: Reported incidence of extrahepatic bile duct cancer is higher in Asians than in Western populations. Korea, in particular, is one of the countries with the highest incidence rates of extrahepatic bile duct cancer in the world. Although research and innovative therapeutic modalities for extrahepatic bile duct cancer are emerging, clinical guidelines are currently unavailable in Korea. The Korean Society of Hepato-Biliary-Pancreatic Surgery in collaboration with related societies (Korean Pancreatic and Biliary Surgery Society, Korean Society of Abdominal Radiology, Korean Society of Medical Oncology, Korean Society of Radiation Oncology, Korean Society of Pathologists, and Korean Society of Nuclear Medicine) decided to establish clinical guideline for extrahepatic bile duct cancer in June 2021. Methods: Contents of the guidelines were developed through subgroup meetings for each key question and a preliminary draft was finalized through a Clinical Guidelines Committee workshop. Results: In November 2021, the finalized draft was presented for public scrutiny during a formal hearing. Conclusions: The extrahepatic guideline committee believed that this guideline could be helpful in the treatment of patients.

Clinical Significance of Expression and Amplification of the DcR3 Gene in Pancreatic Carcinomas

  • Zhou, Jian;Song, Shi-Duo;Li, De-Chun;Zhou, Jin;Zhu, Dong-Ming;Zheng, Shi-Ying
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.2
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    • pp.719-724
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    • 2012
  • This study aimed to investigate the clinical significance of expression and amplification of decoy receptor 3 (DcR3) in pancreatic carcinomas (PC). mRNA expression was detected by PQ-PCR, and amplification was determined. DcR3 protein expression was detected by immunohistochemistry and ELISA. Correlations between DcR3 expression and clinical pathological factors were analyzed. The relative amount of DcR3 in PC tissues and non-cancerous tissues showed a statistically significant difference, 21 cases displaying more than two fold DcR3 amplification, while no such amplification was found in normal pancreatic tissues. DcR3 positive cell staining was located in the cytoplasm. The positive rate of DcR3 in PC and non-cancerous tissues showed a significant difference. DcR3 mRNA expression was correlated with clinical staging, size of the tumor, lymph node metastasis and histological staging, while protein expression was correlated with clinical data like tumor size. DcR3 gene amplification only correlated with tumor size. The level of DcR3 in serum of the PC resectable group before operation was $72.2{\pm}10.2$ pg/ml, showing a significant difference compared to gallbladder carcinoma group (GC) or pancreatic benign tumor (PBT) group (P < 0.01). In conclusion, DcR3 amplification is correlated with DcR3 expression in PC tissues, especially those clinical pathological factors which reflect tumor progression. Assessment of DcR3 level in sera of PC patients may be helpful for the early diagnosis and prognostic judgement.

Galectin-1 Promotes Gastric Carcinoma Progression and Cisplatin Resistance Through the NRP-1/c-JUN/Wee1 Pathway

  • Zhengyang Pan;Guoxi Xu;Yan Zhang;Meiling Wu;Jiahui Yu;Xujun He;Wei Zhang;Junfeng Hu
    • Journal of Gastric Cancer
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    • v.24 no.3
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    • pp.300-315
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    • 2024
  • Purpose: Gastric cancer (GC) is among the deadliest malignancies and the third leading cause of cancer-related deaths worldwide. Galectin-1 (Gal-1) is a primary protein secreted by cancer-associated fibroblasts (CAFs); however, its role and mechanisms of action of Gal-1 in GC remain unclear. In this study, we stimulated GC cells with exogenous human recombinant galectin-1 protein (rhGal-1) to investigate its effects on the proliferation, migration, and resistance to cisplatin. Materials and Methods: We used simulated rhGal-1 protein as a paracrine factor produced by CAFs to induce GC cells and investigated its promotional effects and mechanisms in GC progression and cisplatin resistance. Immunohistochemical (IHC) assay confirmed that Gal-1 expression was associated with clinicopathological parameters and correlated with the expression of neuropilin-1 (NRP-1), c-JUN, and Wee1. Results: Our study reveals Gal-1 expression was significantly associated with poor outcomes. Gal-1 boosts the proliferation and metastasis of GC cells by activating the NRP-1/C-JUN/Wee1 pathway. Gal-1 notably increases GC cell resistance to cisplatin The NRP-1 inhibitor, EG00229, effectively counteracts these effects. Conclusions: These findings revealed a potential mechanism by which Gal-1 promotes GC growth and contributes to chemoresistance, offering new therapeutic targets for the treatment of GC.

