Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

P-Glycoprotein (Pgp) has been shown to mediate multidrug resistance in tumor cell lines. Overexpression of Pgp has been detected in clinical cancer samples of many histological types. The basis and biological significance of such increases in Pgp expression are not well understood. In this study, the expression of Pgp during stepwise progression to rat liver cancer was examined to investigate the possible role of Pgp in carcinogenesis. An immunohistochemical technique was used to detect Pgp at the single-cell level, in a large number of liver nodules, hepatocellular carcinoma, and in distant metastases of the carcinomas. The results showed that distinct changes in Pgp expression occurred during stepwise liver carcinogenesis and that these changes were closely associated with the microscopic anatomy of the lesions. In contrast to gamma-glutamyl transpeptidase and glutathione S-transferase-7.7, whose expression appeared to correlate with the early steps of liver carcinogenesis, Pgp expression was higher in the large hyperplastic nodules and in hepatocellular carcinomas than in the early microscopic lesions. A particularly striking finding was the consistent expression of Pgp in the lung metastases. These findings suggested that Pgp was associated with a more progressed malignant phenotype in liver carcinogenesis.
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PMID:P-glycoprotein expression during tumor progression in the rat liver. 138 36

Forty patients with unresectable liver cancer were treated by hepatic arterial infusion chemotherapy plus embolization (HAI+HAE). Thirty-four patients had huge masses and 6 nodular lesions. After HAI+HAE, the frequency of greater than or equal to 50% reduction in tumor size was 67.5% (27/40); that of reduction in marked and partial disappearance of tumor blood vessels was 90% (36/40); and that of marked decrease and normalized AFP was 90.3% (28/31). The mean survival of 12 patients treated solely by HAI plus HAE was 17.2 months, and one of them has been alive for 48 months. Twenty-eight patients became operable following HAI+HAE and 26 of them underwent hepatic resection. Pathologic examination revealed obvious necrosis in most part of the tumor with a few viable cancer cells in the periphery and inflammatory reaction as well as fibrotic proliferation around the necrotic tumor tissue. The authors believe that hepatic arterial infusion chemotherapy plus embolization for the unresectable liver cancer is effective. If satisfactory shrinkage of the tumor is observed, subsequent resection should be contemplated for cure.
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PMID:[Hepatic arterial infusion chemotherapy plus embolization for unresectable liver cancer--a report on 40 patients]. 139 76

We measured urinary levels of free L-fucose in healthy subjects, patients with benign diseases, and patients with cancer using an automated analyzer and a newly isolated L-fucose dehydrogenase, and evaluated the clinical usefulness of the results. The values obtained were corrected for urinary creatinine as micromoles per gram of creatinine. The cutoff value, set at the mean + 2SD for the healthy subjects, was 250 mumol/g.Cr. Patients with gallbladder cancer, bile-duct cancer, liver cancer, pancreatic cancer, or cirrhosis of the liver had significantly higher levels of L-fucose than the healthy subjects. The diagnostic sensitivity for these five diseases, taken together, was 68% (144/213). Specificity for the detection of cancer was calculated by use of false positives for patients with cholelithiasis, hepatitis, and pancreatitis: it was 73% (76/104). Diagnostic accuracy for these seven diseases taken together was therefore 69% (220/317). We compared the positive ratio of the L-fucose level with that of the tumor markers AFD and CA19-9. The positive ratio of an L-fucose value above the cutoff was higher than the positive ratio of either marker in bile-duct cancer, gallbladder cancer, liver cancer, and pancreatic cancer. The results suggested that the urinary levels of free L-fucose reflected the metabolism of sugar chains of glycoconjugates, and may be usefully clinically as a tumor marker.
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PMID:[Clinical assessment of urinary free L-fucose levels]. 140 61

Radiologists play a vital role in the management of malignant liver disease, both by providing accurate data regarding extent and segmental localization of lesions as well as demonstrating their relationship to major vascular structures. The interrelationship between the major cross-sectional imaging modalities (ultrasound, CT, and MRI) must be understood in order to use each modality effectively and efficiently. Characteristic behavior of certain tumors (such as venous invasion by hepatomas) can help in recognition of tumor type and may have a major impact on decisions regarding resectability. Pitfalls in liver imaging (such as the presence of benign conditions that may mimic malignant lesions) must be well understood in order to avoid errors in diagnosis. Difficulties may arise in underdetection of tumors arising in chronically diseased livers and overstatement of the extent of tumors in livers with coexistent benign and malignant lesions. The appearances and behavior of primary and metastatic liver cancer is reviewed, emphasizing the features listed previously.
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PMID:Correlative imaging of malignant liver tumors. 141 39

