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Cases of extrahepatic bile duct carcinoma are mostly adenocarcinomas and extrahepatic bile duct squamous cell carcinomas are rare. We report here a case of choledochal squamous cell carcinoma in a young woman who underwent surgery and chemotherapy. The woman presented with abdominal discomfort. A physical examination showed tenderness in the upper abdomen. Laboratory tests showed elevated direct bilirubin, total bilirubin, and C-reactive protein levels. Abdominal computed tomography and magnetic resonance imaging showed a cystic-solid mixed soft tissue mass in the common bile duct. Pain symptoms in the patient were not relieved and surgical treatment was performed. Postoperative pathological results showed a choledochal cyst complicated by squamous cell carcinoma. The patient was treated by biliary intestinal anastomosis followed by chemotherapy. However, the patient developed liver metastasis and recurrence at a 6-month follow-up. Primary congenital bile duct cysts with squamous cell carcinoma are extremely rare. Surgical resection is the main treatment option for choledochal squamous cell carcinoma. Postoperative chemoradiotherapy can be used, but the efficacy is poor and chemotherapy does not significantly prolong the patient’s survival.

Background and Aim Altered motility of the gallbladder is associated with an increased risk of gallstones and can result in biliary tract cancers. Cholecystokinin (CCK) is an important modulator of gallbladder motility which functions by activating CCK type-A receptor (CCKAR). The aim of this study was to determine whether genetic variants in CCK and CCKAR are associated with the risk of biliary tract cancers and stones. Methods We investigated the associations between nine single nucleotide polymorphisms in CCK and CCKAR in a population-based case–control study, including 439 biliary tract cancer cases (253 gallbladder, 133 extrahepatic bile duct, and 53 ampulla of Vater cancer cases), 429 biliary stone cases, and 447 population controls in Shanghai, China. Results We found that women with the CCKAR rs1800855 AA genotype had an increased risk of gallbladder cancer (odds ratio = 2.37, 95% confidence interval (CI): 1.36–4.14) compared with subjects with the TT genotype, and remained significant after Bonferroni correction (P = 0.0056). Additionally, female carriers of the CCKAR haplotype C-T-C-T (rs2071011-rs915889-rs3822222-rs1800855) had a reduced risk of gallbladder cancer (odds ratio = 0.61, 95% confidence interval: 0.43–0.86) compared with those with the G-C-C-A haplotype; the association also remained significant after Bonferroni correction. Conclusions These findings suggest that variants in the CCKAR gene may influence the risk of gallbladder cancer in women. Additional studies are needed to confirm our findings.

OBJECTIVE To investigate the relationship between BMI．WHR and billary tract cancers(CBT)． METHODS A population-based case—controI study was conducted in urban Shanghai fromJune 1,1997to May 31,2001 involving interviews with 627 new cases of biliary tract cancers aged 35tO 74 years and 959 frequency-matched population controls bygender and age in five-year groups．All subjects wereinterviewedin person by trained interviewers using a structured questionnaire．An unconditional logistic regression was performed to calculate adjusted odds ratios(ORs) and 95％ confidence intervals(CIs)． RESULTS Obesity was associated with an increased risk of gallbladder cancer across adulthood at ages 20-29 and 30-39 in females．Compared with subjects inthelowest quartile of WHR，ORs for the highestquartile and P for trend for cancers of gallbladder and extrahepatic bile duct both reached significant levels among males andfemales． CONCLUSION Our observationsin urban Shanghai suggested that obesity in early adult life may contribute to the risk of gallbladder cancer，and increasedWHR maysubstantially elevatedrisk of cancers of the gallbladder and extrahepatic bile duct．

Altered motility of the gallbladder can result in gallstone and cholecystitis, which are important risk factors for biliary tract cancer. Motilin (MLN) and somatostatin (SST) are known important modulators of gallbladder motility. To determine whether genetic variants in motilin, somatostatin, and their receptor genes are associated with the risk of biliary tract cancers and stones, nine tag-SNPs were determined in 439 biliary tract cancer cases (253 gallbladder, 133 extrahepatic bile duct and 53 ampulla of Vater cancer cases), 429 biliary stone cases, and 447 population controls in a population-based case–control study in Shanghai, China. We found that subjects with the MLNR rs9568169 AA genotype and SSTR5 rs169068 CC genotype were significantly associated with risk of extrahepatic bile duct cancer (OR = 0.49, 95% CI: 0.27–0.89; OR = 2.40, 95% CI: 1.13–5.13) compared to the major genotypes. MLN rs2281820 CT and rs3793079 AT genotypes had significantly increased risks of gallstones (OR = 1.52, 95% CI: 1.06–2.18; OR = 1.64, 95% CI: 1.20–2.25) compared to TT genotypes. Besides, haplotype analysis showed that MLN T-T-T haplotype (rs2281820–rs3793079–rs2281819) had a non-significantly elevated risk of gallstone (OR = 1.30, 95% CI: 0.91–1.86) compared with C-A-A haplotype. To the best of our knowledge, this is the first study to report an association between genetic polymorphisms in MLN, MLNR and their receptor genes and risk of biliary tract cancers and stones., Highlights • We conduct a population-based case–control study of biliary tract diseases in China. • We examine nine TagSNPs in gallbladder motility genes in this study. • MLNR rs9568169 and SSTR5 rs169068 are related to extrahepatic bile duct cancer risk. • MLN rs2281820 and rs3793079 are associated with gallstone risk.

Purpose: Biliary tract cancer is an uncommon malignancy with a poor survival rate. We evaluated p16 gene alteration as a prognostic marker for this disease. Experimental Design: We studied p16 gene alterations by sequencing, methylation, and loss of heterozygosity of chromosome 9p in 118 biliary tract carcinomas, including 68 gallbladder cancers, 33 extrahepatic bile duct cancers, and 17 ampullary cancers. Survival was evaluated in 57 patients with gallbladder carcinomas, 27 with bile duct carcinomas, and 16 with ampullary carcinomas with and without somatic p16 alterations detected by two different methods. Results: p16 gene alterations including silent mutations were present in 61.8% gallbladder cancers, 54.5% bile duct cancers, and 70.6% ampullary cancers. p16 gene nonsilent mutations, p16 methylation, and loss of chromosome 9p21-22 that targets p14, p15, and p16 genes were present in 13 of 53 (24.5%), 8 of 54 (14.8%), and 32 of 44 (72.7%) gallbladder tumors; 5 of 25 (20.0%), 5 of 31 (16.1%), and 12 of 21 (57.1%) bile duct tumors; and 3 of 13 (23.1%), 6 of 15 (40.0%), and 8 of 16 (50.0%) ampullary tumors, respectively. The mean survival of patients with gallbladder cancers without p16 alterations was 21.5 ± 14.8 months compared with 12.1 ± 11.4 months for patients with p16 alterations (P = 0.02). Conclusions: Alteration of p16 gene alone or in combination with alterations of other tumor suppressor genes on chromosome 9p is a prognostic indicator in gallbladder carcinoma, with more favorable survival rates associated with carcinomas lacking p16 gene alterations.