National Cancer Institute®
Last Modified: July 1, 2002
UI - 11983470
AU - Tseng JH; Wan YL; Hung CF; Ng KK; Pan KT; Chou AS; Liu NJ
TI - Diagnosis and staging of gallbladder carcinoma. Evaluation with dynamic MR imaging.
SO - Clin Imaging 2002 May-Jun;26(3):177-82
AD - First Department of Diagnostic Radiology, Chang-Gung Memorial Hospital at Linkou, College of Medicine and School of Medical Technology, Chang-Gung University, 5 Fu-Hsing Street, Kwei-Shan, Taipei, Taiwan, ROC.
The purpose of this study is to determine the ability of dynamic magnetic resonance imaging (MRI) in the diagnosis and staging of gallbladder cancer (GBC). Images of dynamic MRI of hepatobiliary system combined with MR cholangiography (MRC) of 18 patients with pathologically proved gallbladder cancer were correlated with pathological and operative findings. Focal or diffuse wall thickening was present in 10 patients. In five patients, the tumor appeared as a fungating or intramural mass. A tumor replacing the gallbladder was found in two patients and a small cancer in cystic duct in one patient. The tumor featured early and irregular enhancement, which persisted throughout the dynamic study. Metastatic nodes were found by surgicopathology in 13 patients and were depicted by the dynamic MRI in 11 patients. Local invasion to liver was found by surgery in 12 patients and correctly detected by MRI in 11 patients. MRI detected duodenum invasion in three out of six patients and none of the three cases with omental metastasis. In conclusion, dynamic MRI is useful and reliable in staging of advanced gallbladder cancer. MRI combined with MRC is sensitive in detection of obstructive jaundice, liver invasion as well as liver and lymph nodes metastasis. It is more difficult to delineate the invasion to duodenum and omental metastasis by MRI.
UI - 12057912
AU - Wistuba II; Ashfaq R; Maitra A; Alvarez H; Riquelme E; Gazdar AF
TI - Fragile histidine triad gene abnormalities in the pathogenesis of gallbladder carcinoma.
SO - Am J Pathol 2002 Jun;160(6):2073-9
AD - Department of Anatomic Pathology, Pontificia Universidad Catolica de Chile, Santiago, Chile. firstname.lastname@example.org
There is limited information about the molecular changes involved in the pathogenesis of gallbladder carcinoma (GBC). Our recent allelotyping analyses have indicated that chromosome 3p loss of heterozygosity (LOH), including the fragile histidine triad (FHIT) candidate tumor-suppressor gene locus at 3p14.2, is frequently detected in this neoplasm. To investigate the role of the FHIT abnormalities in the multistage sequential development of GBC, 33 formalin-fixed paraffin-embedded invasive GBC specimens and 76 accompanying histologically normal (n = 43) and dysplastic (n = 33) epithelia were examined by immunostaining for expression of Fhit protein. Allele loss at the FHIT gene locus (3p14.2) was studied in all GBCs and in a subset of accompanying gallbladder epithelia by polymerase chain reaction-based LOH analysis, using three 3p14.2 microsatellite markers. In addition, histologically normal epithelium from chronic cholecystitis (n = 19) and dysplasia (n = 13) from gallbladder specimens without cancer were examined for immunostaining and LOH. There was a progressive increase in both the frequency of loss of Fhit expression and LOH at FHIT with increasing severity of histopathological changes. FHIT abnormalities were occasionally demonstrated in histologically normal gallbladder epithelium. Dysplastic foci demonstrated frequent reduction or absence of Fhit immunostaining (38 to 55%) and FHIT allelic loss (33 to 46%). In invasive tumors, these abnormalities were even higher, with 79% reduction or absence of Fhit immunostaining and 76% FHIT allele loss. A high correlation (70%) was observed between Fhit immunostaining abnormalities and allele loss in GBC specimens (P < 0.05). Although a high frequency of FHIT locus breakpoints were detected in both invasive and dysplastic gallbladder specimens, no intronic homozygous deletions on FHIT were detected in GBCs. FHIT gene abnormalities are nearly universal in GBC and these changes are detected early in the sequential development of this neoplasm. Our findings indicate that the FHIT gene is one of the chromosome 3p putative tumor suppressor genes involved in the pathogenesis of this highly malignant neoplasm.
UI - 11986189
AU - Kohya N; Miyazaki K; Matsukura S; Yakushiji H; Kitajima Y; Kitahara K;
TI - Fukuhara M; Nakabeppu Y; Sekiguchi M Deficient expression of O(6)-methylguanine-DNA methyltransferase combined with mismatch-repair proteins hMLH1 and hMSH2 is related to poor prognosis in human biliary tract carcinoma.
