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Cheol Keun Park

Publications and source records attributed to Cheol Keun Park.

At least 19 recordsLinked to original sources
PubMed2007

Sclerosing hepatic carcinoma: helical CT features.

BACKGROUND: The purpose of this study was to describe our experience, particularly for CT features, with four patients who had pathologically proven sclerosing hepatic carcinoma that mimicked other malignant hepatic tumors with abundant fibrosis at CT. METHODS: Over a 10-year period, we collected four patients with surgically proven sclerosing hepatic carcinoma. All patients were men (age range, 49-63 years; mean, 56 years). Three-phase helical CT images were obtained in all patients, and their CT features were correlated with pathologic findings. RESULTS: The tumor size ranged from 2.7 to 11 cm (mean, 7.2 cm). The tumors were manifested as a hypoattenuating mass with peripheral, rim enhancement at hepatic arterial phase, followed by centripetal enhancement progressively during portal venous and equilibrium phases. Histopathologically, the tumors showed features intermediate between hepatocellular carcinoma and cholangiocarcinoma with abundant fibrosis and surrounding liver had no liver cirrhosis. CONCLUSION: As described above, the CT features of sclerosing hepatic carcinoma may be similar to other malignant hepatic tumors with abundant fibrosis. Although sclerosing hepatic carcinoma is extremely rare, the radiologists should recognize that this tumor may be one of the malignant hepatic tumors with abundant fibrosis, especially in the non-cirrhotic liver.

Biopsy↗
PubMed2006

PKCtheta expression in gastrointestinal stromal tumor.

Gastrointestinal stromal tumor is characterized by a gain of function mutation of KIT gene and the expression of c-kit protein, but in 5% of cases, c-kit expression is negative although histological findings of gastrointestinal stromal tumor are most suspicious. The existence of c-kit-negative gastrointestinal stromal tumors points to the need of additional markers for making the diagnosis. In this study, we studied the expression of PKCtheta and correlated their expression with other immunohistochemical profiles of gastrointestinal stromal tumors and evaluated their usability as a diagnostic marker. For this purpose, 220 gastrointestinal stromal tumors were immunohistochemically stained for PKCtheta, c-kit, CD34, alpha-smooth muscle actin and S-100 protein. Additionally, genetic studies of KIT and PDGFRA genes were performed using c-kit-negative or PKCtheta-negative cases. All the 220 masses were either PKCtheta-positive or c-kit-positive. PKCtheta was positive in 212 (96%) cases and c-kit was positive in 216 (98%) cases in the cytoplasm of tumor cells with a diffuse staining pattern. Out of 212 PKCtheta-positive GISTs, 208 (98%) cases were c-kit-positive, 174 (82%) cases were CD34-positive, 62 (29%) cases were SMA-positive and S-100 protein was positive in 54 cases (26%). Genetic analyses on eight PKCtheta-negative cases showed exon 11 mutations of KIT gene in four cases. Two PKCtheta-positive and c-kit-negative GISTs showed mutations of PDGFRA gene. Our study shows that PKCtheta is a useful marker and it may play a role in the development of gastrointestinal stromal tumors. Together with c-kit, PKCtheta immunostaining can be used as an important diagnostic tool in the pathologic diagnosis of gastrointestinal stromal tumors with its high specificity and sensitivity.

Actins↗
PubMed2006

Encapsulated hepatocellular carcinoma: CT-pathologic correlations.

