Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of 2-naphthylamine and cyclophosphamide on the urinary bladder and liver of female BALB/c mice was investigated. The bladder mucosa of mice treated with 2-naphthylamine alone for 40 weeks showed diffuse hyperplasia. Oral administration of 2-naphthylamine for 40 weeks plus injections of cyclophosphamide produced bladder carcinomas in 30.8 approximately 35.7% of all animals, associated with downward growth of the bladder epithelium. All the bladder carcinomas were of the transitional cell type and most of them contained pseudoglandular areas. Hepatomas seemed to develop in higher incidence in mice treated with 2-naphthylamine plus cyclophosphamide than in mice treated with 2-naphthylamine alone. Most of the hepatomas were solitary and showed a trabecular pattern. Cyclophosphamide seemed to have a summative or promoting effect on carcinogenesis of the bladder mucosa and liver induced by 2-naphthylamine in female BALB/c mice.
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PMID:Histopathological changes induced in the urinary bladder and liver of female BALB/c mice treated simultaneously with 2-naph-thylamine and cyclophosphamide. 52 Jul 55

Tumorigenicity and oncogene expression were examined in HepG2 derived cells, a human hepatoma cell line. HepG2 cells and a single cell clonal HepG2 line, HLD2-6, were equally tumorigenic when injected s.c. into athymic nude mice. Cyclophosphamide pretreatment of both cell lines (500 micrograms cyclophosphamide/ml/two cell cycles) had no effect on tumor incidence or latency (P greater than 0.05). Tumors were nonencapsulated, highly invasive adenocarcinomas and were positive for gamma-glutamyltranspeptidase activity and bile production. Plasma from tumor-bearing mice was positive for human alpha-fetoprotein and negative for hepatitis B virus surface antigen as measured by radioimmunoassay. Two cell lines reestablished into tissue culture from HLD2-6 derived tumors had unaltered cell cycle times. Detailed in vitro translation analysis of RNA isolated from HLD2-6 derived cells and tumors were extremely similar to the translation products of RNA isolated from a normal human liver sample except for a Mr 53,000 polypeptide with an apparent charge shift. c-myc specific transcripts, when compared to a normal human liver sample, were increased in all HLD2-6 cell lines and tumors derived from HLD2-6 cells. This increase in c-myc expression could not be explained by gene amplification or hepatitis B virus integration. N-ras specific transcripts were not elevated in HLD2-6 cells grown in tissue culture but there was a selective increase of the 5.5-kilobase N-ras transcript in HLD2-6 derived tumors grown in nude mice. This increased 5.5-kilobase transcript did not remain elevated if the tumors were reestablished into tissue culture, suggesting some interaction with the host animal. c-Ha-ras expression could not be detected in any HLD2-6 derived tumor or cell line.
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PMID:Tumorigenicity and transcriptional modulation of c-myc and N-ras oncogenes in a human hepatoma cell line. 299 77

Mitoxantrone is similar to Adriblastin in its mechanism of action and antitumor activity. Objective remissions were obtained in 20-30% pretreated patients and in 23-44% of untreated patients by single-drug treatment of patients suffering from metastatic breast cancer. The objective response rates to Mitoxantrone in combination with CTX, 5-FU, MTX, VCR, MMC. Prednimustine or Vindesine were 16-46% in treatment and 38-89% in primary treatment. Randomized studies comparing Mitoxantrone with Adriblastin in single-drug and combination treatment did not show any significant differences in efficacy. However, Mitoxantrone was significantly less toxic. Remission rates of between 24 and 54% were achieved by single-drug treatment in pretreated patients suffering from non-Hodgkin lymphoma. Mitoxantrone appears to be active in ovarian cancer, lung cancer and hepatocellular carcinoma.
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PMID:Mitoxantrone: mechanism of action, antitumor activity, pharmacokinetics, efficacy in the treatment of solid tumors and lymphomas, and toxicity. 332 53

