Biomedical subjects

J J Jang

Publications and source records attributed to J J Jang.

At least 37 records · Page 2Linked to original sources

PubMed2000

Mitomycin C induces apoptosis in a caspases-dependent and Fas/CD95-independent manner in human gastric adenocarcinoma cells.

We investigated the mechanism of mitomycin C (MMC)-induced apoptosis in SNU-16 human gastric adenocarcinoma cells. Caspase-8 and caspase-3 were activated in MMC-treated cells whereas caspase-1 was not activated, and cytochrome c was released from mitochondrial membrane to cytosol suggesting that caspase-9 was activated during the MMC-induced apoptotic process. Protein kinase C (PKC) delta was cleaved to its characteristic 40 kDa fragment in a caspase-3-dependent manner; on the other hand PKC zeta was cleaved to approximately 40 kDa independently of caspase-3 in the drug-induced apoptosis of the cells. Incubation with z-DEVD-fmk and benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk) almost completely abrogated MMC-induced DNA fragmentation, indicating that activation of these caspases was crucially involved in MMC-induced apoptosis. Activation of caspase-8 in response to Fas triggering by recruitment of caspase-8 to the Fas has also been found, however, MMC did not induce FasL and Fas expression, as evidenced by reverse transcriptase-polymerase chain reaction and Western blotting. Taken together, these findings indicate that MMC-induced apoptosis in SNU-16 cells was mediated by caspase-8, caspase-9, and caspase-3 activation independently of FasL/Fas interactions.

Adenocarcinoma↗

PubMed2000

Angiogenesis is impaired by hypercholesterolemia: role of asymmetric dimethylarginine.

BACKGROUND: Many angiogenic factors require endothelium-derived nitric oxide (NO) to exert their effects. Recently, an endogenous competitive antagonist of NO synthase has been characterized: asymmetric dimethylarginine (ADMA). Elevated plasma levels of ADMA reduce NO synthesis in hypercholesterolemia. Accordingly, we hypothesized that hypercholesterolemia impairs angiogenesis by an ADMA-dependent mechanism. METHODS AND RESULTS: Angiogenesis was assessed with the use of a disk angiogenesis system implanted subcutaneously in normal (E(+)) mice or apolipoprotein (apo)E-deficient hypercholesterolemic (E(-)) mice. After 2 weeks, the disks were removed, and the fibrovascular growth area was used as an index of angiogenesis. Basal and fibroblast growth factor-stimulated angiogenesis was impaired in E(-) mice, associated with an elevation in plasma ADMA. Oral administration of L-arginine reversed the impairment of angiogenesis in E(-) mice. By contrast, oral administration of L-nitroarginine (an exogenous antagonist of NO synthase) reduced angiogenesis. When added directly to the disk, ADMA dose-dependently inhibited basal and fibroblast growth factor-induced angiogenesis, an effect that was reversed by oral administration of L-arginine. CONCLUSIONS: The derangement of the NO synthase pathway that occurs in hypercholesterolemia is associated with an impairment of angiogenesis. The lipid-induced impairment of angiogenesis can be reversed by oral administration of L-arginine and can be mimicked in normocholesterolemic animals by administration of an NO synthase antagonist. The data are consistent with the hypothesis that ADMA is an endogenous inhibitor of angiogenesis.

Angiogenesis Inhibitors↗

PubMed2000

Loss of p16 and p27 is associated with progression of human gastric cancer.

We performed the immunohistochemical staining for six G1 check point cell cycle proteins to study their expression patterns and roles in the gastric carcinogenesis. We studied 76 cases of paraffin blocks that included the sections of 18 tubular adenomas (TA), 38 early gastric carcinomas (EGC) (20 cases of mucosal type, nine cases of submucosal type with no nodal metastasis, nine cases of submucosal type with nodal metastasis), 20 advanced gastric carcinomas (AGC) (ten cases with no nodal metastasis, ten cases with nodal metastasis). We found that abnormal expression of p16 and p27 increased with the progression of tubular adenomas to advanced gastric cancers. Inverse relationship between pRb and p16 proteins was found in a small portion of the gastric tumors. Expressions of pRb and cdk4 were consistently high in benign and malignant gastric tumors. Expression of cyclin D1 and cyclin E rather decreased with the tumor progression. In conclusion, losses of p16 and p27 seem to play a significant role during the gastric carcinogenesis, and the G1 checkpoint cell cycle proteins such as pRb, cdk4, cyclin D1, and cyclin E variably participate in the gastric carcinogenesis and metastasis by the mechanisms which are yet unknown; thus, further studies need to be performed to elucidate the mechanisms.

