Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The question whether expression of drug metabolizing enzymes in human liver is altered by liver neoplasm remains controversial; however, the ability or unability of tumour cells to metabolize certain drugs may be important for developing therapeutic strategies. We therefore investigated the abundance and localization of two classes of drug metabolizing enzymes [cytochrome P4503A (CYP3A) and pi-type glutathione-S-transferase] by means of immunohistochemistry (standard ABC technique) in patients with hepatocellular carcinoma (HCC, n = 16) and with liver metastasis from adenocarcinoma (n = 53) in comparison to normal controls (n = 5). The distribution of CYP3A in normal liver samples showed a characteristic pattern of four to five layers of stained hepatocytes surrounding the central vein. Eleven out of 16 cases of HCC showed expression of CYP3A; staining was less intense than in normal liver and zonation was completely lost. In contrast, only 5 out of 53 samples of metastasis stained positively for CYP3A. The difference between primary and secondary neoplasm was statistically significant (chi-square, P < 0.0001). Pi-type glutathione-S-transferase (GST) stained positively in 9 out of 16 HCC and in 48 out of 53 cases of liver metastasis (chi-square, P < 0.01) indicating a higher percentage of immunostaining in liver metastasis. In summary, we observed differences in the abundance and distribution pattern of CYP3A and GST between primary and secondary neoplasma of human liver and in comparison to normal controls. In combination with established methods these data may contribute to the establishment of reliable test systems for distinguishing primary from secondary liver tumours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential expression of drug metabolizing enzymes in primary and secondary liver neoplasm: immunohistochemical characterization of cytochrome P4503A and glutathione-S-transferase. 840 68

Between 1988 and 1992 ultrasound-guided fine needle aspiration biopsies of thromboses in the main branches of the portal vein were carried out in 15 patients with liver cirrhosis. The aims of the study were to evaluate the usefulness, feasibility and diagnostic accuracy of this procedure in cirrhotics with known or suspected hepatocellular carcinoma. The procedure was carried out only in patients with a platelet count > or = 40,000/microL and prothrombin activity > or = 40%. A single pass, with a 22 gauge spinal needle, was performed in the portal vein lumen. Diagnosis of the aetiology of the portal vein thrombosis was obtained in all 15 cases. In 12 cases, a cytological diagnosis of hepatocellular carcinoma was made. In one case, the neoplastic cells aspirated were compatible with adenocarcinoma, and a subsequent colonoscopy confirmed the presence of colonic cancer. The material aspirated was compatible with chemically-induced thrombosis in one patient who had undergone several percutaneous ethanol injection sessions for treatment of hepatocellular carcinoma, and in the last case only blood was aspirated, thus ruling out the coexistence of hepatic cancer. We conclude that fine needle aspiration biopsy of portal vein thrombosis is a feasible, low risk procedure that facilitates the diagnosis of hepatocellular carcinoma when fine needle biopsy of focal liver lesions fails. Fine needle aspiration biopsy of portal vein thrombosis is also useful in excluding neoplastic aetiology of portal vein thrombosis.
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PMID:Ultrasound-guided fine needle aspiration biopsy of portal vein thrombosis in liver cirrhosis: results in 15 patients. 858 Apr 10

The prognosis of primary liver cancer, especially cholangiocarcinoma, is extremely poor. A long term, 12 years survivor of intrahepatic cholangiocarcinoma arising in a local dilatation of the intrahepatic bile duct is presented. A 40-year-old male patient was presented with recurrent upper abdominal pain, fever, and jaundice. Computed tomography revealed a localized duct dilatation, and ultrasound clearly demonstrated a tumor mass arising within the bile duct. At surgery in March, 1982, the tumor mass was resected and histologically confirmed as a well differentiated papillary adenocarcinoma arising. In March, 1994, the patient is alive and cancer-free, 12 years after surgical resection. To our knowledge, there has been no report on a patient surviving more than 10 years after initial treatment. This case suggests that a localized cystic dilatation of the intrahepatic-bile duct on imaging modalities may harbor a bile duct carcinoma, and this in turn may contribute to early diagnosis of carcinomas and improved long term survival.
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PMID:Intrahepatic cholangiocarcinoma with a long-term survival of 12 years after surgical resection: report of a case and review of the literature. 875 Dec 6

