Risk factors of gallbladder cancer: An international collaborative case-contol study

Serra, Miquel; Calvo, Alfonso; Báez, Sergio; Yamamoto, Masahiro; Endoh, Kazuo; Aranda, Waldo

doi:10.1002/(sici)1097-0142(19961001)78:7<1515::aid-cncr21>3.0.co;2-1

Cited by 35 publications

(21 citation statements)

References 9 publications

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“…The association between gallbladder cancer and chronic inflammation due to gallstones has been mentioned in various studies since 1861. [13][14][15] Inflammation of the gallbladder wall is also seen in chronic inflammatory conditions, and found usually to be non-specific. 8 Gallstones are detected in 54-97% of gallbladder cancers.…”

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confidence: 99%

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Incidental findings during routine pathological evaluation of gallbladder specimens: review of 1,747 elective laparoscopic cholecystectomy cases

Başak

Hasbahçeci

Canbak

et al. 2016

annals

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INTRODUCTION Cholecystectomy for benign gallbladder diseases can lead to previously undiagnosed gallbladder cancer during histopathological evaluation. Despite some controversy over its usefulness, histopathological evaluation of all gallbladder specimens is common in most hospitals. We evaluated the results of routine pathology of the gallbladder after cholecystectomy for benign gallbladder diseases with regard to unexpected primary gallbladder cancer (UPGC). METHODS Patients undergoing cholecystectomy because of benign gallbladder diseases between 2009 and 2013 were enrolled in this study. All gallbladder specimens were sent to the pathology department, and histopathological reports were examined in detail. The impact of demographic features on pathological diagnoses and prevalence of UPGC assessed. Data on additional interventions and postoperative survival for patients with UPGC were collected. RESULTS We enrolled 1,747 patients (mean age, 48.7±13.6 years). Chronic cholecystitis was the most common diagnosis (96.3%) and was associated significantly with being female (p=0.001). Four patients had UPGC (0.23%); one was stage T3 at the time of surgery, and the remaining three cases were stage T2. CONCLUSIONS Routine histopathological examination of the gallbladder is valuable for identification of cancer that requires further postoperative management.

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confidence: 99%

“…8 Metaplastic changes to the gallbladder epithelium are known to cause precancerous lesions. 14,16 Association of metaplasia with dysplasia and carcinoma has been studied. 8,17 In the present study, two (50%) of UGPC cases had metaplasia, but this association could not be assessed by statistical means because of only four UPGC cases with a prevalence of 0.23%.…”

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confidence: 99%

Incidental findings during routine pathological evaluation of gallbladder specimens: review of 1,747 elective laparoscopic cholecystectomy cases

Başak

Hasbahçeci

Canbak

et al. 2016

annals

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“…Anchorage-independent growth assays were performed using the CytoSelect™ 96-well Cell Transformation assay kit (Cell Biolabs, San Diego, CA, USA). Briefly, JCRB1033 cells (5x10 4 ) or SNU-308 cells (1x10 5 ) were plated in DMEM containing 10% FBS in a cell suspension agar matrix between layers of base agar matrix. After 2 weeks, the agar matrix was solubilized and the cells were stained with MTT solution.…”

Section: Methodsmentioning

confidence: 99%

The cell adhesion molecule L1 promotes gallbladder carcinoma progression in vitro and in vivo