This study is a retrospective evaluation of the correlations between the presence and integrity of the capsule of nodular hepatocellular carcinomas (HCC) by dynamic CT and histopathology, with histopathologic evidence of tumor propagation to surrounding hepatic parenchyma. Dynamic CT scans of 75 nodular HCCs in 73 patients (61 men, 12 women; age range, 32-81; mean, 53) were evaluated regarding capsule visualization and integrity. Histopathologic findings of HCCs in resected specimens were correlated with the presence of a capsule, tumor invasion onto the capsule, and with the presence of microvascular emboli in the surrounding liver parenchyma. On histopathologic examination, capsules were present in 57 of 75 nodular HCCs; the capsules were invaded by tumor in 18 nodules and there were microvascular emboli around the nodular HCC in 49 cases. Capsule visualization by CT was correlated with the presence of capsule by histopathology (P<0.001). Disruption of capsule by CT was correlated with tumor invasion by histopathology (P=0.003) and with microvascular tumor emboli (P<0.001). The presence and structural integrity of HCC capsules on CT was closely correlated with the presence of capsule on histopathology and the absence of microvascular tumor emboli.

Adult↗
PubMed2006

Hepatic visceral larva migrans of Toxocara canis: CT and sonographic findings.

OBJECTIVE: The aim of this study was to describe the CT and sonographic findings of hepatic visceral larva migrans of Toxocara canis. MATERIALS AND METHODS: Fifty-four patients (44 men, 10 women; age range, 30-80 years; mean age, 53 years) with serologically confirmed visceral larva migrans of Toxocara canis underwent evaluation of the liver with CT (n = 25), sonography (n = 48), or both. Two radiologists used consensus for retrospective evaluation of CT and sonographic findings. Correlation between the presence and severity of hepatic abnormalities on images and the degree of peripheral eosinophilia was assessed. RESULTS: Seventeen (68%) of 25 patients who underwent CT had single or multiple ill-defined, oval or elongated, small, low-attenuating lesions in the liver. Eighteen (38%) of 48 patients who underwent sonography had single or multiple small, poorly defined, oval or elongated, hypoechoic scattered focal lesions in the liver. In the 19 patients who underwent both CT and sonography, the two techniques had no significant difference in rate of detection of hepatic lesions (p = 0.375, McNemar test). The lesion numbers on CT and sonography showed excellent linear correlation (r = 0.844, p = 0.001) by Pearson's correlation test. An independent samples t test showed that eosinophil count and percentage in the peripheral blood were significantly higher in patients with hepatic lesions on CT and sonography than in patients without lesions. CONCLUSION: CT and sonographic findings of hepatic visceral larva migrans of T. canis are multiple, ill-defined, oval or elongated, small, nodular lesions scattered in the liver parenchyma. The presence of hepatic lesions on images was associated with higher peripheral eosinophil count and percentage.

Adult↗
PubMed2006

Mesenchymal hamartomas of the liver: comparison of clinicopathologic features between cystic and solid forms.

Mesenchymal hamartoma (MH) of the liver is an uncommon benign lesion related to ductal plate malformation. It is usually cystic and mainly composed of myxoid mesenchymal tissue with tortuous or cystic bile ducts. In order to characterize the clinicopathological features of MH, the Korean Gastrointestinal Pathology Study Group collected a total of 17 MH cases diagnosed in 7 hospitals from 1992 to 2002 and compared the clinicopathologic findings of cystic MH with those of solid variant. Among the 17 cases, 7 (41%) were solid. The solid form showed a higher serum level of alpha-fetoprotein (AFP), the smaller bile ducts, and more frequent proliferation of vessels. Serum AFP level was related to the amount of hepatocytes. Two of seven solid cases harbored a larger amount of evenly distributed hepatocytes and proliferation of small duct with focal hepatocyte-bile duct transition. These histologic findings are similar to those of mixed hamartoma. Therefore, the mixed hamartoma and the MH of both solid and cystic types could be the variants of one disease spectrum. And hepatocytes within MH might be rather a genuine tumor component than entrapped into the tumor. In conclusion, MH can show various clinicopathological features and recognition of these features will facilitate accurate diagnosis of MH.

Adult↗
PubMed2006

Isolated biliary granulocytic sarcoma followed by acute myelogeneous leukemia with multilineage dysplasia: a case report and literature review.