Biomarkers, Tumor↗

PubMed2000

Expression of cyclin D1, cyclin E, cdk4 and loss of heterozygosity of 8p, 13q, 17p in hepatocellular carcinoma: comparison study of childhood and adult hepatocellular carcinoma.

AIMS/BACKGROUND: In hepatitis B virus-related hepatocellular carcinoma (HCC), at least 20-40 years of continuous necro-inflammation is necessary for the hepato-carcinogenesis to occur. However, HCC in childhood shows an unusually short latent period and rapid progression. In our previous report, mutation of c-met was found only in childhood HCC, but not in adult HCC. In order to determine the specific biological tumorous features of childhood HCC, a comparison study of childhood and adult HCC was performed. METHODS: Eighteen cases of HBV positive HCC (nine children and nine adults aged more than 40 years) were selected. The expression of G1 phase regulatory proteins (cyclin D1, cyclin E and cdk4) was studied using immunohistochemical methods. Loss of heterozygosity (LOH) on chromosomal arms 8p, 13q and 17p was analyzed. RESULTS: Cyclin D1 expression was significantly lower in childhood HCC than in adult HCC (cases of cyclin D1 expression under 3+: childhood 5/9 vs. adult 1/9, p=0.046). No difference in cyclin E and cdk4 expression was found between childhood and adult HCC. LOH frequency on 13q was relatively higher in childhood than in adult HCC (66.7% vs. 22.2%, p=0.058). LOH frequency on 8p and 17p was 44.4% and 33.3% in childhood HCC and 44.4% and 75% in adult HCC with no statistical significance between the two groups. CONCLUSION: Our data suggest that childhood HCC may be less dependent on cyclin D1 protein for tumor growth and progression than adult HCC, and that the LOH on 13q may be an important feature of childhood HCC.

Adolescent↗

PubMed2000

Basaloid squamous carcinoma of the oesophagus: a distinct neoplasm with multipotential differentiation.

AIMS: Basaloid squamous carcinoma (BSC) is an uncommon variant of squamous cell carcinoma, with its prevalent sites being the hypopharynx, tongue base and larynx. In the oesophagus, BSC is rarer than in the head and neck region. This study was aimed to document the clinicopathological features of BSCs of the oesophagus, and to present their relative incidence and immunohistochemical findings. METHODS AND RESULTS: Eighteen cases of BSC of the oesophagus, comprising 3.6% of 502 oesophageal carcinomas, were reviewed for their pathological and clinical features, and examined for the immunohistochemical expression of neuroendocrine markers, cytokeratins, p53, pRb and bcl-2. Oesophageal basaloid squamous carcinomas tended to be biphasic or multiphasic carcinomas, most commonly with basaloid and squamous components (eight cases), or with additional adenocarcinoma (three cases) or with small cell carcinoma (two cases). Each component was microscopically clearly distinguishable from the others, and metastasized separately, chiefly the basaloid component. The remaining five cases were apparently pure basaloid carcinomas, being characterized by lobules and nests of monotonous round undifferentiated cells with frequent comedo necrosis. They resembled, but were differentiated from, the small cell carcinoma on the basis of neuroendocrine markers and cytokeratin expression. p53, pRb and bcl-2 oncoprotein, which are known to normally present in the basal/parabasal cells of the oesophageal epithelium, were detected in 40-50% of cases, with a heterogeneous expression pattern. The patients were all male, with the age ranging 47-74 years (median 57) and presented at variable stages. The plotted 3 years survival rate was 51%, and the immunohistochemical expression of p53, pRb and bcl-2 was not related to the survival of the patients. CONCLUSION: Basaloid squamous carcinoma of the oesophagus is a peculiar neoplasm with a capacity of multidirectional differentiation, often with heterogeneous oncogene expression, probably reflecting the pluripotential stem cell origin.

Aged↗

PubMed2000

Somatic mutations of Fas (Apo-1/CD95) gene in cutaneous squamous cell carcinoma arising from a burn scar.