SO - Ann Surg Oncol 2002 May;9(4):371-9
AD - Department of Surgery, Saga Medical School, Saga, Japan.
BACKGROUND: O(6)-Methylguanine-DNA methyltransferase (MGMT) is a DNA repair enzyme that transfers methyl groups from O(6)-methylguanine to itself. Alkylation of DNA at the O(6) position of guanine is an important step in the induction of mutations in the organism by alkylating agents. The O(6)-methyl G:T mismatch is recognized by the mismatch-repair (MMR) pathway. The biliary duct is highly exposed to alkylating agents because of its anatomical location. METHODS: We examined 39 surgically resected gallbladder carcinomas and 35 extrahepatic bile duct carcinomas and evaluated the expression of MGMT and MMR protein (hMLH1 and hMSH2) by immunohistochemical staining. RESULTS: MGMT-negative staining was detected in 59.0% of gallbladder carcinoma specimens and 60.0% of extrahepatic bile duct carcinoma specimens. In gallbladder carcinoma, hMLH1- and hMSH2-negative staining was observed in 51.3% and 59.0%, respectively, whereas in extrahepatic bile duct carcinoma, the respective values were 57.1% and 65.7%. MGMT-negative staining correlated with hepatic invasion in gallbladder carcinoma and with poor prognosis in both types of tumor. Furthermore, a combined MGMT and MMR status was shown to be a more significant prognostic biomarker in both tumor types. CONCLUSIONS: Combined MGMT and MMR is a possible prognostic marker that probably reflects an accumulation of genetic mutations.
UI - 11986191
AU - Suzuoki M; Hida Y; Miyamoto M; Oshikiri T; Hiraoka K; Nakakubo Y;
TI - Shinohara T; Itoh T; Okushiba S; Kondo S; Katoh H RCAS1 expression as a prognostic factor after curative surgery for extrahepatic bile duct carcinoma.
SO - Ann Surg Oncol 2002 May;9(4):388-93
AD - Department of Surgical Oncology, Division of Cancer Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido, Japan. email@example.com
BACKGROUND: RCAS1 (receptor-binding cancer antigen expressed on SiSo cells) is a cancer cell-surface antigen and has been identified as a prognostic factor in several cancers. It is thought that tumor cells escape from immune attack by expressing RCAS1, which induces apoptosis in receptor-positive immune cells. We investigated the relationship between RCAS1 expression and clinicopathologic features and clinical outcome in patients with extrahepatic bile duct carcinoma (EBDC) who underwent curative resection. METHODS: RCAS1 expression was determined by immunohistochemistry in 60 patients with EBDC who underwent curative resection from 1992 to 1999. The patients were divided into two groups on the basis of the extent of RCAS1 expression: a low-expression group (immunoreactivity in <25% of cells) and a high-expression group. Expression was correlated with clinicopathologic features and prognosis. RESULTS: RCAS1 was expressed in 52 (86.7%) of 60 tumors and at a high frequency in all histopathologic stages. High expression of RCAS1 was detected in 46 (76.7%) of 60 cases. No correlation existed between the pattern of RCAS1 expression and any clinicopathologic feature, although high expression did correlate with poor prognosis. High RCAS1 expression was an independent negative predictor for survival. CONCLUSIONS: RCAS1 expression predicts poor outcome in resectable EBDC.
UI - 12082617
AU - Laghi L; Orbetegli O; Bianchi P; Zerbi A; Di Carlo V; Boland CR; Malesci
TI - A Common occurrence of multiple K-RAS mutations in pancreatic cancers with associated precursor lesions and in biliary cancers.
SO - Oncogene 2002 Jun 20;21(27):4301-6
AD - Division of Gastroenterology, Istituto Clinico Humanitas, Rozzano, Milan, 20089 Italy.
Recent studies on small series of pancreatic cancer (PC) with foci of pancreatic intraepithelial neoplasia (PanIN), a putative precursor lesion, have shown that multiple K-RAS mutations may coexist in the same neoplastic pancreas. To see whether mutant-K-RAS polyclonality is a common and specific feature of pancreatic carcinogenesis, we investigated a unselected series of periampullary cancers (41 pancreatic, 13 biliary and two ampullary adenocarcinomas). After hemi-nested polymerase chain reaction (PCR), mutations identified with single strand conformation polymorphism (SSCP) were confirmed by allele-specific PCR and sequencing. K-RAS codon 12 was mutated in 34 (83%) pancreatic cancers and in 11 (85%) biliary cancers. Multiple distinct K-RAS mutations were found in 16 PC (39% of all cases, 47% of those with mutated K-RAS) and in eight biliary cancers (62 and 72%, respectively). In PC, multiple K-RAS mutations were more frequent (P<0.001) in cancers with (nine of 12, 75%) than in those without detectable PanIN (seven of 29, 24%). Individual precursor lesions of the same neoplastic pancreas were found to harbor distinct mutations. Results show that multiple K-RAS mutations are frequent both in PC with associated PanIN and in biliary cancers, and indicate that clonally distinct precursor lesions of PC might variably contribute to tumor development.