et al. 2011

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Abstract. Recent studies have demonstrated that the cell adhesion molecule, L1, is expressed in several malignant tumor types and its expression correlates with tumor progression and metastasis. However, the role of L1 in gallbladder carcinoma (GBC) remains unclear. Here, we demonstrate that L1 is expressed in GBC cells and plays an important role in the growth, motility, invasiveness, and adhesiveness of GBC cells. Specific depletion or overexpression of L1 in the GBC cell lines JCRB1033 and SNU-308, respectively, was achieved by lentivirus-mediated transduction and expression of an L1 mRNA-specific short hairpin RNA or full-length human L1. Stable depletion of L1 led to a significant decrease in GBC cell proliferation, migration and invasion, as well as decreased intracellular signaling through AKT and FAK. Overexpression of L1 in GBC cells enhanced these cellular activities. In a GBC xenograft nude mouse model, suppression of L1 markedly reduced tumor growth and increased the survival of tumorbearing mice whereas L1 overexpression stimulated tumorigenicity. Taken together, these results suggest that L1 plays a crucial role in GBC progression and may be a novel therapeutic target in GBC treatment. IntroductionGallbladder carcinoma (GBC) is the most common malignancy of the biliary tract. Although occurrence is rare compared to other gastrointestinal tract neoplasms such as gastric and colorectal cancers, GBC has a distinctly higher incidence in certain demographic groups and geographic areas (1,2). The prevalence of GBC in China, Thailand and Northern India is much higher than in the United States and Europe (3). Surgical resection is currently the most effective and potentially curative treatment for GBC. However, many patients present late in the course of the disease when surgical intervention is no longer effective; most patients with advanced GBC experience frequent recurrence after surgery. Therefore, the overall survival rate remains quite poor (4). Although the most important risk factor for the development of GBC is cholelithiasis (up to 95% of GBCs are associated with gallstones) (5), the molecular mechanisms involved in early carcinogenesis and the factors affecting disease progression remain unclear. Therefore, the identification of factors crucial for GBC progression is necessary for development of new therapeutic strategies.L1 is a transmembrane glycoprotein of 200-220 kDa that belongs to the immunoglobulin superfamily of cell adhesion molecules. It consists of six immunoglobulin-like domains and five fibronectin type III repeats in the extracellular region, a single-pass transmembrane domain and a cytoplasmic tail (6). L1 was originally described as a neural cell adhesion molecule and has been shown to initiate a variety of dynamic motile processes, including cerebellar cell migration and neurite extension in the central nervous system (7,8). L1 is also expressed in other cell types such as endothelial cells, certain epithelial cells, reticular fibroblasts, and cells of lymphoid and myelomonocyt...

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“…Although the most important risk factor for the development of GBC is cholelithiasis (up to 95% of GBCs are associated with gallstones; ref. 5), the molecular mechanisms involved in early carcinogenesis and the factors affecting disease progression remain unclear. Therefore, identification of factors crucial for GBC progression is necessary for the development of new therapeutic strategies.…”

Section: Introductionmentioning

confidence: 99%

Chemokine (C-X-C Motif) Ligand 12 Is Associated with Gallbladder Carcinoma Progression and Is a Novel Independent Poor Prognostic Factor

Lee

et al. 2012

Clinical Cancer Research

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Purpose: Although recent studies have suggested that chemokine (C-X-C motif) ligand 12 (CXCL12) is important in the progression of various malignancies, its role in gallbladder carcinoma (GBC) remains unknown. We investigated CXCL12 expression in GBC and its biologic and prognostic role in GBC tumorigenesis.Experimental Design: We examined CXCL12 expression in tumor specimens from 72 patients with GBC by immunohistochemistry and analyzed the correlation between CXCL12 expression and clinicopathologic factors or survival. The functional significance of CXCL12 expression was investigated by CXCL12 treatment and suppression of CXCR4, a major receptor of CXCL12, as well as by CXCL12 overexpression in in vitro and in vivo studies.Results: CXCL12 was differentially expressed in GBC tissues. CXCL12 expression was significantly associated with a high histologic grade (P ¼ 0.042) and nodal metastasis (P ¼ 0.015). Multivariate analyses showed that CXCL12 expression (HR, 8.675; P ¼ 0.014) was an independent risk factor for patient survival. CXCL12 significantly increased anchorage-dependent and -independent growth, migration, invasion, adhesiveness, and survival of GBC cells in vitro, and these effects were dependent on CXCR4. Consistent with these results, overexpression of CXCL12 significantly promoted GBC tumorigenicity in a xenograft model.Conclusions: Our results indicate that GBC cells express both CXCL12 and its receptor CXCR4, and CXCL12 may have a role in GBC progression through an autocrine mechanism. In addition, CXCL12 is a novel independent poor prognostic factor in patients with GBCs. Thus, targeting CXCL12 and CXCR4 may provide a novel therapeutic strategy for GBC treatment.

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Risk factors of gallbladder cancer: An international collaborative case-contol study

Cited by 35 publications

References 9 publications

Incidental findings during routine pathological evaluation of gallbladder specimens: review of 1,747 elective laparoscopic cholecystectomy cases

Incidental findings during routine pathological evaluation of gallbladder specimens: review of 1,747 elective laparoscopic cholecystectomy cases

The cell adhesion molecule L1 promotes gallbladder carcinoma progression in vitro and in vivo

Chemokine (C-X-C Motif) Ligand 12 Is Associated with Gallbladder Carcinoma Progression and Is a Novel Independent Poor Prognostic Factor

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