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)

PLC/PRF/5 is a human liver cancer cell line which synthesizes hepatitis B virus surface antigen (HgsAB). These cells produced tumor in 6 of 8 (75%) congenitally athymic nude mice at 13 of 28 subcutaneous injection sites and in 13 of 14 (93%) mice inoculated intraperitoneally. Tumors were successfully transplanted to 4 of 6 additional nude mice. Tumor growth was rapid. Growth of cephalad tumors was significantly greater than for caudal tumors (0.39 mm/day versus 0.28 mm/day). Microscopic examination of tumors showed moderately well-differentiated hepatocellular carcinoma. Foci of identical cells were present in pulmonary veins in 7 of 14 tumor-bearing animals. Tumor cell karyotype was identical with that of PLC/PRF/5 cells. In addition, HBsAg was detectable in high titer in animals with extensive tumor. Biological features of PLC/PRF/5-induced tumors in nude mice appeared to closely resemble human hepatocellular carcinoma. Moreover, HBsAg may provide a marker of tumor growth.
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PMID:A human hepatoma cell line (PCL/PRF/5) produces lung metastases and secretes HBsAg in nude mice. 688 16

The antitumor effect of an angiogenesis inhibitor, TNP-470 (AGM-1470, 6-0-(N-chloroacetylcarbamoyl)-fumagillol), administered via the hepatic artery in a medium-chain triglyceride (MCT) solution, in which TNP-470 is very stable, was examined in rats bearing Walker 256 carcinosarcoma in the liver. The MCT solution containing 0.1 mg of TNP-470 completely suppressed tumor growth after a single arterial injection, and the solutions containing 0.5 approximately 5 mg of TNP-470 caused tumor regression function. These antitumor effects lasted for at least 2 weeks. Moreover, the administration of the MCT solution containing 5 mg of TNP-470 also caused remarkable regression of well-developed enlarged tumors 2 weeks after inoculation, indicating potential in the treatment of unresectable hepatic cancer. When the MCT solution containing radiolabeled TNP-470 was injected via the hepatic artery, the initial radioactivity in the tumor was 22 times that in the normal part of the liver and 5.7 times that in the tumor when an aqueous solution of radiolabeled TNP-470 was injected. Also, in the case of the MCT solution, the radioactivity in the tumor was maintained at a relatively high level for over 2 weeks after injection. These results indicate that the remarkable antitumor effect resulted from the selective delivery and prolonged retention of TNP-470 at the tumor site.
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PMID:Antitumor activity of a medium-chain triglyceride solution of the angiogenesis inhibitor TNP-470 (AGM-1470) when administered via the hepatic artery to rats bearing Walker 256 carcinosarcoma in the liver. 752 53

Twenty-five cases of small hepatocellular carcinoma (HCC; diameter < or = 30 mm) were evaluated for overall morphologic features and growth patterns. The tumors often showed a well-differentiated, normotrabecular histologic pattern and insidious interstitial invasion, which resembled benign hepatocytes scattered in connective tissues. As the tumor grew, a less-differentiated tumor area became predominant. Portal tracts included in small HCC nodules were quantitatively assessed, revealing that they progressively reduced in number with tumor growth. The tumor margin was often reported to be unclear. The present results indicate that the histologic grade of tumor differentiation, capsular formation, existence of liver cirrhosis and patterns of interstitial invasion are important factors for determining the nature of the margin. The score of argyrophilic nuclear organizer regions (AgNOR) was examined in 5 cases showing typical interstitial invasion with the insidious type. In each case, the AgNOR score of the invading tumor cells was lower than that of tumor cells within the HCC nodules, but higher than benign hepatocytes in cirrhotic parenchyma. It clarified that the growth activity of well-differentiated HCC was rather suppressed upon their interstitial invasion.
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PMID:Growth patterns and interstitial invasion of small hepatocellular carcinoma. 764 31