Fas (Apo-1/CD95) is a cell-surface receptor involved in cell death signaling, and recent reports have suggested that defects within the Fas receptor pathway such as Fas mutation play an important part in the development and progression of human tumors. Burn scar-related squamous cell carcinoma of skin is a unique subtype of cutaneous squamous cell carcinoma, and tends to be more aggressive in nature than conventional squamous cell carcinoma. The molecular mechanisms underlying the development and progression of burn scar-related squamous cell carcinoma, however, are not clear. In this study, we analyzed the entire coding region and all splice sites of the Fas gene for the detection of the somatic mutations in a series of 50 conventional squamous cell carcinomas and 21 burn scar-related squamous cell carcinomas by polymerase chain reaction, single strand conformation polymorphism, and DNA sequencing. We detected mis-sense mutations in three of 21 burn scar-related squamous cell carcinomas (14.3%), whereas no mutation was detected in 50 conventional squamous cell carcinomas. Of the three Fas mutations detected in the burn scar-related squamous cell carcinomas, one was found in Fas ligand-binding domain, another one was identified in the death domain known to be involved in the transduction of an apoptotic signal, and the other one was found in the transmembrane domain. Our data show that some burn scar-related squamous cell carcinomas have Fas gene mutations in important regions for the apoptosis function and suggest that these mutations might be involved in the pathogenesis of burn scar-related squamous cell carcinomas. In addition, our results provide an important clue to understanding the difference between burn scar-related squamous cell carcinoma and conventional squamous cell carcinoma at the molecular level.

Adolescent↗

PubMed2000

Overexpression of human telomerase RNA in Helicobacter pylori-infected human gastric mucosa.

Telomerase, an enzyme associated with cellular immortality and malignancy, plays an important role in cellular immortalization and tumorigenesis. Furthermore, overexpression of the RNA component of the telomerase, called human telomerase RNA (hTR), has been demonstrated in various human cancers as an early event. The pattern of hTR expression following Helicobacter pylori (H. pylori) infection in human gastric mucosa was investigated by a radioactive in situ hybridization (ISH) assay. Paraffin-embedded sections of 50 biopsy specimens taken from the gastric antrum of individual patients infected to different extents with H. pylori, as well as normal gastric mucosa, were studied. In normal gastric mucosa, only weak hTR expression was noted and the expression was limited to basal cells of the gastric glands. However, the degree of hTR expression gradually increased in parallel with the degree of H. pylori infection. The mean scores of gastric mucosa with mild, moderate and severe degrees of H. pylori infection were 2.3, 2.8, and 3.7 times higher than that of normal gastric mucosa, respectively. The results of this study suggested that up-regulation of hTR expression is a frequent and early event associated with H. pylori infection in the gastric mucosa and may play some role in gastric carcinogenesis. Sufficient synthesis of hTR during this early stage may be a prerequisite for telomerase reactivation to occur in gastric cancer.

Adult↗

PubMed2000

Clinicopathologic study of Castleman's disease in Korea.

Castleman's disease represents an atypical lymphoproliferative disorder, infrequently associated with various immunologic abnormalities or subsequent development of malignancy such as Kaposi sarcoma, malignant lymphoma and plasmacytoma. Its clinicopathologic features depend on various etiologic factors such as Kaposi sarcoma herpesvirus (KSHV), oversecretion of IL-6, adhesion molecule and follicular dendritic cell dysplasia, etc. To investigate the relationship of Castleman's disease (CD) and the above factors, we reviewed 22 cases of CD. Four cases of KSHV positive CD were detected, all multicentric, plasma cell type, and these cases displayed prominent vascular proliferation, characteristic 'Kaposi-like lesion'. IL-6 and CD54 positive mononuclear cells were scattered in interfollicular areas of KSHV positive cases. Follicular dendritic cell hyperplasia, vascular proliferation, expression of IL-6 and CD54 did not show any significant difference between solitary vs multicentric type, and plasma cell type vs hyaline vascular type. Our study suggests that KSHV positive CD reveals unique pathologic features, and the probable relationship of KSHV and IL-6 and CD54 is discussed.

Adolescent↗

PubMed2000

TNF-alpha induces apoptosis mediated by AEBSF-sensitive serine protease(s) that may involve upstream caspase-3/CPP32 protease activation in a human gastric cancer cell line.

