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A Tannapfel

Publications and source records attributed to A Tannapfel.

At least 73 records · Page 4Linked to original sources
PubMed2001

[Anatomy and pathology of intrahepatic and extrahepatic bile duct tumors].

Adenocarcinomas of the intra- and extrahepatic bile ducts are rare tumors that begin with malignant transformation of the bile duct epithelia. Intrahepatic cholangiocarcinomas derive from the small bile ducts located proximally to the right and left hepatic ducts. Extrahepatic bile duct carcinomas originate in the right or left hepatic duct, the cystic duct, or the choledochal duct. Tumors located at the bifurcation are called Klatskin tumors. The intrahepatic cholangiocarcinomas are classified according to the TNM classification of liver tumors, while the extrahepatic bile duct tumors have their own TNM classification. Several factors, accompanied by a chronic inflammatory reaction, have been discussed in the etiopathogenesis of these tumors: schistosomiasis, ulcerative colitis with primary sclerosing cholangitis, and inborn bile duct cysts of the liver as a consequence of a disturbance of the ductal plate formation. Over 95% of bile duct tumors are adenocarcinomas. In the nomenclature of precursor lesions a two-grade classification of dysplasia (low-grade versus high-grade) has been found to be more reproducible.

Adenocarcinoma↗
PubMed2001

[Carrent state of molecular pathology of stomach carcinomas].

Gastric carcinoma is one of the commonly diagnosed malignancies and remains an important cause of mortality in the Western hemisphere. Various sequences of genetic alterations may be responsible for the development of gastric cancer, as there exist two histological types: well-differentiated or intestinal-type and poorly differentiated or diffuse-type gastric cancers. While new genetic findings open new perspectives on carcinogenesis and molecular biology of gastric cancer, they have not been widely applied in routine diagnostic procedures, classification systems, disease monitoring, or prognostic assessment. We discuss the mechanisms molecular pathology in relation to their potential clinical relevance.

Apoptosis↗
PubMed2001

[Preneoplasia of the liver. Definition--differential diagnosis--clinical consequences].

The great advances in radiological imaging techniques and their widespread availability have focused attention on hepatic premalignant nodular lesions. The histological differential diagnosis of these nodules can often be difficult, especially in needle biopsy specimens with limited material. Diagnostic considerations differ significantly between livers with and without cirrhosis: In the noncirrhotic liver, the differential diagnosis includes liver cell adenoma, nodular regenerative hyperplasia, and hepatocellular carcinoma. In cirrhosis, dysplastic nodules (low and high grade), dysplasia (large and small cell) as well as hepatocellular carcinoma may occur. The standardization and the uniform use of the nomenclature of these entities are necessary for a better understanding of the biological nature and etiopathology of these lesions. Only a commonly accepted nomenclature makes a comparison of different therapeutic treatment regimens feasible.

Adenoma, Liver Cell↗
PubMed2001

Tumor markers in squamous cell carcinoma of the head and neck: clinical effectiveness and prognostic value.

Despite recent advances in tumor surgery and multimodal treatment regimens the prognosis of squamous cell carcinomas of the head and neck is still relatively poor and has shown only slow progress. Additional clinical and biological factors are therefore urgently needed that aid tumor diagnosis, early detection of tumor recurrences, prediction of the results of therapeutic interventions, and identification of subsets of patients with unfavorable outcome during follow-up. A tumor marker should fulfill the criteria of specificity and clinical effectiveness. So far none of the known serological and biological markers fits all these criteria. Although some biological markers can be determined serologically without the need for tumor tissue, their low specificity limits their applicability to early detection of tumor recurrences during follow-up. A large number of molecular or genetic markers have been examined in squamous cell carcinomas of the head and neck. All of these are controversial regarding their prognostic value and clinical effectiveness. UICC tumor stage and patient's age and performance still remain the basis for therapeutic decisions. Further search for more sensitive and specific markers is needed to improve individual treatment and prognostic statements.

Autoantibodies↗
PubMed2001

High prevalence of K-ras-2 mutations in hepatocellular carcinomas in workers exposed to vinyl chloride.

