Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although autopsy reports show that the adrenal gland is the second most common organ of hematogeneous metastasis from hepatocellular carcinoma (HCC), paradoxically there is found to be a very scarce number of the adrenal metastasis in clinical practice. We have recently experienced rare patients with right adrenal metastasis from HCC. Case 1: A 51 year-old man with a 5-year history of chronic hepatitis was admitted with hematemesis to Nippon Medical School Hospital. CT revealed a main tumor associated with a few daughter tumors in the hepatic posterior segment and in addition another tumor located between the right hepatic lobe and right kidney. The diagnosis of HCC with a right adrenal gland metastasis was made, and hepatectomy and right adrenalectomy was performed. Twenty months after operation he was alive and free of disease. Case 2: A 78 year-old man underwent resection of the lateral segment of the left hepatic lobe for HCC. Twelve months later, recurrent foci in the residual liver were found and those were treated with transarterial embolization (TAE). Right adrenal metastasis was found on CT 26 months after hepatectomy. TAE was done for the hepatic recurrent tumors and adrenal metastasis. Twelve months after, he survived in good condition. Case 3: A 47 year-old man presented with liver cirrhosis with a long history. He was diagnosed as having HCC with multiple intrahepatic metastases and was treated with TAE 4 times. Follow-up CT revealed right adrenal metastasis. TAE was done for hepatic recurrent tumor and right adrenal metastasis. Three months later the patient died of liver failure.
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PMID:Adrenal metastasis from hepatocellular carcinoma (HCC): report of 3 cases. 1052 32

To determine the role of retinoblastoma (Rb) gene alteration in hepatocarcinogenesis, we examined Rb protein expression immuno-histochemically in a series of surgically resected specimens including non-cancerous liver tissues with cirrhosis or chronic hepatitis, large regenerative nodules, pre-cancerous adenomatous hyperplasias as well as primary and metastatic lesions of hepatocellular carcinoma (HCC). All of the non-cancerous liver tissues, large regenerative nodules and adenomatous hyperplasias showed normal Rb protein expression. Altered Rb protein expression was observed in 31 (lack of Rb protein in 16 and over-expression in 15) of the 81 primary HCCs (38%) and was significantly associated with tumor differentiation grade: altered Rb protein expression occurred in 1 of 23 (4%), 16 of 43 (37%) and 14 of 15 (93%) well-, moderately and poorly differentiated tumors (moderately vs. well-differentiated p < 0.01; poorly vs. moderately differentiated p < 0.001). Incidences of both Rb protein absence and over-expression were higher for moderately differentiated than for well-differentiated tumors and even higher for poorly differentiated tumors. Rb protein absence and over-expression were observed in 9 (39%) and 10 (44%) of the 23 metastatic lesions of HCC, respectively, and the incidence of altered Rb protein expression (absence or over-expression) was significantly higher than in primary lesions (83% vs. 38%, p < 0.001). Our observations suggest that elevated and absent Rb protein are closely associated with tumor progression and developing metastatic disease rather than tumor initiation in cases of HCC. Int. J. Cancer (Pred. Oncol.) 84:604-608, 1999.
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PMID:Over-expression and lack of retinoblastoma protein are associated with tumor progression and metastasis in hepatocellular carcinoma. 1056 6