Granulocytic sarcoma is a rare extramedullary tumor composed of myeloid progenitor cells. Primary involvement of the biliary tract without evidence of leukemia is exceedingly rare. Here, we report an isolated biliary granulocytic sarcoma in a 30-yr-old man who presented with jaundice, fever, and chill without any evidence of leukemia. However, five months after the diagnosis, he developed acute myelogenous leukemia with multilineage dysplasia and chromosomal abnormality. A rare possibility of biliary granulocytic sarcoma should be considered as a differential diagnosis in patients with obstructive jaundice. A histologic evaluation by aggressive diagnostic intervention is important and may improve prognosis.

Adult↗
PubMed2006

Gastric syphilis mimicking adenocarcinoma: a case report.

Syphilis is an unexpected diagnosis in the stomach, and the reduced incidence of syphilis has made its clinical presentation less widely appreciated. We report a 43-yr-old man suffering from epigastric tenderness with an initial diagnosis of gastric carcinoma; gastric syphilis was confirmed by demonstrating spirochetes in a gastric biopsy specimen by silver impregnation. Excessive lymphoplasmacytic infiltration with diffuse thickening of gastric rugae should raise suspicion of gastric syphilis, which should be considered in the differential diagnosis of diffuse erosive gastritis and infiltrative lesions of the stomach.

Adenocarcinoma↗
PubMed2005

Tracing origin of serrated adenomas with BRAF and KRAS mutations.

Serrated neoplasm of the colorectum raised many as-yet unanswered issues. To characterize serrated neoplasia pathway, we investigated BRAF and KRAS mutations in 35 traditional serrated adenomas. BRAF exons 11 and 15, and KRAS exon 2 were amplified by polymerase chain reaction and directly sequenced. BRAF V599E mutation was found in 27 serrated adenomas (77.1%), and KRAS mutations were found in 3 (8.6%) of 35 traditional serrated adenomas. In 13 cases, mixed polyps composed of traditional serrated adenomas and hyperplastic (serrated) polyps were observed, and seven of them showed the same BRAF mutations in both components. Somatic mutations of BRAF and KRAS genes were mutually exclusive. These findings suggest that BRAF mutations are early and a critical event in the serrated adenomas, and most serrated adenomas in both sides of colon may progress from microvesicular hyperplastic polyps via BRAF mutations, and some left-sided serrated adenomas develop via KRAS mutations.

Adenoma↗
PubMed2005

Mutational analysis of EGFR and K-RAS genes in lung adenocarcinomas.

Both epidermal growth factor receptor (EGFR) and RAS gene mutations contribute to the development of non-small cell lung cancer (NSCLC). Because RAS is one of the downstream molecules in the EGFR signal transduction, the association between the somatic mutations of EGFR and RAS may be important in the pathogenesis of NSCLC . However, to date, such data are lacking. In this study, we analyzed the hotspot regions of K-RAS gene (codons 12, 13, 59 and 61) and EGFR gene (exons 18, 19 and 21) in 153 NSCLC tissue samples including 69 adenocarcinomas. Overall, we detected 30 EGFR mutations (19.6%) and 6 K-RAS mutations (3.9%) in the 153 NSCLCs. In the 69 adenocarcinomas, 26 EGFR mutations (37.7%) and six K-RAS mutations (8.7%) were detected. Of note, the 26 tumors with EGFR mutations did not harbor any K-RAS mutations, and the six tumors with K-RAS mutations did not harbor any EGFR mutations. Inverse relationship between K-RAS and EGFR mutations in the lung adenocarcinoma was statistically significant (P=0.046, chi2 test). As regards smoking history, EGFR mutation was significantly associated with never-smoking history, whereas K-RAS mutation was significantly associated with smoking history. Our data suggest that mutations of EGFR and K-RAS genes might separately, but not cooperatively, contribute to lung adenocarcinoma pathogenesis, and that EGFR and K-RAS mutants could separately be anti-neoplastic targets in lung adenocarcinomas.