Estrogen withdrawal versus tamoxifen (TAM) treatment was compared in two human breast cancer xenografts, the estrogen-dependent ZR75-1 and its estrogen-independent subline ZR75/LCC-3. The following parameters were determined: tumor growth, NTP:P(i) by 31P magnetic resonance spectroscopy, apoptotic index, and creatine kinase (CK) activity. Tumors of each line were grown in ovariectomized nude mice during stimulation from a s.c. 17 beta-estradiol pellet. At a tumor size of approximately 350 mm3, the pellet was removed from one-half of the animals. The remaining one-half served as controls. In parallel experiments, injections of TAM were initiated instead of estrogen withdrawal. Estrogen withdrawal as well as TAM induced growth inhibition of ZR75-1 tumors, whereas ZR75/LCC-3 was resistant to both types of therapy. Growth inhibition of ZR75-1 by estrogen withdrawal, but not by TAM, was accompanied by an 80% increase of the NTP:P(i) ratio (P < 0.01) and a significantly decreased cytosolic CK activity (P < 0.01). No significant change in pH was observed. These changes seemed not to be related to changes in apoptotic index. None of the described changes occurred in ZR75/LCC-3. The present data indicate: (a) ZR75-1 and ZR75/LCC-3 xenografts respond differently to estrogen withdrawal and TAM with regard to growth inhibition, 31P magnetic resonance spectroscopy, and CK activity; (b) estrogen withdrawal, but not TAM, induced a decrease in the CK activity of estrogen-dependent tumor tissue, and (c) increased apoptosis did not explain the growth inhibition and the increase in NTP:P(i) induced by estrogen withdrawal. The results indicate other growth inhibitory mechanisms of TAM in addition to competitive inhibition of the estrogen receptor.
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PMID:Growth inhibition in response to estrogen withdrawal and tamoxifen therapy of human breast cancer xenografts evaluated by in vivo 31P magnetic resonance spectroscopy, creatine kinase activity, and apoptotic index. 766 92

The effectiveness of combined administration of Ftorafur (FT) and Krestin (PSK) on experimentally-induced liver cancer has not been established. This study was undertaken to elucidate the effect of combined administration of these drugs on tumor growth and temporal changes in the immuno-endocrine system under this immunochemotherapy. Male inbred WKA/H strain rats were used. The drugs used were FT and PSK, each dissolved in water and fed orally. The drugs were administered separately but concomitantly in standardized cycles to the tumor-bearing animals. KDH-8 ascitic liver cancer cells were subcutaneously transplanted into WKA rats. The tumor growth inhibition rate of FT and PSK was then determined. Twenty-one days after subcutaneous transplantation, tumor growth in the combined administration transplantation, tumor growth in the combined administration group was significantly inhibited, compared to the control group (p < 0.001). At fourteen days, plasma ACTH levels of the FT + PSK combined group were significantly lower than those of the control group (p < 0.001).
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PMID:Efficacy of immunochemotherapy with Ftorafur and Krestin in rats. 773 25

The effectiveness of the combined administration of 5-fluorouracil (5-FU) and Krestin (PSK) on experimentally induced liver cancer has not been established. This study was undertaken to elucidate the effect of the combined administration of these drugs on tumor growth and metastasis. Male inbred WKA/H strain rats were used. The drugs used were 5-FU and PSK, each dissolved in water and fed orally. The drugs were administered separately or concurrently in standardized cycles to the tumor-bearing animals. KDH-8 ascitic liver cancer cells were subcutaneously transplanted into WKA rats. The tumor growth inhibition rates of 5-FU and PSK were then determined. Eighteen days after subcutaneous transplantation, tumor growth in the combined administration group was significantly inhibited, compared to the control group and the single treatment groups (p < .05). In addition, a liver metastatic model was prepared by transplanting KDH-8 cells into the spleen. Then the metastatic inhibitory effects of 5-FU and PSK were analyzed. At 14 days, the mean number of liver metastatic nodules was approximately 63 in the control group. However, the combined-medicated group showed a much lower number of nodules (40), indicating that metastasis was significantly inhibited (p < .05).
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PMID:Inhibitory effects of combined administration of 5-FU and Krestin on liver cancer KDH-8 in WKA/H rats. 773 28