Chemosensitivity of liver cell carcinoma was studied by subrenal capsule assay. The method of assay was based on Bogden's one, but the antitumor activity was evaluated by tumor growth inhibition rate (TG-IR). The anticancer agent with more than 50% TG-IR was judged as positive in the chemosensitivity test. Of 3 human hepatoma cell lines transplanted in the subcutaneous space of nude mice, all of 3 were evaluable. The positive rates of ADR, MMC, CDDP, 5-FU and CPA were 66.7%, 100%, 66.7%, 100% and 0%, respectively. Of 24 patients who provided fresh tumor specimens for the assay, 12 (50%) were evaluable. The positive rates of ADR, MMC, CDDP, 5-FU and CPA were 25%, 16.7%, 16.7%, 33.3% and 8.3%, respectively. Our study suggested that 5-FU, MMC and ADR were comparatively active against the hepatoma cell, CDDP was less active than these 3 agents, CPA was inactive. These results seem to justify the use of current anticancer agents against hepatic cell carcinoma and indicate the usefulness of SRC assay for selecting chemotherapeutic agents against liver cell carcinoma.
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PMID:[Study on the chemosensitivity of liver cell carcinoma by subrenal capsule assay]. 334 29

Hypoxia, leading to cells in resting or slow replication phases may be a cause of chemotherapy and radiation therapy resistance in some tumors. Perfluorochemicals (PFC) may potentiate response to these therapies by increasing oxygen delivery to the tumor, forcing cells into more therapy-responsive replicating phases. To assess the effects of PFC on tumor growth and chemotherapy response, 91 ACI rats bearing 1 cc flank Morris hepatoma tumors were divided into groups: Group I, control; Group II, Adriamycin (ADR) 10 mg/kg intraperitoneally (IP); Group III, Cytoxan (CTX) 100 mg/kg IP; Group IV, PFC 20 mL/kg IV; Group V, ADR and PFC; Group VI, CTX and PFC. Animals were kept in 0.5 FiO2 for 24 hours after treatment, and mortality and tumor volumes determined 2 weeks later. Tumor DNA turnover was measured using opposing pathways assay of 14C-thymidine uptake and degradation. In a separate group, tumor tissue pO2 was measured polarographically with an oxygen microelectrode before and after injection of PFC (20 mL/kg). The survival was significantly reduced in group IV (4%) compared with group I, control (73%). Both ADR and CTX slowed the growth of the tumor, while PFC alone significantly accelerated tumor growth. The tumor response to ADR was potentiated by the addition of PFC. These results were confirmed by DNA synthesis evaluation. The mean pO2 level prior to injection was 6.6 +/- 1.96 mmHg compared with 18.92 +/- 1.00 mmHg after PFC injection (P less than or equal to .01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of perfluorochemicals on tumor growth and chemotherapy response. 344 Sep 9

Second malignancies were observed in 181 cases after treatment of antecedent breast cancer, among 5,302 primary breast cancer cases. The accumulated incidence of double cancer was as follows: 2.8% for 5 years, 5.2% for 10 years, 7.6% for 15 years, and 10.0% for 20 years. The observed incidence of second malignancy for all sites was 1.58 times as frequent as in the normal group. Statistically significant increased risks were observed for opposite breast cancer (O/E ratio 5.92), ovarian cancer (O/E ratio 4.47), corpus uterine cancer (O/E ratio 5.97) and thyroid cancer (O/E ratio 5.07). Among 5,302 cases, 2,431 (45.9%) underwent adjuvant chemotherapy. In chemotherapy groups, significantly increased risk of stomach cancer, thyroid cancer, leukemia and hepatoma was observed, but there were no remarkable differences between the MMC group and the CPA group. However, in the MMC + CPA combination treatment group, the risk of stomach cancer and leukemia was higher than in the single drug treatment groups. When multiple drugs were administered in large doses as long-term adjuvants, the risk of second malignancy seemed to become greater.
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PMID:[Effects of surgery and adjuvant chemotherapy of breast cancer on the incidence of a second malignancy]. 372 65

Fifty-two patients received one of two doxorubicin (DOX)-based admixtures; DOX plus cyclophosphamide (CTX) or DOX plus vinblastine (VBL) administered as a continuous 24-hour infusion for protracted periods. Compatibility and stability of the two-drug admixture was established for a minimum of 7 days. Twenty patients on the DOX/CTX admixture were infused for a median of 20 days (range, 7-56 days). DOX/VLB was infused in 32 patients for a median of 18 days (range, 5-48 days). Dose limiting toxicity was leukopenia observed in 14/52 patients; 4/20 on DOX/CTX and 10/32 on DOX/VLB. Additional toxicities observed included stomatitis (15%) and subclavian vein thrombosis (23%). Tumor responses were observed in 11 patients, including 6/13 breast cancer; 2/2 hepatoma; 2/4 sarcoma and 1/1 ovarian cancer. Responses were relatively short-lived and no responses were noted in known anthracycline resistant tumors. Admixtures of chemotherapeutic agents represents a novel, but feasible, mechanism for delivery of multiple drugs with an infusion schedule and can be considered for Phase III comparative clinical trials.
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PMID:Doxorubicin/vinblastine and doxorubicin/cyclophosphamide combination chemotherapy by continuous infusion. 373 Oct 35