Reactivation of the hepatitis B virus (HBV) is a rare, but well described complication of cytotoxic chemotherapy that may result in hepatic failure. Patients who are chronic carriers of the HBV and who have a G to A mutation at nucleotide 1896 in the precore region may develop more severe liver disease, possibly because of rapid selection and enhanced replication ability of the mutant strain. Such mutant viruses have been implicated occasionally in chemotherapy induced reactivation of hepatitis B virus. In this report, 5 patients with solid tumours were identified to have developed severe hepatitis B virus related liver disease during treatment with cytotoxic agents (with dexamethasone as anti-emetic). All had clinical and serological evidence of reactivation of the HBV. Three patients developed icteric hepatitis; 2 fully recovered, and 1 had died from progressive metastatic disease while recovering from the reactivation. The other two died from progressive liver failure. Direct sequencing of the polymerase chain reaction (PCR) products of the precore (preC) and precore promoter region of the HBV-DNA was carried out on the patients' serum samples taken during the episode of reactivation. In each case, similar mutations (G to A) in nucleotide 1896 of the preC region were found, together with additional mutations in the preC promoter. The present findings suggest that reactivation involving a mutant hepatitis B virus may lead to liver failure, which is possibly more severe than that caused by wild type HBV, and can be triggered by cytotoxic chemotherapy, or the administration of corticosteroids. In Eastern Asia the HBV carriage rate in adults is high. HBV reactivation and severe liver disease during cytotoxic treatment may become a serious and common problem in this region as cytotoxic chemotherapy is more widely used. Patients should be screened routinely for HBsAg in endemic areas of chronic hepatitis B virus infection prior to receiving cytotoxic treatment. The possibility of HBV reactivation should be considered in patients developing liver dysfunction. Patients who are HBeAg negative/Anti-HBe positive, and are suspected to be having an HBV reactivation, should have HBV-DNA levels measured for confirmation as they may carry a mutant HBV.
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PMID:Hepatitis B virus reactivation in patients undergoing cytotoxic chemotherapy for solid tumours: precore/core mutations may play an important role. 1063 Sep 55

A 65-year-old man with chronic hepatitis C showed a markedly elevated serum alpha-fetoprotein concentration. Computed tomography revealed a huge tumor occupying the entire right hepatic lobe. Three months later, the tumor regressed spontaneously from 12 cm to 7 cm in diameter without any medical treatment. A right hepatic lobectomy was performed 4 months after the initial diagnosis. The main tumor, located in the posterior inferior segment, was completely necrotic, and had a thick fibrous capsule. Many inflammatory cells had also infiltrated into the tumor. Only a small portion of a tumor thrombus in the portal vein and one of three intrahepatic metastases contained viable cancer cells. The tumor was found to be poorly differentiated hepatocellular carcinoma. Tumor regression may have been caused by a disturbance in hepatic circulation associated with the portal vein thrombus.
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PMID:Spontaneous regression of a large hepatocellular carcinoma with portal vein tumor thrombi: report of a case. 1064 91

This is a case report of a 53-year-old male with chronic hepatitic C infection presenting with weight loss and elevated liver function tests. Repeated ultrasonography, computed tomography and magnet resonance imaging showed multiple intrahepatic lesions suggestive of metastatic disease. Repeated ultrasound-guided biopsies from the lesions as well as from the adjacent normal appearing liver tissue revealed no malignancy but showed inflammation and significant fibrotic tissue, consistent with chronic hepatitis C. 2 years after the first admission liver function tests were all within the normal range and remained so until today. Computed tomography at that time showed complete remission of all intrahepatic lesions. The exact diagnosis remained elusive but the rare case of reversible focal fibrosis is the most likely cause of these spontaneously regressive lesions.
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PMID:Spontaneous regression of intrahepatic lesions mimicking metastatic disease. 1107 78

A 62-year-old man with chronic hepatitis C was found to have a hepatic tumor by ultrasonography. Computed tomography of the liver disclosed a tumor 4 cm in diameter occupying the posterior segment and associated with a portal tumor thrombus and enlargement of hilar and paraaortic lymph nodes. At laparotomy multiple nodal metastases were seen involving hilar, hepatoduodenal, common hepatic arterial, and paraaortic nodes. We performed right hepatic lobectomy and systematic lymph node dissection. Histologic examination of both the main tumor and nodal metastases showed poorly-differentiated hepatocellular carcinoma. Severe postoperative ascites persisted for 1 month. Fifteen months after surgery the patient died of multiple intrahepatic and systemic nodal recurrences. Our experience confirms that surgical treatment of hepatocellular carcinoma with nodal metastases is likely to benefit only a few carefully selected patients, since the prognosis is commonly poor and hepatectomy with lymph node dissection carries the risk of severe complications.
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PMID:A surgically treated case of hepatocellular carcinoma with extensive lymph node metastases. 1114 39