Adenocarcinoma↗
PubMed2005

Local radiotherapy for patients with unresectable hepatocellular carcinoma.

PURPOSE: To evaluate the response to local radiotherapy (RT) for unresectable hepatocellular carcinoma (HCC) and to analyze the dose-response relationship and the treatment-related morbidities. METHODS AND MATERIALS: Between 1998 and 2002, 59 patients who were treated with localized RT were evaluated. RT was delivered with a curative intent, and the radiation dose was 30-55 Gy (biologic effective dose of 39.0-70.2 Gy(10) using the alpha/beta ratio of 10 Gy) with 2-3 Gy as a daily dose. The tumor response was evaluated by the change in maximum tumor size on serial CT scans, and the morbidity was evaluated by the Common Terminology Criteria for Adverse Events v3.0. RESULTS: An objective tumor response was achieved in 39 of 59 patients (66.1%) with complete response (CR) in 5 patients and partial response (PR) in 34 patients. More than 50 Gy(10) had a significant response; CR or PR was 72.8% with >50 Gy(10) and 46.7% with < or =50 Gy(10) (p = 0.0299). The 2-year overall survival rate after RT was 27.4% (median survival time: 10 months), and this was affected by the tumor response (p = 0.0640); the 2-year overall survival rate after RT was 50.0% for CR and 21.8% for PR. There was no Grade 3 or 4 acute toxicity, and 3 patients (5.1%) developed gastric or duodenal ulcer. CONCLUSIONS: Radiotherapy for unresectable HCC resulted in 66.1% of tumor response with acceptable toxicity, and the radiation dose seems to be a significant prognostic factor in RT response for HCC.

Adult↗
PubMed2005

Molecular changes from dysplastic nodule to hepatocellular carcinoma through gene expression profiling.

Progression of hepatocellular carcinoma (HCC) is a stepwise process that proceeds from pre-neoplastic lesions--including low-grade dysplastic nodules (LGDNs) and high-grade dysplastic nodules (HGDNs)--to advanced HCC. The molecular changes associated with this progression are unclear, however, and the morphological cues thought to distinguish pre-neoplastic lesions from well-differentiated HCC are not universally accepted. To understand the multistep process of hepato-carcinogenesis at the molecular level, we used oligo-nucleotide microarrays to investigate the transcription profiles of 50 hepatocellular nodular lesions ranging from LGDNs to primary HCC (Edmondson grades 1-3). We demonstrated that gene expression profiles can discriminate not only between dysplastic nodules and overt carcinoma but also between different histological grades of HCC via unsupervised hierarchical clustering with 10,376 genes. We identified 3,084 grade-associated genes, correlated with tumor progression, using one-way ANOVA and a one-versus-all unpooled t test. Functional assignment of these genes revealed discrete expression clusters representing grade-dependent biological properties of HCC. Using both diagonal linear discriminant analysis and support vector machines, we identified 240 genes that could accurately classify tumors according to histological grade, especially when attempting to discriminate LGDNs, HGDNs, and grade 1 HCC. In conclusion, a clear molecular demarcation between dysplastic nodules and overt HCC exists. The progression from grade 1 through grade 3 HCC is associated with changes in gene expression consistent with plausible functional consequences.

Carcinoma, Hepatocellular↗
PubMed2005

Clinicopathologic features and prognosis of combined hepatocellular cholangiocarcinoma.