Magnetic resonance imaging during arterio-portography (MR-AP) was performed in 2 patients of hepatic cancer. Low dose of meglumine gadopentetate (4 ml of a 0.5 mmol/L solution) was injected into a superior mesenteric artery during acquisition of a Turbo-FLASH sequence. An increase in liver to lesion contrast was obtained with MR-AP and it is also useful in the late phase to distinguish a flow defect lesion due to portal obstruction from the tumor.
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PMID:[MR imaging during arterio-portography (MR-AP) in the detection of hepatic cancer]. 143 39

For colorectal carcinomas, the rate of tumor development is proportional to the fourth to sixth power of elapsed time, suggesting that four to six independent events are necessary. Although similar calculations have not been made for HBV-associated HCCs, it is likely that this is also the case for HCCs, since individuals with persistent HBV infection do not usually develop HCC until they are 45 or greater years old. As evidence for specific genetic and epigenetic changes in HCCs accumulate, the important players in multistep hepatocarcinogenesis are becoming clearer. However, even though Myc family oncogenes are clearly implicated in woodchuck HCC, similar integrations have not been found in human HCCs. Therefore, although rodent and human systems have many similarities, we must realize that important differences may also exist. Regarding tumor suppressor genes, the evidence for p53 alterations in HCC is strong. A growing body of evidence suggests further that alterations in the retinoblastoma gene and one or more tumor suppressor genes on chromosome 11 are also involved in HCC. HBV integrations may certainly play a role in the generation of chromosome aberrations leading to loss of tumor suppressor alleles, since chromosomes 11 and 17 are the most common integration sites. Finally, the role of X proteins as participants in malignant transformation has been demonstrated for certain immortalized, nontransformed hepatocytes. Altered autocrine mechanisms of cell growth control, possibly involving IGF-II, are clearly implicated in HCC. Paracrine mechanisms for the control of hepatocyte growth and differentiated functions may also be altered as a result of the synthesis and secretion of a complex array of interleukins, HGF, and basic and acidic FGFs by cells in the inflammatory and cirrhotic lesions of precancerous livers. Whether the order of molecular changes in the hepatocyte is important for malignant progression is presently not clear. What is clear, however, is that hepatocarcinogenesis involves alterations in the concerted action of protooncogenes, growth factor, and tumor suppressor genes. How these factors interact will provide a more complete understanding of the mechanism or mechanisms of hepatic oncogenesis.
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PMID:Cellular and molecular mechanisms of hepatocarcinogenesis. 143 79

As an effective therapy for hepatocellular carcinoma, hepatic arterial chemo-embolization therapy has been widely used, and many embolizing materials have been extensively investigated. In the present study, we prepared various types of cis-diamminedichloroplatinum(II) (CDDP) albumin microspheres using chitin and chitosan, both of which have attracted considerable attention as new non-toxic biological polymer materials having favorable characteristics such as immune adjuvant activity, biological compatibility, and biodegradation. Hepatic artery of rabbit hepatic cancer models, which had transplanted VX2 tumors, were embolized with various types of microspheres. The anti-tumor effects and tumor-targeting of the microspheres, and the effects of the microspheres administration on the hepatic tissue were investigated. As a result, anti-tumor activity of the microspheres was increased by the addition of chitin-containing or chitosan treated materials; tumor growth rates of chitin addition and chitosan treated groups were approximately 160% and 120%, respectively, and were significantly lower than that of the non-treatment groups with a rate of approximately 580%. However, complete inhibition of tumor growth might have been impossible. Anti-tumor activity was increased by the addition of chitin-containing or chitosan treated materials. Whereas the growth inhibitory effect was insufficient, in order to potentiate anti-tumor activity, higher CDDP contents and sustained release of CDDP at a high level from microsphere and so on should be essentially improved for the near future. The CDDP level in hepatic tissue following the administration of microspheres was increased by adding chitin to the microspheres or by treating the microspheres with chitosan.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A study of embolizing materials for chemo-embolization therapy of hepatocellular carcinoma: antitumor effect of cis-diamminedichloroplatinum(II) albumin microspheres, containing chitin and treated with chitosan on rabbits with VX2 hepatic tumors. 146 14