Vascular endothelial growth factor plays an important role in neovascularization both in normal tissues and most tumors. It has been extensively investigated recently in various hepatic diseases such as primary and secondary hepatocellular carcinoma, liver cirrhosis, hepatitis and even benign tumors in liver. Vascular endothelial growth factor has been verified to be closely involved in the development and metastases of hepatocellular carcinoma and correlated to the high risk of hepatic metastases and a poor prognosis in gastrointestinal cancer. Using antibodies to vascular endothelial growth factor or other drugs to suppress its expression has also been successfully tried to restrain hepatocellular carcinoma cells and metastases in vitro and in animal models. The protein of vascular endothelial growth factor has an inclination to increase in acute and chronic hepatitis and tends to decrease in cirrhosis both in tissue expression and circulating levels. This circulating level is closely related to the Child-Pugh classification in cirrhotic liver. However, there are indeed some disagreements concerning vascular endothelial growth factor and liver disease, for example, opinions on the positive rates of vascular endothelial growth factor in protein and mRNA level are far from reaching a general consensus. Further study should be performed in the future in antitumor research and its significance in the process of liver cirrhosis.
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PMID:Vascular endothelial growth factors and liver diseases. 1149 Aug 20

The potent immunomodulatory, antiproliferative and antiviral properties of interferons (IFNs), together with their availability in large amounts thanks to the recombinant DNA technique, have resulted in their widespread clinical use in a variety of viral and nonviral proliferative disorders. In dermato-oncology, IFNs have been used primarily in melanoma, but also in nonmelanoma skin cancer, such as squamous and basal cell carcinomas, Kaposi sarcomas and lymphomas. Trials with IFNs have been performed in patients with melanoma in an adjuvant setting (stage II and III) and in metastatic disease (stage IV). While the response rates with IFNs as single agents in stage IV disease usually do not exceed 15%, the use of adjuvant IFNs has been claimed to increase disease-free survival (stage II), or even overall survival (stage III), in low- or high-dose regimens, respectively; the latter, however, involved numerous side-effects and were beset with lack of compliance and acceptance, as well as being very costly. Pegylated IFN (PEG-IFN) is a form of recombinant human IFN that has been chemically modified by the covalent attachment of a branched metoxpolyethylene glycol moiety. Pharmacogenetic and pharmacodynamic data obtained in animal and in phase I studies have indicated that PEG-IFN injected once a week has the potential to be superior in efficacy to human IFN injected three times a week. The safety profiles of PEG-IFN and IFN are comparable in healthy volunteers and in chronic hepatitis C (CHC) patients. PEG-IFN is currently being evaluated for the treatment of CHC, renal cell carcinoma, chronic myelogenous leukaemia, and malignant melanoma, the last in both stage IV and stage III disease.
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PMID:Perspectives of pegylated interferon use in dermatological oncology. 1207 10

Immunohistochemistry is a strong tool in hepatopathologic diagnosis: the technique is relatively simple and inexpensive. New and very sensitive detection methods have been recently developed (e.g., the EnVision technique and the microwave antigen retrieval method). This article discusses the role of immunohistochemistry in differentiating chronic cholestatic diseases from chronic hepatitis and in characterizing infectious agents. Algorythms for the typing of lymphomas and for the differentiation of primary tumors versus metastases are proposed as well. The immunohistochemical criteria for the diagnosis of premalignant lesions are discussed.
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PMID:The role of immunohistochemistry in diagnosis. 1212 71

A 65-year-old Japanese man with chronic hepatitis C was found to have a hepatic tumor by ultrasonography. Both dynamic computed tomography and hepatic angiography showed a hypervascular tumor with a central defect. Since a diagnosis of hepatocellular carcinoma was made, transcatheter arterial embolization was performed. However, the tumor metastasized to systemic lymph nodes and the patient died 3 months after treatment. An autopsy was performed. Histologic examination of the hepatic tumor revealed that the peripheral part was completely necrotic and the central area was composed of strands of pleomorphic cells with focal gland formation surrounded by fibrosis. No production of mucin or bile was evident. The microscopic findings of metastatic lymph nodes were similar to those of the central portion of the hepatic tumor. Immunohistochemical strains of the hepatic tumor and lymph node metastases showed diffuse positivity for cytokeratins 7 and 19, while hepatocyte paraffin 1 was focally reactive. These findings suggest that the hepatic tumor was a combined hepatocellular carcinoma and cholangiocarcinoma. Since the tumor expressed dual phenotypic markers of both hepatocytes and bile duct cells, the tumor might have an intermediate phenotype between hepatocytes and bile duct cells.
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PMID:Primary liver cancer with dual expression of hepatocyte and bile duct epithelial markers. 1214 10


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