A 66-year-old man with ascites and marked edema in the lower extremities was suspected of having secondary Budd-Chiari syndrome due to primary liver cancer, based on imaging diagnosis, i.e., ultrasonography, computed tomography, and inferior venacavogram. At autopsy, an encapsulated small liver cancer was found to have extended into the inferior vena cava and right atrium. There have been few reports of small hepatocellular carcinoma with intravascular tumor growth into the right atrium.
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PMID:Small hepatocellular carcinoma with intravascular tumor growth into the right atrium. 819 95

In this study we investigated temporal changes in both the endocrine system and immunity in rats under immunochemotherapy with 5-FU and Krestine (PSK). This immunochemotherapy was performed on two types of groups, non-cancer-bearing rats and cancer-bearing rats. As hosts, inbred strain WKA/HA 5-week-old male rats and as tumors, transplantable ascitic liver cancer KDH-8 cells were used. Our results indicated that 1) in the non-cancer-bearing rats, 5-FU administration led to an increase in serum cortisol and IAP, however, PSK concurrent administration clearly lowered the levels of cortisol and IAP; 2) in the cancer-bearing rats, the levels of ACTH, cortisol and IAP increased as the cancer progressed, but in the immunothemotherapy administration groups these levels were lower; 3) the immunothemotherapy administration group had greater effects on both tumor growth and liver metastasis.
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PMID:Temporal changes in ACTH, cortisol and IAP in rats under immunochemotherapy with 5-FU and Krestine. 839 7

To characterize the effect(s) of transforming growth factor alpha (TGF alpha) during multistage carcinogenesis, we examined tumor development in pancreas and liver of transgenic mice that coexpressed TGF alpha with either viral (simian virus 40 T antigens [TAg]) or cellular (c-myc) oncogenes. In pancreas, TGF alpha itself was not oncogenic, but it nevertheless dramatically accelerated growth of tumors induced by either oncogene alone, thereby reducing the host life span up to 60%. Coexpression of TGF alpha and TAg produced an early synergistic growth response in the entire pancreas together with the more rapid appearance of preneoplastic foci. Coexpression of TGF alpha and c-myc also accelerated tumor growth in situ and produced transplantable acinar cell carcinomas whose rate of growth was TGF alpha dependent. In liver, expression of TGF alpha alone increased the incidence of hepatic cancer in aged mice. However, coexpression of TGF alpha with c-myc or TAg markedly reduced tumor latency and accelerated tumor growth. Significantly, expression of the TGF alpha and myc transgenes in hepatic tumors was induced up to 20-fold relative to expression in surrounding nonneoplastic liver, suggesting that high-level overexpression of these proteins acts as a major stimulus for tumor development. Finally, in both pancreas and liver, combined expression of TGF alpha and c-myc produced tumors with a more malignant (less differentiated) appearance than did expression of c-myc alone, consistent with an influence of TGF alpha upon the morphological character of c-myc-induced tumor progression. These findings demonstrate the importance of TGF alpha expression during multistage carcinogenesis in vivo and point to a major role for this growth factor as a potent stimulator of tumor growth.
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PMID:Transforming growth factor alpha dramatically enhances oncogene-induced carcinogenesis in transgenic mouse pancreas and liver. 841 34

Long-term tamoxifen has generally only few and usually mild adverse side effects. More serious, potentially life-threatening toxicities are rare. Aside from the ocular effects, most documented side effects appear to be related to the estrogenic properties of tamoxifen, for instance, thrombembolic disease and endometrial cancer. On the other hand, these properties may also be beneficial, for instance, they may contribute to a decreased risk of cardiac disease and osteoporosis. The potential association between tamoxifen and other possibly estrogenic side effects such as liver cancer and tamoxifen-induced tumor growth in patients with acquired tamoxifen resistance remain controversial.
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PMID:Long-term toxicity of tamoxifen. 850 24


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