There is no high risk group for cholangiocarcinoma as there is for hepatocellular carcinoma, and it has a poor prognosis because many cases are diagnosed after it has become advanced. To date, there is no effective chemotherapy or radiation therapy for cholangiocarcinoma, and extended hepatectomy is the only effective treatment. In Japan, regional lymph node dissection and extended hepatectomy have been performed aiming at curative resection, but the 5-year survival in Japan is still low, only 26.1%. The Committee on the Japanese General Rules for the Clinical and Pathological Study of Primary Liver Cancer has divided macroscopic type into 3 patterns: mass-forming type, periductal infiltrating type, and intraductal growth type, to access prognosis on a common basis. According to these groups, our patients with the intraductal growth type had a good outcome, but patients with the mass-forming type and periductal infiltrating type had a poor outcome. Many papers have reported that the presence of lymph node metastasis makes the prognosis poor. Among our cases, the 5-year survival rate for all patients who underwent hepatectomy was 26.1% and the rate for patients positive for lymph node metastasis was 10.8%, as opposed to 45.1% for patients negative for lymph node metastasis. We examined the outcome according to histological type and found that based on the histological findings, the prognosis was increasingly poor in the following order: papillary adenocarcinoma, macrotubular carcinoma, microtubular carcinoma. To achieve curative treatment in the future it will be important to clearly define the extent of hepatectomy and determine the extent of lymph node dissection required, and clearly identify other prognostic factors.
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PMID:[Intrahepatic bile duct carcinoma (cholangiocarcinoma)]. 921 13

Zymosan, a non-specific macrophage-stimulating agent, modifies favourably tumour growth in the liver but has minor effect on renal tumours. The mechanism accounting for variation is still to be clarified. The effect of zymosan on liver cancer may be mediated by the macrophage-monocyte system. Kupffer cells are in vitro cytotoxic against colon cancer cell lines. The kidney is sparse in macrophage elements. The prostaglandin synthesis inhibitor, indomethacin, inhibits tumor growth. In Wistar-FU rats inoculated in the liver and the kidney with an adenocarcinoma cell suspension, pretreatment with zymosan (3 mg x 100 g[-1]) significantly reduced both tumour take and liver volume. This effect was attenuated by concomitant administration of indomethacin (0.2 mg x 100 g[-1]). After 2 weeks there was still reduced liver tumour volume. No significant effects on tumour take or growth were observed when the cells were inoculated into the kidney. There was no significant effect of zymosan on an hepatoma in Lister-Hooded rats. Pretreatment with indomethacin had no effect on tumor take or initial growth.
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PMID:The influence of zymosan and indomethacin on liver and kidney tumor growth. An experimental study in rats. 938 96

To provide the pattern and outcome, 131 patients admitted to Tikur Anbessa Hospital, Department of Surgery, between 1992 and 1996 with a diagnosis of lower gastrointestinal tract (colo-anorectal and small bowel) cancer were analysed. Lower gastrointestinal tract cancer accounted for 30% of all gastrointestinal tract malignancies, excluding hepatic cancer, seen in the Department during the study period. The female to male ratio was 1.0:1.8. The mean age was 47.1 +/- 15.7 (range 17-85) years. Among the 131 cases, 52.7% and 16% were under 50 and 30 years of age, respectively. The mean duration of symptoms on admission was 11.2 +/- 8.9 (range 0.2-43) months. The most frequent clinical features included weight loss (93%), pain (86%), rectal bleeding (79%), tenesmus (74%) and anorectal lesion (62%). Adenocarcinoma accounted for 92% of the pathology. Among 94 surgically staged cases, 63 had Dukes' C and D lesions. The most common site of primary tumours was the rectum (61.1%). Ninety per cent of the cases were operable and of these, 63 had resections with curative intent. Twenty patients refused surgery. There were fifteen postoperative hospital-stay deaths. The mean follow up was 5.7 +/- 3.1 (range 0.2-48) months. Cancer of the lower gastointestinal tract seemed to occur in rather younger age and diagnosis was late.
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PMID:Cancer of the lower gastrointestinal tract: a five year experience in Ethiopia. 980 17

The LCC15-MB cell line was established from a femoral bone metastasis that arose in a 29-year-old woman initially diagnosed with an infiltrating ductal mammary adenocarcinoma. The tumor had a relatively high (8%) S-phase fraction and 1/23 positive lymph nodes (LN). Both the primary tumor and LN metastasis were positive for estrogen receptor (ER) and progesterone receptor (PgR), but lacked erbB2 expression. Approximately one year later, the patient presented with a 0.8 cm comedo-type intraductal mammary adenocarcinoma in the left breast that was negative for ER and PgR, but positive for erbB2. Thirty-five months after the initial diagnosis she was treated for acute skeletal metastasis, and stabilized with a hip replacement. At this time, tumor cells were removed from surplus involved bone, inoculated into cell culture, and developed into the LCC 15-MB cell line. The bone metastasis was a poorly differentiated adenocarcinoma lacking ER, PgR, and erbB2, characteristics shared by the LCC15-MB cells, although ER can be re-expressed by treatment of the LCC15-MB cells for 5 days with 75 microM 5-aza-2'-deoxycytidine. The LCC15-MB cell line is tumorigenic when implanted subcutaneously in NCr nu/nu mice and produces long-bone metastases after intracardiac injection. Although the bone metastasis from which the LCC15-MB cell line was derived lacked vimentin (VIM) expression, the original primary tumor and lymph node metastasis were strongly VIM positive, as are LCC15-MB cells in vitro and in nude mice. The karyotype and isozyme profiles of LCC15-MB cells are consistent with its origin from a human female, with most chromosome counts in the hypertriploid range. Thirty-two marker chromosomes are present. These cells provide an in vitro/in vivo model in which to study the inter-relationships between ER, VIM, and bone metastasis in human breast cancer.
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PMID:LCC15-MB: a vimentin-positive human breast cancer cell line from a femoral bone metastasis. 1043 4

