BackgroundCarcinoma of the gallbladder (GBC) clinically mimics benign gallbladder diseases and often escapes detection until advanced stage. Despite the frequency of cholecystectomy, diagnosis of GBC remains problematic in many situations. We sought to identify pathologic features that contribute to the difficulty in recognition of GBC.MethodsWe identified 23 patients (ranged from 45 to 86 years, male to female ratio 1:4.5) with carcinoma involving the gallbladder referred to an academic medical center over a period of 10 years for study. This includes 10 cases of primary GBC, 6 cases of metastatic tumor to gallbladder, 6 cases of directly invasive adenocarcinoma arising elsewhere in the biliary tree, and one case of unidentified origin adenocarcinoma. Primary tumors include adenocarcinoma not otherwise specified (NOS) in 6 cases, papillary adenocarcinoma in 2 cases, and single cases of undifferentiated carcinoma and combined adenocarcinoma and neuroendocrine carcinoma (NEC). Metastatic tumors to gallbladder were from a wide range of primary sites, predominantly the gastrointestinal tract.ResultsThese cases illustrate seven potential pitfalls which can be encountered. These include: 1) mistakenly making a diagnosis of adenocarcinoma of gallbladder when only benign lesions such as deeply penetrating Rokitansky-Aschoff sinuses are present (overdiagnosis), 2) misdiagnosing well-differentiated invasive carcinoma with minimal disease as benign disease (underdiagnosis), 3) differentiating between primary NEC of gallbladder and metastasis, 4) confusing primary mucinous adenocarcinoma of gallbladder with pseudomyxoma peritonei from a low grade appendiceal neoplasm disseminated to gallbladder, 5) confusing gangrenous necrosis related to cholecystitis with geographic tumoral necrosis, 6) undersampling early, grossly occult disease, and 7) misinterpreting extracellular mucin pools.ConclusionsClinical history and a high index of suspicion are prerequisite to detecting GBC. Detection of GBC at an early stage is difficult because the symptoms mimic benign gallbladder diseases. Misinterpretation of subtle microscopic abnormalities contributes diagnostic failures in early cases. Careful attention to any evidence of mural thickening, thorough sampling, particularly in older patients, and close examination of any deeply situated glandular structures are critical. Correlations with radiographic and clinical findings are important helps to avoid misdiagnosis in this commonly resected organ.
Carcinomas of the oral cavity sometimes arise as multiple, independent lesions and this observation has led to the concept of field cancerization. Howerever, the mechanism of multiple occurrences of oral squamous cell carcinoma (OSCC) is still unknown. Thirty-one cases of synchronous and/or metachronous multiple OSCCs were selected from biopsy and operation materials of the Dental Hospital, Tokyo Medical and Dental University. Histopathogenetic study and investigation were carried out. The clonality of the tumor tissues was analyzed by immunohistochemistry for Ki-67, Bcl-2, p53, cyclinB1 and cyclinD1. Histologic observation showed two patterns of occurrence of OSCC: de novo type and premalignancy-associated type. Twenty-one patients with multiple OSCCs were classified into 3 groups. Group I was de novo type, Group II was mixed type and Group III was premalignacy-associated type. Seventeen of 21 patients (80.9%) revealed p53-positivity in the epithelium apart from the tumor. Fifty-two of 69 tumors (75.4%) showed a different expression rate between Cyclin B1 and Cyclin D1. This data suggests that those patients are at high risk of developing second primary tumors. It also suggests the possibility of polyclonal development of the multiple OSCCs.
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