Two Cases of Unresectable Pancreatic Cancer Treated with Neoadjuvant Chemotherapy and Surgical Resection

  • Huh, Gunn;Chun, Jung Won;You, Min Su;Paik, Woo Hyun;Lee, Sang Hyub;Kim, Yong-Tae;Ryu, Ji Kon
    • Journal of Digestive Cancer Reports
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    • v.7 no.2
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    • pp.61-64
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    • 2019
  • We report two cases of patients with unresectable pancreatic cancer treated with neoadjuvant chemotherapy and surgical resection. In the first case, main mass was located at the neck of the pancreas, encasing superior mesenteric artery and peritoneal seeding was suspected. In the second case, main mass was located at the body of pancreas and superior mesenteric artery was encased. Both patients received FOLFIRINOX chemotherapy regimen, consisting of 5-FU, folinic acid, irinotecan and oxaliplatin. In both cases, tumor size decreased and vascular involvement regressed in response to chemotherapy. After subsequent chemoradiation therapy, both patients underwent surgical resection with negative resection margin. The pathological stages were ypT1cN0 and ypT1aN0, respectively. Both patients received postoperative adjuvant chemotherapy with 6 cycles of 5-FU/folinic acid and remained without evidence of disease for more than 6 months after the surgery.

Overexpression of Tbx3 Predicts Poor Prognosis of Patients with Resectable Pancreatic Carcinoma

  • Wang, Hong-Cheng;Meng, Qing-Cai;Shan, Ze-Zhi;Yuan, Zhou;Huang, Xin-Yu
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.4
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    • pp.1397-1401
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    • 2015
  • Background: To determine the expressions of Tbx3, a member of subgroup belonging to T-box family, and its prognostic value in pancreatic carcinoma. Materials and Methods: We determined the expression levels of Tbx3 on both mRNA and protein levels in 30 pairs of fresh tumor tissues and paratumor tissues by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting, respectively. In addition, protein level of Tbx3 were identified using immunochemistry in 80 pairs of paraffin-embedded specimen. The correlations between Tbx3 expression and various clinicopathological parameters as well as overall survival were evaluated. Results: Tbx3 mRNA and protein levels in tumor tissues were significantly higher than in the paratumor tissues by qRT-PCR ($0.05{\pm}0.007$ vs. $0.087{\pm}0.001$, p<0.001) and western blotting ($1.134{\pm}0.043$ vs. $0.287{\pm}0.017$, p<0.001). The statistical analysis based on immunohistochemical evaluation suggested that Tbx3 aberrant expression was significantly associated with several conventional clinicopathological variables, such as gender, age, tumor position, preoperative CA19-9 level, pathological T staging and N staging. Univariate and multivariate analyses revealed that Tbx3 expression was an independent prognostic factor for overall survival (<0.001). Conclusions: Our results suggest that overexpression of Tbx3 is associated with poor prognosis of pancreatic cancer patients. However, additional clinical trials are needed to accurately validate this observation.

What are the Appropriate Surgery and Postoperative Surveillance for Intraductal Papillary Mucinous Neoplasm?

  • Ideno, Noboru;Nakata, Kohei;Nakamura, Masafumi
    • Journal of Digestive Cancer Reports
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    • v.9 no.1
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    • pp.8-18
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    • 2021
  • Although many guidelines for pancreatic cystic neoplasms focus on the management of intraductal papillary mucinous neoplasm of the pancreas (IPMN) at the highest oncological risk, there are many issues that surgeons need to consider at the time to plan the surgical procedures based on characteristics of IPMN subtypes, such as multiplicity of branch duct-IPMN (BD-IPMN) and intraductal spreading of main duct-IPMN (MD-IPMN). For multifocal BD-IPMN, partial pancreatectomy would be selected to remove BD-IPMN with predictors of malignancy, while the other lesions without risk factors can be left, although total pancreatectomy might be considered if the patients have a strong family history of pancreatic cancer. Partial pancreatectomy would be also adequate procedure for MD-IPMN if negative surgical margin for high-grade dysplasia or invasive carcinoma were achieved. It has become to be well-known that patients with BD-IPMN are at increased risk for developing not only IPMN-associated pancreatic ductal adenocarcinoma (PDAC) but also PDAC independent from the IPMN. Hence, the detection of a concomitant PDAC is also an important focus for strategies after resection of BD-IPMNs. Our recent analysis of patients after partial pancreatectomy for MD-IPMN with negative surgical margin identified an unexpected recurrence pattern, which we called "monoclonal skip" recurrence. MD-IPMN seems to be disseminated in the pancreatic ductal systems and MD-IPMN with identical genetic background was detected in the remnant pancreas even in a long time after index surgery. We proposed strategies of postoperative surveillance based on characteristics and natural history of each morphological subtype.