BACKGROUND: Clinicopathologic features and prognosis of combined hepatocellular cholangiocarcinoma (HCC-CC) have not been established. METHODS: Data of patients who underwent surgical resection for HCC-CC were compared with those of hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (CC) patients. RESULTS: The prevalence of hepatitis B positivity (54.0%) and that of cirrhosis (54.2%) in the HCC-CC group were of intermediate tendency between the HCC group and the CC group. The HCC-CC group presented with a higher prevalence of multiplicity and microvascular emboli and portal vein or hepatic vein invasion, but a lower prevalence of capsular formation compared with the other groups. One- and 3-year survival rates in the HCC-CC group (81.9% and 47.0%, respectively) were lower than those in the HCC group and higher than those in the CC group. The cumulative recurrence rates at 6 months and at 1 year in the HCC-CC group (25.0% and 33.3%, respectively) were higher than those in the HCC group and lower than those in the CC group. CONCLUSIONS: The HCC-CC group has distinct clinicopathologic features compared with the HCC or CC groups. In addition, the HCC-CC group has a prognosis that is better than the CC group but worse than the HCC group.

Adult↗
PubMed2005

Mutations of beta-catenin and AXIN I genes are a late event in human hepatocellular carcinogenesis.

BACKGROUND: Hepatocellular carcinoma (HCC) is a well-known cancer involving the Wnt pathway in its carcinogenesis. AIMS: However, it is not clear whether these genetic changes are early genetic events in hepatocarcinogenesis or not. METHOD: In this study, we performed mutational analysis of the beta-catenin and AXIN I genes, and immunohistochemistry for beta-catenin in a series of 114 hepatocellular nodular lesions, including premalignant lesions such as low-grade dysplastic nodules (LGDNs) and high-grade dysplastic nodules (HGDNs). RESULTS: In the present study, mutations of the beta-catenin and AXIN I genes were detected in 16% (13 out of 81) and 6.2% (five of 81) of the HCCs, respectively. However, no mutations were found in 14 LGDNs and 19 HGDNs. Moreover, abnormal nuclear beta-catenin immunostaining was observed in 30 of 81 HCCs, but not in dysplastic nodules. CONCLUSION: Taken together, our data suggest that beta-catenin stabilization because of either beta-catenin or AXIN I mutation might be a late event for malignant progression rather than an early genetic event involving the initiation of HCC development.

Adult↗
PubMed2005

Neoangiogenesis and sinusoidal capillarization in hepatocellular carcinoma: correlation between dynamic CT and density of tumor microvessels.

PURPOSE: To retrospectively evaluate the correlation between the degree of contrast enhancement on dynamic computed tomographic (CT) scans and the degree of neoangiogenesis and sinusoidal capillarization in hepatocellular carcinoma (HCC). MATERIALS AND METHODS: The institutional review board did not require approval or informed patient's consent for the review of medical records or images. Dynamic CT scans of 97 nodular HCCs in 97 patients (79 men, 18 women; age range, 29-73 years; mean age, 54 years) were evaluated in terms of the attenuation change in the arterial, portal venous, and delayed phases, and the results were correlated with the number of unpaired arteries and the degree of sinusoidal capillarization at histopathologic examination. The mean attenuation value of the nodular HCCs on triple-phase helical CT scans was correlated with the number of unpaired arteries and the degree of sinusoidal capillarization. Statistical analysis was performed with the Spearman rank correlation test. RESULTS: The number of unpaired arteries in the nodular HCCs was found to correlate with the degree of contrast enhancement in the arterial phase (r = 0.225, P = .027), but did not correlate with the degree of contrast enhancement in the portal and delayed phases. The degree of sinusoidal capillarization did not correlate linearly with the mean attenuation of the nodular HCCs in any phase of contrast enhancement. CONCLUSION: The degree of contrast enhancement of the nodular HCCs in the arterial phase tended to correlate with the number of unpaired arteries, but no correlation was evident between the degree of contrast enhancement and sinusoidal capillarization in any phase of CT imaging.

Adult↗
PubMed2005

Promoter methylation of E-cadherin in hepatocellular carcinomas and dysplastic nodules.