UI - 12115514
AU - Gallus S; Negri E; Chatenoud L; Bosetti C; Franceschi S; La Vecchia C
TI - Post-menopausal hormonal therapy and gallbladder cancer risk.
SO - Int J Cancer 2002 Jun 10;99(5):762-3
AD - Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. firstname.lastname@example.org
The relation between post-menopausal hormone replacement therapy (HRT) and gallbladder cancer was analyzed in women above age 45 years, using data of a case-control study conducted in Italy between 1985 and 1997, on 31 incident, histologically confirmed cases and 3,702 controls in hospital for acute, non-neoplastic conditions. The multivariate odds ratio (OR) was 3.2 (95% confidence interval: 1.1-9.3) for those who had ever used HRT and the OR tended to rise with longer duration. Although based on small numbers, due to the rarity of the disease, these findings provide the first direct epidemiological evidence of an association between HRT and gallbladder cancer. Copyright 2002 Wiley-Liss, Inc.
UI - 11824055
AU - Frena A; Catalano P; La Guardia G; Martin F
TI - [Radical surgery for gallbladder carcinoma]
SO - Chir Ital 2001 Nov-Dec;53(6):801-7
AD - Chirurgia Generale 2, Ospedale Regionale, Via Lorenz Bohler, 5, 39100 Bolzano.
The aims of the study were to evaluate the adequacy of the surgical treatment and results of curative extended resections for gallbladder cancer. To this end we carried out a retrospective analysis of 59 patients operated on at our institution from 1983 to 2000. Nineteen patients received a curative resection with a radical intent (4 stage I-II patients and 15 stage III-IV patients, according to the AJCC classification). Kaplan-Meyer survival was 100% after one year and 66.6% after five years for stage I-II patients; 44.4% after one year and 0% after 5 years for stage III patients; 75.0% after one year and 0% after 5 years for stage IV patients. Our analysis confirms the poor prognosis of gallbladder carcinoma. In stage I-II patients surgical treatment offers a good chance of survival. In stage III-IV patients surgery affords good palliation. "Curative" extended resection is, however, a safe surgical procedure and offers a real possibility of enhancing survival.
UI - 12115390
AU - Oohashi Y; Shirai Y; Wakai T; Nagakura S; Watanabe H; Hatakeyama K
TI - Adenosquamous carcinoma of the gallbladder warrants resection only if curative resection is feasible.
SO - Cancer 2002 Jun 1;94(11):3000-5
AD - Division of Digestive and General Surgery, Niigata University Graduate School of Medical and Dental Sciences, Niigata City, Japan.
BACKGROUND: Adenosquamous/squamous cell carcinoma of the gallbladder generally has been considered a lethal disease. The objective of this study was to clarify the effectiveness of resection for patients with adenosquamous/squamous cell carcinoma of the gallbladder. METHODS: Twenty-nine patients who underwent resection for either adenosquamous carcinoma (n = 28 patients) or squamous cell carcinoma (n = 1 patient) were analyzed retrospectively. Sixteen patients underwent radical resection, whereas the other patients underwent primary tumor resection alone. To elucidate the factors that influenced postresectional survival, 10 variables (age, gender, presence or absence of gallstones, size of the primary tumor, lymphatic vessel invasion, blood vessel invasion, perineural invasion, TNM stage, residual tumor status, and type of resection) were examined. RESULTS: Twenty-three patients (79.3%) were categorized with T3 or T4 tumors that invaded adjacent organs. The outcome after undergoing radical resection (cumulative 5-year survival rate, 48.6%) was significantly better compared with the outcome of patients after undergoing primary tumor resection alone (cumulative 3-year survival rate, 7.7%; P = 0.004). The outcome after undergoing resection was better in 14 patients who had no residual tumor (cumulative 5-year survival rate, 62.9%) compared with the outcome in 15 patients who had residual tumor (cumulative 5-year survival rate, 0%; P < 0.001). Univariate analysis revealed that residual tumor status (P < 0.001), type of resection (P = 0.004), patient age (P = 0.012), and blood vessel invasion (P = 0.017) were significant prognostic factors. Residual tumor status (P = 0.026) was the only significant independent prognostic factor. CONCLUSIONS: Adenosquamous/squamous cell carcinoma of the gallbladder warrants resection only if potentially curative (R0) resection is feasible. Copyright 2002 American Cancer Society.
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