OBJECTIVES: Vinyl chloride (VC) and its metabolites are human carcinogens associated with liver angiosarcomas (LAS) and also with hepatocellular carcinomas (HCCs). In VC associated LAS mutations of the K-ras-2 gene have been reported, however, no data about the prevalence of such mutations in VC-associated HCCs are available. The aim of the study was to evaluate possible specific K-ras-2 oncogene mutations in the case of HCCs due to VC. METHODS: The presence of K-ras-2 mutations was analysed in tissue from 12 patients with VC-associated HCCs. All patients had known long-term exposure to VC (average exposure amount: 9,942 ppm-years). Twenty patients with hepatocellular carcinoma due to hepatitis B (n = 7), hepatitis C (n = 5) and alcoholic liver cirrhosis (n= 8) served as a control group. The specific mutations were determined by direct sequencing of codons 12 and 13 of the K-ras-2 gene in carcinomatous and adjacent non-neoplastic liver tissue after microdissection. Immunohistochemical analysis was performed to detect p21ras protein. RESULTS: K-ras-2 mutations were found in five of 12 (42%) examined HCCs and in three cases of adjacent non-neoplastic liver tissue (25%). There were three guanine to adenine (G --> A) point mutations in the tumour tissue. All three mutations found in non-neoplastic liver from VC-exposed patients were also G --> A point mutations (codon 12- and codon 13-aspartate mutations). Within the control group, K-ras-2 mutations were found in three of 20 (15%) examined HCCs. CONCLUSIONS: Mutations of the K-ras-2 gene in hepatocellular carcinomas associated with VC exposure are frequent events. We observed a K-ras-2 mutation pattern characteristic of chloroethylene oxide, one of the carcinogenic metabolites of VC analysed in animal models. Our results suggest that VC had direct toxic effects not only on endothelial cells but also on hepatocytes, as it was previously only described in animal models.

Adult↗
PubMed2001

Adenoma of the papilla and ampulla--premalignant lesions?

Ampullary adenomas arising in the papilla or the ampulla Vateri, are rare, benign, neoplastic lesions. No specific aetiological factors, such as diet, chemical or environmental causes, have been identified yet. An established risk factor which is accompanied by the development of adenoma is the presence of genetically inherited polyposis syndromes, e.g. familial adenomatosis coli (FAP). Adenomas assume tubular, tubulovillous, or villous architecture and are not different from adenomas arising elsewhere in the gastrointestinal tract. The full neoplastic spectrum, ranging from mild to high grade dysplasia, up to invasive carcinoma, resembles the adenoma-carcinoma sequence of the large bowels.

Adenoma↗
PubMed2001

Expression of a glypican-related 62-kDa antigen is decreased in hepatocellular carcinoma in correspondence to the grade of tumor differentiation.

A monoclonal mouse antibody, Be-F4, was generated by means of immunization with a synthetic oligopeptide. In Western blots, this antibody recognizes an antigen with an apparent molecular mass of 62 kDa, termed p62. Immunohistochemical analysis of p62 in hepatocellular carcinoma (HCC) specimens (n=33) and in corresponding non-cancerous liver tissue was performed using monoclonal antibody Be-F4. All non-neoplastic hepatic cells showed, without exception, a moderate or strong staining intensity of the 62-kDa antigen, recognized by Be-F4. In contrast to the non-neoplastic hepatocytes, the cellular p62 content was unambiguously reduced in all malignant cells. The extent of decrease of p62 corresponded to the grade of histological differentiation of HCC cells (P<0.001). Using a semiquantitative scoring system, the median of p62 expression, which was 2.1 for normal hepatocytes, was significantly reduced to 1.2 for G1, 1.0 for G2, and 0.2 for G3 HCCs. These data suggest that neoplastic transformation is associated with a reduced p62 content.

Animals↗
PubMed2001

C282Y and H63D mutation of the hemochromatosis gene in German porphyria cutanea tarda patients.

BACKGROUND AND AIMS: Patients with porphyria cutanea tarda (PCT) have a susceptibility to reversible inactivation of hepatocyte uroporphyrinogen decarboxylase, which can be triggered by alcohol, hepatitis C virus, and other agents. Inherited factors that may predispose to PCT include the C282Y mutation in the hemochromatosis (HFE) gene. METHODS: We analyzed the hemochromatosis mutations C282Y and H63D in liver biopsies and serum samples of 190 German patients (mean age 48+/-12.5 years) with sporadic PCT. The hepatic iron concentration was determined within the liver tissue. Age-matched healthy blood donors (115 donors) served as controls. RESULTS: The C282Y and H63D mutations were found in 75 (39%) and 85 (45%) of 190 patients with PCT, respectively. Twenty-two patients (12%) were homozygous for the C282Y mutation, and eighteen patients (9%) were compound heterozygotes, displaying both the C282Y and the H63D mutation. Within the control group, 3 of 115 patients were heterozygous for C282Y (3%) and 12 for H63D (10%). Serum and hepatic iron, ferritin, transferrin saturation, or liver enzymes did not differ significantly between patients with or without HFE mutations. CONCLUSIONS: The high frequency of homo- and heterozygosity for the C282Y and H63D alleles strongly suggests that these mutations are important predisposing factors for PCT in German patients.