In order to clarify the significance of E-cadherin methylation in multistep hepatocarcinogenesis, we examined the methylation status of the E-cadherin promoter region, using methylation-specific polymerase chain reaction in 64 hepatocellular carcinomas (HCCs) and 13 dysplastic nodules (DNs), and correlated these results with E-cadherin protein expression and clinicopathologic factors of HCCs. Promoter methylation was detected in 1 of 13 (7.7%) DNs, in 5 of 13 (38.5%) Edmondson and Steiner grade I HCCs, and in 27 of 51 (52.9%) grade II or III HCCs, and a significant correlation was observed between the methylation status and the stepwise progression of hepatocarcinogenesis (p=0.004). Reduced E-cadherin immunoreactivity was found in 18 of 64 (28%) HCCs, but in none of DNs. E-cadherin methylation status in HCCs was significantly correlated with microvascular invasion (p=0.02) and tumor recurrence (p=0.04), but not with reduced E-cadherin immunoreactivity. The Kaplan-Meier method showed that methylation status did not have a significant influence on the recurrence-free survival of HCC patients (p=0.15). Our results indicate that methylation of the E-cadherin promoter region is a frequent event in HCC, which may play an important role in the stepwise progression of hepatocarcinogenesis. And the promoter methylation of E-cadherin in HCC was found to be significantly correlated with microvascular invasion and recurrence.

Adult↗
PubMed2005

Gastrointestinal stromal tumors in Koreans: it's incidence and the clinical, pathologic and immunohistochemical findings.

Seven hundred forty seven cases of gastrointestinal stromal tumors (GISTs) in Koreans who were diagnosed between 2001 and 2002 were analyzed to evaluate their occurrence and their clinical, pathologic and immunohistochemical findings. The most frequent location of tumor was in the stomach (63%), followed by the small intestine (30%), the colorectum (5%), and the esophagus (2%). c-kit expression was found in 93.6% of the cases, while CD34, SMA and S-100 protein was positive in 80.1%, 28.2%, and 20.2%, respectively. c-kit positivity was high in the stomach (94.2%) and small intestine (94.6%), while it was relatively low in the colorectum (85.0%), and esophagus (81.2%). The positivity for CD34 was correlated with the higher risk of GISTs (p = 0.04). Follow up of the patients showed that 58 primary GISTs patients died and 20 of these patients were recurrent or metastatic at the time of diagnosis. The pathologic diagnosis to predict the risk of aggressive behavior of GISTs was correlated with the numbers of tumor, clinical stage, epithelioid histologic type, cellularity, cellular atypia, necrosis, and mucosal invasion (p = 0.00). GISTs with a poor prognosis were closely related to the clinical stage at presentation, the locations of the tumor, and the ages of the patients.

Actins↗
PubMed2005

Prognostic significance of p53 overexpression after hepatic resection of hepatocellular carcinoma.

BACKGROUND/AIMS: p53 mutation is the most common genetic abnormality in human cancers. However, although it has been reported that p53 overexpression in hepatocellular carcinoma (HCC) is associated with the aggressive behavior of tumor, the prognostic significance of p53 overexpression in HCC remains controversial. The aims of the present study were to examine the correlations between p53 overexpression and the clinicopathologic parameters of HCCs, and to determine the prognostic significance of p53 overexpression in HCC. METHODS: Immunohistochemical analysis of p53 overexpression was performed in 105 consecutive cases of HCC who underwent curative hepatic resection. Survival curves were calculated using the Kaplan-Meier method and multivariate analysis of outcome predictors for HCCs was assessed by logistic regression analysis. RESULTS: p53 overexpression was observed in 20 of 105 HCCs (19.0%). Multivariate analysis identified significant correlations between p53 overexpression and microvascular invasion (p=0.027), liver cirrhosis (p=0.035), 1-year survival rate (p=0.016), multiple tumors (p=0.014), and the presence of tumor capsule (p=0.010). The 2-year survival rate was poorer in patients without tumor capsule (p=0.043). CONCLUSIONS: Our results show a positive association between p53 overexpression and microvascular invasion in HCC, and indicate that p53 overexpression is a poor prognostic factor of survival, especially within 1 year after liver resection in HCC patients.

Adult↗