In the present study, we investigated the role of caspase-3/CPP32 and serine protease(s) in cell death induced by TNF-alpha in SNU-16 human gastric adenocarcinoma cells. Apoptosis induced in SNU-16 cells by TNF-alpha was accompanied by the activation of caspase-3/CPP32. After treatment with TNF-alpha, PKCdelta cleaved to its characteristic 40 kDa fragment in a caspase-3/CPP32 dependent manner. Incubation with z-DEVD-fmk completely abrogated TNF-alpha-induced DNA fragmentation, indicating that activation of caspase-3/CPP32 was crucially involved in TNF-alpha-induced apoptosis. In addition, serine protease inhibitor, 4-(2-aminoethyl)benzenesulfonyl fluoride (AEBSF), clearly inhibited all the features of apoptosis including DNA fragmentation and chromatin condensation. Furthermore, in the AEBSF treated SNU-16 cells, only intact PKCdelta was detected by immunoblot analysis, suggesting that activation of caspase-3/CPP32 was blocked. Thus, the AEBSF-sensitive step may involve an upstream caspase-3/CPP32 protease activation. Taken together, these results suggest that both caspase-3/CPP32 and serine protease(s) are activated and play an important role in TNF-alpha induced apoptosis in SNU-16 cells.

Adenocarcinoma↗

PubMed1999

Point mutations and deletions of the Bcl10 gene in solid tumors and malignant lymphomas.

The Bcl10 gene, which encodes a protein with proapoptotic activity, recently has been identified on chromosome 1p22. In this study, we analyzed somatic mutations and deletions of the Bcl10 gene in a series of 439 tumor tissues from various histological origins that are known to have frequent loss of heterozygosity at chromosome 1p22. According to the LOH study at intragenic polymorphic sites, deletion of Bcl10 in informative cases was detected in 50% of malignant mesotheliomas, 33% of gastric carcinomas, 23% of breast carcinomas, 20% of hepatocellular carcinomas, 17% of lymphomas, 15% of colorectal carcinomas, 13% of laryngeal carcinomas, and 10% of male germ cell tumors (GCTs). In contrast, we detected Bcl10 mutations in 4 of 120 lymphomas (3.3%) and 2 of 78 GCTs (2.6%), respectively, but no mutation was found in the remaining solid tumors analyzed. Taken together, these data imply that Bcl10 may occasionally be involved in the pathogenesis of lymphoma and GCTs. However, the absence or low frequency of the mutation suggests that either Bcl10 is inactivated by other mechanisms or it is not the only target of chromosome 1p22 deletion in human tumors.

Adaptor Proteins, Signal Transducing↗

PubMed1999

Alterations of the DR5/TRAIL receptor 2 gene in non-small cell lung cancers.

Chromosome 8p21-22 is a frequent site of allelic deletions in many types of human tumors, including non-small cell lung cancer (NSCLC). Tumor necrosis factor-related apoptosis-inducing ligand-receptor 2 (TRAIL-R2) is a cell-surface receptor involved in cell death signaling. The TRAIL-R2 gene recently has been mapped to chromosome 8p21-22. To explore the possibility that the TRAIL-R2 gene might be the relevant gene to the frequent deletion of 8p21-22 in NSCLC, we have analyzed the entire coding region and all splice sites of TRAIL-R2 for the detection of the somatic mutations in a series of 104 NSCLCs. Overall, 11 tumors (10.6%) were found to have TRAIL-R2 gene mutations in the death domain known to be involved in the transduction of an apoptotic signal. Our data indicate that somatic mutation of TRAIL-R2 may play a role in the pathogenesis of some NSCLCs and that the TRAIL-R2 gene is one of the genes relevant to the frequent loss of chromosome 8p21-22 in NSCLC.

Adenocarcinoma↗

PubMed1999

2-(Allylthio)pyrazine inhibition of aflatoxin B1-induced hepatocarcinogenesis in rats.