DNA↗
PubMed2001

Efficacy of surgical measures in preventing port-site recurrences in a porcine model.

BACKGROUND: Port-site recurrences are serious complications of laparoscopy performed for cancer. Incidences reported in the literature vary between 0% and 21%, suggesting an influence of the surgeon. METHODS: The aim of this experimental, prospective, randomized, single-blind study was to investigate the influence that the quality surgery has on the incidence of port-site recurrences. After a 12-mmHg carbon dioxide (CO2) pneumoperitoneum was created, 10(7) human HeLa cell were injected into the peritoneal cavity of 18 pigs, creating a xenogeneic tumor. Laparoscopic sigmoid resections then were performed using four trocars and a transanal double-stapling technique. The following protective measures were applied in nine animals: trocar fixation, prevention of gas leaks, rinsing of instruments with povidone-iodine, minilaparotomy protection, rinsing of trocars before removal, peritoneal closure, and rinsing of all wounds with povidoneiodine. Surgeons and type of procedures were randomized. After 4 weeks, the animals were killed and all portsites excised. Blinded immunohistologic analysis with antihuman pancytokeratin antibody was performed. RESULTS: Tumor recurrence was present in 23 of 36 port sites (63.8%) in the control group, but only in 5 of 36 port sites (13.8%) in the group that received protective measures (p = 0.002; Fisher's exact test). No peritoneal carcinosis nor anastomotic recurrences were observed. CONCLUSION: These results strongly suggest that the quality of surgical technique has an influence on the incidence of port-site recurrences. From now on, we propose to use these protective measures routinely in cancer laparoscopy.

Animals↗
PubMed2001

p16INK4A-alterations in primary angiosarcoma of the liver.

BACKGROUND/AIMS: Alterations in the p16 (CDKN2/MTS-1/INK4A) gene have been implicated in the tumorigenesis of different human cancers. Recent evidence shows that transcriptional silencing as a consequence of hypermethylation of CpG islands is the predominant mechanism of p16INK4a gene inactivation in malignant epithelial tumors. This study was performed to determine whether alterations of p16 are involved in the development of angiosarcoma of the liver. METHODS: The status of p16 was evaluated in 17 angiosarcomas of the liver by methylation-specific PCR (MSP), microsatellite analysis, DNA sequencing and immunohistochemical staining. The results obtained were correlated with histopathological variables and with patient survival. RESULTS: Hypermethylation of the 5' CpG island of the p16 gene was found in 12 out of 17 (71%) angiosarcomas examined. Homozygous deletion at the p16 region was present in one case (6%), and loss of heterozygosity was present in two cases (12%). We failed to detect p16 gene missense mutations. The status of p16 correlated with neither histopathological factors nor with the prognosis of the patients with angiosarcomas. CONCLUSIONS: These data suggest that inactivation of the p16 gene is a frequent event in angiosarcomas of the liver. The most common somatic alteration is promotor methylation of the p16 gene. We failed to establish p16 as independent prognostic factors in these tumors.

Aged↗
PubMed2001

Long-term combination of interferon alfa-2b and ribavirin for hepatitis C recurrence in liver transplant patients.

The purpose of this study was to evaluate the feasibility, tolerability and efficacy of long-term combination therapy with interferon-alfa 2b (IFNalpha-2b) and ribavirin (Rb) for recurrent hepatitis C after liver transplantation. Fifteen patients with histologically confirmed hepatitis C after liver transplantation were treated. After a basic course of 12 months (IFNalpha-2b 3 MU/3 times a week; Rb 3 x 200 mg/day), patients achieving clearance of viremia underwent maintenance therapy with ribavirin (3 x 200 mg/day). Patients without virological response continuously received combination therapy. Levels of HCV RNA, aminotransferases and bilirubin were followed. Therapy led to a significant decline of transaminases and bilirubin in all patients (p < 0.05). Sixty-four per cent of patients had clearance of viremia after 12 months. Sustained virolo gical response was 88%. In patients without virological response, continuation of combination therapy prevented another biochemical relapse of hepatitis. Treatment was accompanied by severe hematological side-effects, requiring medical support in a majority of patients. In two patients (13.5%), therapy finally had to be withdrawn because of major hematological disorders. These results indicate that long-term combination therapy with IFNalpha-2b and Rb is effective in the treatment of recurrent hepatitis C and in preventing further relapse of disease after liver transplantation, but side-effects may require cessation of therapy.

