1.Microsatellite Instability of Gastric and Colorectal Cancers as a Predictor of Synchronous Gastric or Colorectal Neoplasms.
Young Beak KIM ; Sun Young LEE ; Jeong Hwan KIM ; In Kyung SUNG ; Hyung Seok PARK ; Chan Sup SHIM ; Hye Seung HAN
Gut and Liver 2016;10(2):220-227
BACKGROUND/AIMS: Microsatellite instability (MSI) plays a crucial role in gastrointestinal carcinogenesis. The aim of this study was to clarify whether MSI is a useful marker for predicting synchronous gastric and colorectal neoplasms. METHODS: Consecutive patients who underwent both esophagogastroduodenoscopy and colonoscopy before the resection of gastric or colorectal cancers were included. MSI was analyzed using two mononucleotide and three dinucleotide markers. RESULTS: In total, 434 gastric cancers (372 microsatellite stability [MSS], 21 low incidence of MSI [MSI-L], and 41 high incidence of MSI [MSI-H]) and 162 colorectal cancers (138 MSS, 9 MSI-L, and 15 MSI-H) were included. Patients with MSI gastric cancer had a higher prevalence of synchronous colorectal cancer, colorectal adenoma, and gastric adenoma than those with MSS gastric cancers (4.8% vs 0.5%, p=0.023; 11.3% vs 3.2%, p=0.011; 3.2% vs 1.2%, p=0.00, respectively). The prevalence of synchronous colorectal adenomas was highest in MSI-L gastric cancers (19.0%), compared with MSI-H (7.3%) or MSS (3.2%) gastric cancers (p=0.002). In addition, there were no significant differences in the prevalence rates of synchronous colorectal adenoma among the MSI-H (13.3%), MSI-L (11.1%), and MSS (12.3%) colorectal cancers (p=0.987). CONCLUSIONS: The presence of MSI in gastric cancer may be a predictor of synchronous gastric and colorectal neoplasms, whereas MSI in colorectal cancer is not a predictor of synchronous colorectal adenoma.
Adenoma/*genetics/surgery
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Aged
;
Colonoscopy
;
Colorectal Neoplasms/*genetics/surgery
;
Endoscopy, Digestive System
;
Female
;
Humans
;
Male
;
*Microsatellite Instability
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Middle Aged
;
Neoplasms, Multiple Primary/*genetics/surgery
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Predictive Value of Tests
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Stomach Neoplasms/*genetics/surgery
2.Benign hepatocellular nodules of healthy liver: focal nodular hyperplasia and hepatocellular adenoma.
Massimo RONCALLI ; Amedeo SCIARRA ; Luca Di TOMMASO
Clinical and Molecular Hepatology 2016;22(2):199-211
Owing to the progress of imaging techniques, benign hepatocellular nodules are increasingly discovered in the clinical practice. This group of lesions mostly arises in the context of a putatively normal healthy liver and includes either pseudotumoral and tumoral nodules. Focal nodular hyperplasia and hepatocellular adenoma are prototypical examples of these two categories of nodules. In this review we aim to report the main pathological criteria of differential diagnosis between focal nodular hyperplasia and hepatocellular adenoma, which mainly rests upon morphological and phenotypical features. We also emphasize that for a correct diagnosis the clinical context such as sex, age, assumption of oral contraceptives, associated metabolic or vascular disturbances is of paramount importance. While focal nodular hyperplasia is a single entity epidemiologically more frequent than adenoma, the latter is representative of a more heterogeneous group which has been recently and extensively characterized from a clinical, morphological, phenotypical and molecular profile. The use of the liver biopsy in addition to imaging and the clinical context are important diagnostic tools of these lesions. In this review we will survey their systematic pathobiology and propose a diagnostic algorithm helpful to increase the diagnostic accuracy of not dedicated liver pathologists. The differential diagnosis between so-called typical and atypical adenoma and well differentiated hepatocellular carcinoma will also be discussed.
Adenoma/*diagnosis/surgery
;
Carcinoma, Hepatocellular/diagnosis
;
Diagnosis, Differential
;
Focal Nodular Hyperplasia/*diagnosis/surgery
;
Hepatocyte Nuclear Factor 1-alpha/metabolism
;
Humans
;
Liver/pathology
;
Liver Neoplasms/*diagnosis/surgery
;
beta Catenin/genetics/metabolism
3.Benign hepatocellular nodules of healthy liver: focal nodular hyperplasia and hepatocellular adenoma.