The inhibitory effect of 6-keto-prostaglandin E1 (pGE1) on the growth and survival of ascitic hepatoma (AH-130) cells in vivo was compared with currently used chemotherapeutic agents. Three days after receiving an intraperitoneal injection of 3 X 10(6) AH-130 tumor cells, Donrhyu rats were injected intravenously or intraperitoneally with one of the following: Thromboxane B2 (TXB2) (0.5 mg/kg), 6-keto-pGE1 (0.5 mg/kg), Mitomycin C (MMC) (1.5 mg/kg), or MMC + 6-keto-pGE1 (1.5 mg/kg + 0.5 mg/kg). The mean survival time, median survival time, and increase of life survival percent (ILS%) during a 60 day period revealed that both 6-keto-pGE1 and 6-keto-pGE1 + MMC significantly inhibited AH-130 tumor cell growth, while TXB2 promoted tumor cell growth. We conclude that 6-keto-pGE1 like anti-tumor agents such as MMC, Diketocoriolin B, Carbazilquinon, Endoxan, and 5-Fluorouracil, can significantly inhibit growth of AH-130 tumor cells in vivo, particularly when administered in combination with the anti-tumor agent MMC.
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PMID:Effects of 6-keto-prostaglandin E1 on ascitic hepatoma-130 in vivo comparison with chemotherapeutic agents. 392 Jul 29

DMG, a degraded D-manno-D-glucan with a host-mediated antitumor activity did not significantly enhance nor inhibit the development of suppressor cells for either the antibody-forming response or the delayed hypersensitivity reaction to sheep red blood cells. Cyclophosphamide (CY), which inhibited the generation of suppressor cells, was combined with DMG in treatment of murine syngeneic tumors to obtain a higher antitumor activity. The antitumor activity of the combination against MH134 hepatoma was synergistically higher than that of either component alone. A marked antitumor effect of the combination treatment against MM46 mammary carcinoma was also shown. High levels of antitumor delayed hypersensitivity reactions were observed with this combination therapy. The possible roles of DMG and CY in this combination therapy are discussed.
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PMID:Combination therapy of murine tumors with a degraded D-manno-D-glucan (DMG) from Microellobosporia grisea, and cyclophosphamide. 624 May 52

The treatment of 205 patients with primary hepatocellular carcinoma in Singapore from 1975 to 1980 is reviewed. Adriamycin given at a dose of 40 mg/m(2) intravenously every 4 weeks for irresectible tumours achieved a response rate of 32% alone and has significantly prolonged the median survival time to 4 1/2 months (135 days) in these individuals. Despite this response only 1/34 (3%) patient showed complete remission and is alive at 2 1/2 years. Use of other combinations with Adriamycin e.g. 5 Fluorouracil and Vincristine produced a significant response in the first 16 weeks (p < 0.005) but not thereafter, when completed with the historical group. To improve the response and to consolidate this response, split doses of total hepatic irradiation (to a maximum of 3,150 rads) and alternate day administration of intravenous Adriamycin 10 mg (to a maximum of 90 mg) were given. 12/23 patients (50%) responded. This was followed by a four weekly Adriamycin, 5 F.U. and Vincristine. Median survival time was 5 1/2 months (165 days). Relapse occurred in all patients. Similarly in 5 patients who had resections, early recurrences occurred in 3/5 (60%) within 3 months, inspite of postoperative chemotherapy with Adriamycin, 5 F.U., Vincristine and Cyclophosphamide given every four weeks. In view of the high recurrence rate following effective treatment, further studies on the biological behaviour of these abnormal livers is required.
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PMID:Adriamycin in the treatment of resectible and irresectible primary hepatocellular carcinoma. 625 16


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