2-(Allylthio)pyrazine (2-AP), a synthetic pyrazine derivative with an allylsulfur moiety, has hepatoprotective effects against toxicants. Effect of 2-AP on hepatic tumorigenesis in association with glutathione S-transferase (GST) induction was examined in rats exposed to aflatoxin B1 (AFB1). Both AFB1-DNA adduct formation in the liver and urinary elimination of 8,9-dihydro-8-(N7-guanyl)-9-hydroxy-aflatoxin B1 (AFB1-N7-guanine) adduct were also determined. Male Sprague Dawley rats were treated with 2-AP at the daily oral doses of 10, 25 and 50 mg/kg for 16 consecutive days, during which four repeated doses of AFB1 (1.0 mg/kg) were given to the animals. Rats were then subjected to two-thirds of hepatectomy, followed by administration of phenobarbital (PB). Focal areas of hepatocellular alteration were identified after 44 days and preneoplastic foci expressing the placental form of glutathione S-transferase P (GST-P) were quantified by immunostaining of liver sections. 2-AP reduced the volume of liver occupied by GST-P foci by 65-96%. Under these experimental conditions, 2-AP treatment resulted in significant elevations in GST activity in the liver. Levels of radiolabeled AFB1 covalently bound to hepatic DNA, RNA and proteins were significantly reduced in rats treated with 2-AP for 5 days. 2-AP pretreatment also caused a 45% reduction in the urinary elimination of AFB1-N7-guanine adduct over the 24-h postdosing period. The present findings demonstrated that 2-AP exhibited protective effects against AFB1-induced hepatocarcinogenesis in rats with a marked decrease in the level of AFB1-DNA adduct. Reduction of hepatic DNA adducts might result from elevations of activity of GST, which catalyzes detoxification of the carcinogen.

Aflatoxin B1↗

PubMed1999

Alterations of Fas (APO-1/CD95) gene in transitional cell carcinomas of urinary bladder.

Fas (Apo-1/CD95) is a cell-surface receptor involved in cell death signaling. The key role of the Fas system in negative growth regulation has been studied mostly within the immune system, and somatic mutations of Fas in cancer patients have been described solely in lymphoid-lineage malignancies. We analyzed somatic mutations and loss of heterozygosity of Fas gene in 43 transitional cell carcinomas of urinary bladder. Overall, 12 tumors (28%) were found to have Fas mutations, including 11 missense mutations and 1 frameshift mutation. Ten of the 12 mutations were located in the death domain known to be involved in the transduction of an apoptotic signal, and 8 of these 10 mutations showed an identical G to A transition at bp 993, indicating a potential hotspot in bladder cancers. Three of eight (38%) informative tumors carrying Fas mutations showed LOH at polymorphic sites in the promoter region. This is the first report on the Fas gene mutations in nonlymphoid malignancies, and our data suggest that alterations of the Fas gene might lead to the loss of its apoptotic function and contribute to the pathogenesis of some bladder cancers.

Amino Acid Substitution↗

PubMed1999

Progressive changes of the nuclear matrix protein composition in diethylnitrosamine-induced rat hepatocarcinogenesis.

The nuclear matrix proteins (NMPs) consist of common and tissue-specific nuclear proteins, which can be altered by extracellular environments such as radiation, chemicals and virus infection. Thus, NMP profiles were analyzed in diethylnitrosamine (DEN)-treated rat liver. Male F344 rats (6 weeks old) were treated continuously with DEN (40 ppm) in drinking water. All animals were sacrificed at 10, 20 or 30 weeks during the experiment. The profiles of NMPs and cytoskeletal proteins (CSPs) progressively changed in their number and amount in DEN-treated rats. Four peptides increased in their relative amounts, while three decreased in the 10- and 20-week groups. Many NMPs were detected in DEN-induced hepatocellular carcinomas. These results suggest that the alteration of the NMPs may be involved in DEN-induced hepatocarcinogenesis.

Animals↗

PubMed1999

Somatic mutations in the kinase domain of the Met/hepatocyte growth factor receptor gene in childhood hepatocellular carcinomas.

The MET protooncogene encodes a transmembrane tyrosine kinase identified as the receptor of a polypeptide known as hepatocyte growth factor/scatter factor. We performed PCR-based single-strand conformational polymorphism and sequencing analysis of the tyrosine kinase domain of the MET gene (exon 15-19) in 75 primary liver cancers. Three missense mutations were detected exclusively in 10 childhood hepatocellular carcinomas (HCCs), while no mutations were detected in 16 adult HCCs, 21 cholangiocarcinomas, or 28 hepatoblastomas. The extremely short incubation period from hepatitis B virus infection to the genesis of childhood HCC as compared with the adult HCC suggests that there may be an additional mechanism that accelerates the carcinogenesis of childhood HCC. Our results indicate that mutations of the tyrosine kinase domain of the MET gene may be involved in the acceleration of the carcinogenesis in childhood HCC.