Adult↗
PubMed2001

[Colorectal carcinoma in Cronkhite-Canada syndrome].

We report a 63-year-old lady with Cronkhite-Canada syndrome, who developed colorectal cancer. A hemicolectomy was performed, and the tumor specimen was prepared for DNA-analysis and immunohistochemical screening. We found a mutation of p53 gene without APC- and ras-gene alteration and expression of erbB2-protooncogen. The polyps in non-hereditary Cronkhite-Canada-syndrom are neither adenomatous nor hyperplastic, but patients often develop colorectal cancers. The steps of mutation do not follow the adenoma-carcinoma sequence, first described by Vogelstein 1988. This and previous observations suggest that carcinogenesis in Cronkhite-Canada syndrome follows another independent sequence.

Adenocarcinoma↗
PubMed2001

[Pancreatic intraepithelial neoplasia in chronic pancreatitis].

Chronic pancreatitis causes destruction of the pancreatic gland which leads to tissue fibrosis and regenerative hyperplasia of the epithelium of pancreatic ducts and ductules. Morphological studies revealed distinct proliferative lesions in the pancreatic ducts and ductules adjacent to infiltrating adenocarcinomas of the pancreas. A stepwise progression from mild to severe dysplasia in these hyperplastic lesions has been reported. These lesions, called Pancreatic Intraepithelial Neoplasia (PanIN), harbour a number of well-characterised genetic alterations. Therefore, PanINs were defined as true clonal neoplastic lesions with minimal to moderate and severe cytological and architectural atypia. Almost all of the genetic alterations that have been identified in pancreatic adenocarcinomas have also been identified in PanIN lesions. The prevalence of genetic changes increases as the degree of cytological atypia and histological dysplasia in the PanIN lesions increases. However, some genetic abnormalities have also been found in chronic pancreatitis and normal pancreas, e. g. K-ras mutations. However, due to intratumorous heterogeneity of the genetic changes, further studies are necessary to search for more specific and homogeneous expressed molecular markers. A better understanding of the molecular genetic changes occurring during neoplastic progression in the pancreas will form the basis for future strategies of early tumour detection and improved therapy.

Adenocarcinoma↗
PubMed2001

[Surgery for complications of chronic pancreatitis].

At least 50 % of all patients with chronic pancreatitis require surgical treatment in the course of their disease. Indications for surgery are intractable pain, intra- and extrapancreatic complications and the suspicion of a carcinoma. The basic principles of surgery are resection and drainage. The choice of the surgical procedure depends on the morphological expression and the localization of the pathological changes. Regarding resections in the head-area, previous studies demonstrated uniformly the superiority of the duodenum-preserving pancreas head resection (DPPHR) compared to the Kausch-Whipple operation with and without maintenance of the pylorus. Drainage procedures (pain recurrence in 20-40 % in the long-term course) and left pancreatic resections (de-novo diabetes mellitus in up to 45 %) should be considered critically. Between May 1994 and November 2000 117 patients underwent surgical therapy for complications of chronic pancreatitis at our institution. Resections were performed in 68 % of the patients and drainage procedures in 20 %. There was no mortality. Over the years the proportion of the DPPHR increased in comparison to the Kausch-Whipple procedure and the number of the drainage operations decreased continuously. The DPPHR was significantly superior to the Kausch-Whipple procedure with regard to the glucose metabolism and the quality-of-life. In the spectrum of surgical procedures in chronic pancreatitis, the DPPHR represents a modern, organ-preserving procedure for patients with complications in the pancreas head.

Adolescent↗
PubMed2001

Importance of microcirculatory disturbances in the pathogenesis of pancreatitis.

Pancreatic microvascular control is a complex physiological process which is incompletely understood. Blood flow in the pancreas is altered by a large number of endogenous and exogenous factors in the context of acute and chronic pancreatitis. The frequency of progression from acute pancreatitis to a chronic form is a controversial question. In acute pancreatitis reductions in blood flow and alterations of microvascular integrity resulting in impaired tissue oxygenation play an important part in the progression and possibly the initiation of the disease. Endothelin and nitric oxide are believed to be two of the most effective vasoactive mediators. The beneficial effect of therapeutic strategies affecting vasoactive mediators is confirmed in experimental studies. Chronic disease is associated with decreased pancreatic blood flow and histological changes in the vasculature in both patients and animal models. Further studies are needed to clarify whether ischemia in chronic pancreatitis is more important in perpetuating the disease or as primary cause of the inflammatory processes.

Acute Disease↗