Massimo RONCALLI ; Amedeo SCIARRA ; Luca Di TOMMASO
Clinical and Molecular Hepatology 2016;22(2):199-211
Owing to the progress of imaging techniques, benign hepatocellular nodules are increasingly discovered in the clinical practice. This group of lesions mostly arises in the context of a putatively normal healthy liver and includes either pseudotumoral and tumoral nodules. Focal nodular hyperplasia and hepatocellular adenoma are prototypical examples of these two categories of nodules. In this review we aim to report the main pathological criteria of differential diagnosis between focal nodular hyperplasia and hepatocellular adenoma, which mainly rests upon morphological and phenotypical features. We also emphasize that for a correct diagnosis the clinical context such as sex, age, assumption of oral contraceptives, associated metabolic or vascular disturbances is of paramount importance. While focal nodular hyperplasia is a single entity epidemiologically more frequent than adenoma, the latter is representative of a more heterogeneous group which has been recently and extensively characterized from a clinical, morphological, phenotypical and molecular profile. The use of the liver biopsy in addition to imaging and the clinical context are important diagnostic tools of these lesions. In this review we will survey their systematic pathobiology and propose a diagnostic algorithm helpful to increase the diagnostic accuracy of not dedicated liver pathologists. The differential diagnosis between so-called typical and atypical adenoma and well differentiated hepatocellular carcinoma will also be discussed.
Adenoma/*diagnosis/surgery
;
Carcinoma, Hepatocellular/diagnosis
;
Diagnosis, Differential
;
Focal Nodular Hyperplasia/*diagnosis/surgery
;
Hepatocyte Nuclear Factor 1-alpha/metabolism
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Humans
;
Liver/pathology
;
Liver Neoplasms/*diagnosis/surgery
;
beta Catenin/genetics/metabolism
4.Clinicopathologic features of metanephric adenoma.
Zhu-lei SUN ; Xin-hua ZHANG ; Jiang WU ; Qiu RAO ; Heng-hui MA ; Xuan WANG ; Qun-li SHI ; Xiao-jun ZHOU
Chinese Journal of Pathology 2012;41(2):119-120
Adenoma
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genetics
;
metabolism
;
pathology
;
surgery
;
Adult
;
Carcinoma, Renal Cell
;
genetics
;
metabolism
;
pathology
;
Chromosomes, Human, Pair 3
;
genetics
;
Chromosomes, Human, Pair 7
;
genetics
;
Diagnosis, Differential
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Diploidy
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Female
;
Follow-Up Studies
;
Humans
;
Kidney Neoplasms
;
genetics
;
metabolism
;
pathology
;
surgery
;
Male
;
Middle Aged
;
Retrospective Studies
;
S100 Proteins
;
metabolism
;
Vimentin
;
metabolism
;
WT1 Proteins
;
metabolism
;
Wilms Tumor
;
metabolism
;
pathology
5.Hyalinizing trabecular tumor of thyroid: a clinicopathologic study.
Bo CHEN ; Chang-shui LI ; Gu ZHANG ; Wen-juan YIN ; Jian-qiang ZHAO ; Jun-ying CHEN ; Wen-yong SUN
Chinese Journal of Pathology 2012;41(8):560-561
Adenoma
;
genetics
;
metabolism
;
pathology
;
surgery
;
Adult
;
Carcinoma, Papillary
;
genetics
;
metabolism
;
pathology
;
Diagnosis, Differential
;
Exons
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Female
;
Follow-Up Studies
;
Humans
;
Ki-67 Antigen
;
metabolism
;
Male
;
Mutation
;
Nuclear Proteins
;
metabolism
;
Proto-Oncogene Proteins B-raf
;
genetics
;
Thyroglobulin
;
metabolism
;
Thyroid Neoplasms
;
genetics
;
metabolism
;
pathology
;
surgery
;
Thyroid Nuclear Factor 1
;
Transcription Factors
;
metabolism
6.Clinicopathological features and molecular genetic analysis of endolymphatic sac tumor: report of 2 cases.
Qiu RAO ; Xiao-jun ZHOU ; Xing-zao JIN ; Heng-hui MA ; Hang-bo ZHOU ; Zhen-feng LU
Chinese Journal of Pathology 2010;39(6):412-413
Adenoma
;
metabolism
;
pathology
;
Adult
;
Carcinoma, Renal Cell
;
metabolism
;
pathology
;
Diagnosis, Differential
;
Ear Neoplasms
;
complications
;
genetics
;
metabolism
;
pathology
;
surgery
;
Endolymphatic Sac
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Female
;
Follow-Up Studies
;
Humans
;
Kidney Neoplasms
;
metabolism
;
pathology
;
Middle Aged
;
Paraganglioma
;
metabolism
;
pathology
;
Point Mutation
;
Von Hippel-Lindau Tumor Suppressor Protein
;
genetics
;
von Hippel-Lindau Disease
;
complications
;
genetics
;
metabolism