Adolescent↗

PubMed1999

In vivo expression of soluble Fas and FAP-1: possible mechanisms of Fas resistance in human hepatoblastomas.

Many tumour cells express both Fas and its ligand (FasL) on their surface and it has remained a mystery why such cells do not simply kill themselves. It remains to be determined whether Fas and FasL are expressed in human hepatoblastomas and if so, what is responsible for the possible Fas resistance of these tumours. In this study, the expression of Fas and FasL was examined in 23 cases of human hepatoblastoma by immunohistochemical staining. To elucidate possible Fas resistance in hepatoblastomas, Fas-resistance pathways including the expression of bcl-2 and Fas-associated phosphatase-1 (FAP-1), and the expression of soluble Fas (sFas) mRNA, were analysed by immunohistochemistry and in situ reverse transcription-polymerase chain reaction (in situ RT-PCR). Fas gene mutation in the death domain was also examined. Fas and FasL were expressed in all hepatoblastomas analysed. Twenty (87 per cent) and 18 (78 per cent) cases of hepatoblastoma were positive for sFas mRNA and FAP-1, respectively, but none of the hepatoblastomas expressed bcl-2. Mutation in the death domain of the Fas gene was not found in hepatoblastomas. Taken together, these findings demonstrated that Fas, a death receptor, and its ligand are co-expressed in hepatoblastomas in vivo, but some inhibitors of Fas-mediated apoptosis are also expressed in these tumours. These results suggest that it is probably due to the action of inhibitory molecules of the Fas pathway that the tumour cells of hepatoblastomas do not kill themselves in an autocrine-driven cycle and that in this manner hepatoblastomas avoid apoptosis.

Apoptosis↗

PubMed1999

The effect of tumor size on F-18-labeled fluorodeoxyglucose and fluoroerythronitroimidazole uptake in a murine sarcoma model.

The purpose of this study was to evaluate the effect of tumor size on the uptake of 18F-fluorodeoxyglucose (FDG) and fluoroerythronitroimidazole (FETNIM) in a murine sarcoma model. ICR mice were xenografted with sarcoma 180 cell line and tumors were allowed to grow to a weight of 0.26-5.82 grams. 18F-FDG and 18F-FETNIM were injected intravenously in separate groups of mice, and after 1 hr, the tumors were excised and radiotracer uptake was measured. In another group of mice tumors were autoradiographically analyzed and subjected to H & E staining. In both the FDG and FETNIM group, per-gram radiotracer uptake by a tumor was inversely proportional to tumor weight. 18F-FETNIM correlated more (r = -0.593, p < 0.05) than 18F-FDG (r = -0.447, p < 0.05). Autoradiographic studies revealed that FDG accumulated in viable tumor areas, whereas FETNIM accumulated in both viable and partially necrotic areas. In the case of 18F-FETNIM, a direct correlation between tumor weight and the no-uptake-area to total-tumor-area was demonstrated. We concluded that increased tumor size is associated with decreased uptake of 18F-FDG and FETNIM, though this depends on the type of radiotracers and distribution of necrosis.

Animals↗

PubMed1999

Solid and papillary epithelial neoplasm of the pancreas in children.

Solid and papillary epithelial neoplasm of the pancreas is an uncommon low-grade malignant tumor found predominantly in young females. In this paper, the authors report the tumor's clinical characteristics and the results of surgery in six children. Six cases of solid and papillary epithelial neoplasm of the pancreas pathologically verified at Seoul National University Children's Hospital between 1985 and 1997 were retrospectively analyzed. Four were girls and two were boys, and their mean age at surgery was 11.2 years (range 8-13 years). All patients presented with an abdominal mass and tumor ranging in size from 6.5 x 6.0 cm to 10.5 x 8.0 cm. Five were located in the head and one in the tail of the pancreas; exploration showed that no case involved local invasion or metastasis. All patients underwent complete resection, which involved five pancreaticoduodenectomies and one distal pancreatectomy. No patient died during surgery, and after a mean follow-up period of 5.5 years (range 1.5-12.5 years) all were alive with no recurrences. We believe that the malignancy of this tumor is low grade and that the prognosis is good. For a neoplasm arising anywhere in the pancreas, complete resection is the treatment of choice. Solid and papillary epithelial neoplasm of the pancreas of children shows less female preponderance in children than in adults.

Adolescent↗