Pancreaticobiliary Ductal Anatomy in the Normal Population

  • Jirasiritham, Jakrapan;Wilasrusmee, Chumpon;Poprom, Napaphat;Larbcharoensub, Noppadol
    • Asian Pacific Journal of Cancer Prevention
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    • v.17 no.9
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    • pp.4363-4365
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    • 2016
  • Background: The complex anatomy of the pancreaticobiliary duct was crucial in management of pancreatic and biliary tract disease. Materials and Methods: Fresh specimens of pancreas, common bile duct (CBD), and duodenum were obtained en bloc from autopsies of 160 patients. Results: Ninety-three male and 67 female patients were included. The length of the pancreas ranged from 9.8-20 cm (mean, 16.20 +/- 1.70 cm). The intrapancreatic portion of the CBD showed patterns of three types: most common (85.30%) was type A, in which the anterior surface of the common bile duct was totally covered, while its posterior surface was partially covered, by the pancreatic parenchyma. On dissection of the accessory duct of Santorini, the accessory duct was traceable to the duodenal wall in 67.6%. The anatomy of the Wirsung-choledochus confluence was grouped into five different types. The common channel was found in 75.60% and its length varied from just a common junction (so-called "V-type" anatomy) to 15 mm (Y-type-b). Separate papillae (so-called "II-type") were found in 15.3% of specimens. Conclusions: Several important points regarding the anatomy of the pancreaticobiliary junction and pancreatic ductal system were illustrated in this study.

Impact of sarcopenia on biliary drainage during neoadjuvant therapy for pancreatic cancer

  • Kunio Kataoka;Eizaburo Ohno;Takuya Ishikawa;Kentaro Yamao;Yasuyuki Mizutani;Tadashi Iida;Hideki Takami;Osamu Maeda;Junpei Yamaguchi;Yukihiro Yokoyama;Tomoki Ebata;Yasuhiro Kodera;Hiroki Kawashima
    • Clinical Endoscopy
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    • v.57 no.1
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    • pp.112-121
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    • 2024
  • Background/Aims: Since the usefulness of neoadjuvant chemo(radiation) therapy (NAT) for pancreatic cancer has been demonstrated, recurrent biliary obstruction (RBO) in patients with pancreatic cancer with a fully covered self-expandable metal stent (FCSEMS) during NAT is expected to increase. This study investigated the impact of sarcopenia on RBO in this setting. Methods: Patients were divided into normal and low skeletal muscle index (SMI) groups and retrospectively analyzed. Patient characteristics, overall survival, time to RBO (TRBO), stent-related adverse events, and postoperative complications were compared between the two groups. A Cox proportional hazard model was used to identify the risk factors for short TRBO. Results: A few significant differences were observed in patient characteristics, overall survival, stent-related adverse events, and postoperative complications between 38 patients in the normal SMI group and 17 in the low SMI group. The median TRBO was not reached in the normal SMI group and was 112 days in the low SMI group (p=0.004). In multivariate analysis, low SMI was the only risk factor for short TRBO, with a hazard ratio of 5.707 (95% confidence interval, 1.148-28.381; p=0.033). Conclusions: Sarcopenia was identified as an independent risk factor for RBO in patients with pancreatic cancer with FCSEMS during NAT.

Overexpression of CXCL2 inhibits cell proliferation and promotes apoptosis in hepatocellular carcinoma

  • Ding, Jun;Xu, Kangdi;Zhang, Jie;Lin, Bingyi;Wang, Yubo;Yin, Shengyong;Xie, Haiyang;Zhou, Lin;Zheng, Shusen
    • BMB Reports
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    • v.51 no.12
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    • pp.630-635
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    • 2018
  • C-X-C motif chemokine ligand 2 (CXCL2) is a small secreted protein that exhibits a structure similar to the proangiogenic subgroup of the CXC chemokine family. Recently, accumulating evidence suggests that chemokines play a pivotal role in cancer progression and carcinogenesis. We examined the expression levels of 7 types of $ELR^+$ CXCLs messenger RNA (mRNA) in 264 clinical samples. We found that CXCL2 expression was stably down-regulated in 94% of hepatocellular carcinoma (HCC) specimens compared with paired adjacent normal liver tissues and some HCC cell lines. Moreover, CXCL2 overexpression profoundly attenuated HCC cell proliferation and growth and induced apoptosis in vitro. In animal studies, we found that overexpressing CXCL2 by lentivirus also apparently inhibited the size and weight of subcutaneous tumours in nude mice. Furthermore, we demonstrated that CXCL2 induced HCC cell apoptosis via both nuclear and mitochondrial apoptosis pathways. Our results indicate that CXCL2 negatively regulates the cell cycle in HCC cells via the ERK1/2 signalling pathway. These results provide new insights into HCC and may ultimately lead to the discovery of innovative therapeutic approaches of HCC.