Tumor metastasis to a cirrhotic liver is rare. It has been suggested that colorectal cancer does not metastasize to the cirrhotic liver. We reported a 65 year-old man, a known carrier of hepatitis B surface antigen, diagnosed to have hepatocellular carcinoma with routine screening. A partial hepatectomy with resection of segments VI and VII was performed. The hepatectomy specimen revealed a 4.5 cm diameter HCC in a cirrhotic liver. Incidentally, 0.8 cm diameter ulcer at the descending colon. Histological examination of the left hemicolectomy specimen showed a moderately differentiated adenocarcinoma.
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PMID:Carcinoma of the colon with synchronous hepatic metastasis in a cirrhotic liver harboring a hepatocellular carcinoma. 1052 97

The relationship between aflatoxins and liver cancer is well established. In addition the inhalation exposure to carcinogen aflatoxin B1 (AFB 1) is considerable. Genotoxic chemical is known to react with DNA either directly or after metabolic activation to form adducts, a step thought to be relevant with respect to chemical carcinogenesis. The presence and the amount of specific DNA adducts provide a good indication of chemical exposure and genetic damage resulting the exposure to carcinogens and account for same of factors affecting individual susceptibility to cancer. Analysis of DNA adducts requires that the sensitivity of the methods to be sufficient high to allow detection of about 1 adduct/109 normal nucleotides. Most suitable method is based in physiochemical technique such as HPLC. Because circumstantial epidemiological evidence suggests that AFB1 inhalation may cause primary lung cancer. We investigate AFB1 by HPLC in three different tobacco sources, and in 39 patients with compatible lung cancer or chronic bronchitis. The patients were divided by clinical manifestations in lung cancer (n: 25) and chronic bronchitis (n: 14). Twenty-three of 25 patients presented epidermoid lung cancer within smoking habit, and 2 of 25 presented adenocarcinoma without smoking habit. In chronic bronchitis group 12 of 14 cases presented smoking habit. The control PBS liquid was negative to AFB1; the different tobacco sources, a) Virginia of Jujuy, b) Brasilero and c) black of Salta presented AFB1 positive determinations respectively. The bronchial tissues obtained by lung biopsies presented positive AFB1 in lung epidermoid cancer at 0.68 +/- 0.82 mg/L. The adenocarcinoma presented AFB1 negative determinations. In chronic bronchitis patients with smoking habit (n: 12) presented AFB1 positive with a level less than the epidermoid lung cancer group, 0.21 +/- 0.109 mg/L, p < .025.
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PMID:[Relationship between lung cancer and aflatoxin B1]. 1118 61

We focused our studies on single endothelial cells (ECs) scattered in extracellular matrix in lung cancer tumors. Neovascularization was evaluated in 100 tumors obtained from patients operated for lung cancer, in relation to histological type, tumor differentiation and clinical stage of the disease. Angiogenic objects (single endothelial cells and microvessels) were identified by immunohistochemistry using monoclonal antibodies against von Willebrand factor. The count of angiogenic objects per 1 mm2 in each section was determined in a "hot spot" located at the margin of the tumor. We used an arbitrary scale of angiogenesis intensity: 1 - 0-200, 2 - 201-400, 3 - >400 angiogenic objects/mm2. A majority (57%) of the examined cases belonged to the group 2. The angiogenesis intensity measured by the single EC numbers/mm2 correlates with the histological type and the differentiation of the tumors. There was no such a correlation when the angiogenesis intensity was measured by counting total angiogenic objects (microvessels + EC) number/mm2. Single EC number/mm2 in different histological types of cancer were as follows: 162+/-121 in squamous cell (SqCC), 194+/-71 in adenocarcinoma (AdC), 225+/-145 in large cell (LCC), 264+/-52 in small cell (SCC), 279+/-173 in combined cancer. The differences between the EC counts in the different histological types of lung cancers were statistically significant in the following pairs: SqCC vs SCC (p=0.0233) and AdC vs SCC (p=0.0409). The correlation between EC count in the "hot spot" and the grade of tumor differentiation was statistically significant for G1 vs G4 (p=0.0007) and G1 vs G2 (p=0.0411). Our results suggest that higher numbers of EC/mm2 may confirm rapid development of angioneogenesis. These relations should be examined in larger series of cases.
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PMID:Endothelial cells and angiogenesis intensity in lung cancer. 1153 81


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