During the period of 1958-1986, a series of 125 patients with pathologically proven hepatocellular carcinoma (HCC) surviving more than 5 years was collected in authors' institute. Thirty seven of them survived more than 10 years, the longest being 30 years. Of the entire series, 55.2% of patients was discovered by screening, 48.0% of patients was subclinical HCC, 80.0% of patients had solitary tumor, and 53.6% of patients had tumor size smaller than 5 cm. Pathological findings revealed that 90.2% of tumor was grade I and II (Edmondson grading) and 81.6% of patients associated with cirrhosis. The serum HBsAg was positive in 63% and anti-HBc in 80% of the patients who had checked the HBV markers. Of the 125 patients, 108 patients received resection, 67 patients were small HCC resection, 41 patients were non-small HCC resection, re-resection for subclinical recurrence or solitary lung metastasis was done in 26 patients with resection. Limited resection amounted to 54.6% of patients with resection. Of the 125 patients, 17 patients received palliative surgery other than resection, including hepatic artery ligation, cannulation, or their combination, etc. Eight out of the 17 patients received second stage resection due to marked shrinkage of tumor. It is concluded that early resection remained the major approach to get a long-term survivor, re-resection for subclinical recurrence is also of proved merit. Resection of huge tumor is still useful but less effective. Cyto-reduction and sequential resection is a new trend. Primary liver cancer (PLC) has long been recognized as incurable malignancy with extremely low 5-year survival rate. According to the cancer statistics in the United States, the relative 5-year survival rates for patients with PLC was 2% in 1960-1963, 3% in 1970-1973, 4% in 1974-1976, 3% in 1977-1980 and 5% in 1981-1986. Patients with PLC survived more than 5 years were rarely reported in the literature. In 1971, Curutchet collected worldwide data from 45 authors covering the period for 65 years (1905-1970), only 45 patients with PLC were found to be 5-year survivors. Thanks to the progress in tumor markers, particularly alpha fetoprotin (AFP) and new localization measurements, diagnosis and treatment are possible in subclinical stage. Based on combined strategies to the treatment of PLC including resection of small liver cancer, re-resection of subclinical recurrence after curative resection, multimodality treatment, and sequential resection after shrinkage of tumor, the 5-year survival of PLC has gradually increased.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Analysis of one hundred and twenty five patients with primary liver cancer surviving more than five years. 151 34

Nineteen patients with metastatic liver tumor (9 of gastric cancer, 5 of colon cancer, 2 of pancreatic cancer, one each of mammary cancer, cholecystic cancer, carcinoid of biliary tract) and one patient with primary liver cancer were treated by endogenously induced LAK therapy consisting of transhepatic arterial infusion with ADM or MMC for induction therapy and OK-432 and rIL-2 (TGP-3) for immunotherapy. The following results were obtained. 1) Clinical response for liver tumor showed no CR but 8 cases of PR, for an overall response rate of 42.1%. 2) Reduced tumor marker value was noted in 76.5% cases, and 50% survival term became 349 days after the therapy. 3) Many CD4 and CD8 positive mononuclear cells had infiltrated around liver tumor after therapy by immuno-histochemical staining of surface marker. 4) NK activity of peripheral blood lymphocytes was markedly reduced soon after the therapy and continued for about 4-7 days, while in cases of combined subcutaneous administration with OK-432, NK activity showed only a slight decrease.
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PMID:[Significance of antitumor effects and immunological response on endogenously induced LAK therapy for primary or metastatic liver tumor]. 153 Feb 92

To investigate therapeutic strategies for hepatoma, it is necessary to have a reproducible animal model with a tumor growth pattern allowing accurate assessment of results. Many techniques of intrahepatic tumor implantation (IHTI) have been devised for intrahepatic tumor models. Most of them, however, have the disadvantage of high rates of artificial tumor dissemination during tumor implantation, which interferes with the evaluation of therapy. To overcome this problem, we have developed a technique of IHTI in which a piece of Gelfoam is placed into a small incision in the liver for the purpose of both hemostasis and formation of a tension-free pocket to accept the tumor implant. In 583 ACI rats receiving IHTI with Morris hepatoma 3924A, the tumor take rate was 100%. Resembling the natural course of human hepatoma, the implanted tumor grows locally early in the course of disease and eventually invades the surrounding organs causing ascites and also metastasizes to the lung. Liver microangiography demonstrated that the tumor received blood supply mainly from the hepatic artery. This IHTI technique was also compared to two other methods of IHTI: insertion of fragments without using Gelfoam and implantation with a tumor cell suspension. A significantly lower rate of early lung metastases was achieved with our technique (0%) in comparison with other two techniques (41 and 80%). We conclude that this rat liver cancer model is reproducible and allows efficient evaluation of treatment modalities for liver cancer without interference from tumor at undesirable sites.
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PMID:A reproducible rat liver cancer model for experimental therapy: introducing a technique of intrahepatic tumor implantation. 153 93


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