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)

A pilot study of continuous or intermittent low dose 5-FU and cisplatin chemotherapy (low-dose FP therapy) was conducted at the Department of Surgery of Sapporo Medical University School of Medicine (Group A) and Sapporo Tsukisamu Hospital, and at the Department of Internal Medicine of the Kochi Prefectural Center Hospital (Group B). The cases with esophageal cancer, stomach cancer, pancreatic cancer, hepatocellular carcinoma or colonic cancer co-existing with their inoperable lesion(s) were considered in this chemotherapy. The rates of complete and partial response and of side effects were studied. Also, the effects of low-dose FP on the prognosis of the patients with pancreatic or colonic cancers were investigated. The procedure consisted of continuous 5-FU 320 mg/m2 i.v. with daily CDDP 2.5 mg/m2 i.v. for five days/week rescue was performed for at least four weeks as a rule. The rates of complete response and partial response were 64% (Group A) and 56% (Group B) in esophageal cancer, 62% (Group A and B) in stomach cancer, 48% (Group A) and 57% (Group B) in colonic cancer, and 8% (Group A) and 21% (Group B). The overall response rate was 57.8%. The frequencies of severe side effect(s) (grades 3 and 4) were within three to eight percent, and no death from side effect(s) was experienced. The effects of low-dose FP therapy on the prognosis of stage IV colonic cancer and stage IV b pancreatic cancer were studied retrospectively. It is suggested that this chemotherapy might contribute to the survival of patients with these two cancers. Otherwise, the chemotherapy of intermittent administration (day by day) of 5-FU 750 mg/m2 i.v. and CDDP 2.5 mg/m2 i.v. was selected in order to decrease the rate of side effects and their severity. The pilot study encountered no severe side effects, no cases with grade 4 side effect were experienced but the remission rates were mostly similar to that of sequential low-dose FP therapy. However, the side effect of low grade ones as symptoms in gastrointestinal tract were observed in more patients. We concluded that sequential or intermittent 5-FU/CDDP therapy might be fairly effective, and since the adjuvant chemotherapy of choice for advanced or recurrent gastrointestinal cancer, their FP therapy might be one of the adjuvant treatments.
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PMID:[Biochemical modulation of 5-FU--effect of low dose CDDP]. 1009 43

The synergistic mechanism of cisplatin (CDDP) and 5-fluorouracil (5-FU) in combination remains unclear, despite its substantial antitumor activity, which has been demonstrated clinically. To clarify the mechanism(s), we determined the sensitivity or resistance factors to either drug in seven gastrointestinal cancer cell lines and then analyzed the altered gene expression after different exposures to CDDP and 5-FU. At the basal gene expression level, glutathione S-transferase pi (GSTpi) expression correlated with the observed resistance to CDDP, whereas dihydropyrimidine dehydrogenase (DPD) and multidrug resistance-associated protein (MRP) expression was related to 5-FU resistance. GSTpi, DPD, and MRP expression increased in response to the respective drug, but they also increased in response to the other drug as well. Additionally, 5-FU revealed a drastically increased thymidylate synthase (TS) gene expression in 5-FU-resistant cells. However, the increasing actions of CDDP and 5-FU on GSTpi, DPD, MRP, and TS expression varied according to the exposure time, concentration, and schedule. A low concentration of CDDP (1 microg/ml, 30 min) followed by 5-FU (0.5 microg/ml, 72 h) was found to cause a less increased expression of DPD, MRP, GSTpi, and TS than either drug alone, thus resulting in synergistic cytotoxicity in 5-FU-resistant COLO201 and CDDP-resistant HCC-48 cells. The sequential combination of CDDP and 5-FU inhibited the growth of human normal renal proximal tubule cells by less than 20%. Low concentrations of CDDP followed by continuous exposure to 5-FU can repress increased gene expression related to both drug resistances, thereby being synergistically cytotoxic in human gastrointestinal cancer cells.
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PMID:Low-dose cisplatin and 5-fluorouracil in combination can repress increased gene expression of cellular resistance determinants to themselves. 1049 41

Serum levels of melanoma inhibiting activity (MIA) and S100, both markers in malignant melanoma, are increased only in few patients with non-melanocytic tumors. We examined a series of serum samples from patients with colorectal (CRC) (N=56), gastric (GC) (N=43), pancreatic (PC) (N=29), hepatocellular (HCC) (N=30), cholangiocellular and gallbladder carcinoma (CCC) (N=18). MIA and S100 were measured by commercially available assays. Positive serum levels for MIA and S100 were found in 16.1% and 5.4% of the patients with CRC, 11.6% and 9.3% with GC, 34.5% and 13.8% with PC, 0% and 30% with HCC and 16.7% with CCC, respectively. All patients with sera positive for either MIA or S100 suffered from advanced tumors and received palliative treatment. Elevated serum levels of MIA and S100 are frequent in patients with gastrointestinal cancer. Further investigation is warranted to define the role of MIA or S100 seropositivity in gastrointestinal cancer with regard to follow-up.
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PMID:Seropositivity for MIA and S100 in patients with gastrointestinal carcinomas. 1071 58

Primary gastrointestinal cancer frequently spreads to the mesentery, omentum and other parts of the peritoneum, and these deposits are generally considered to be induced by intraperitoneal seeding from the primary lesion. However, a few peritoneal metastatic cases or cases with positive intraperitoneal lavage cytology, without serosal infiltration, have been reported. Most of peritoneal dissemination is certainly attended with serosal involvement of gastrointestinal malignancy. Nevertheless, we observe an unusual case of peritoneal dissemination without definite serosal invasion of the malignancy. And peritoneal dissemination is likely to be concomitant with lymph node metastasis in both cases with and without definite serosal invasion. In this study, we examined peritoneal cancer dissemination from the viewpoint of lymphogenous metastasis. For the model of lymphatic invasion, we established an animal experimental model of mesenteric lymph vessel obstruction. With these models, lymphangiographical studies were made on the fourth postoperative day (ten animals each) and we obtained mesenteric lymphangiograms of extensive mesenteric lymph vessels and reflux of lymph distal to the obstruction point from all ten animals. Next, in these experimental models, fluorescent-labelled tumor cells (rat hepatoma cell line, N1-S1) were infused from the mesenteric lymph node distal to the obstruction point on the fourth postoperative day (five animals each), and the migration of these tumor cells was investigated via fluorescent micrography. Subsequently, the fluorescent-labelled tumor cells were revealed in the mesenteric lymph nodes, mesenteric lymph vessels, interstitial tissues of the mesentery, submucosal lymph nodules and mucosal layer of the small intestine. Hence, lymphatic invasion and obstruction may cause extensive peritoneal dissemination via the lymphatic route.
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PMID:Experimental study of lymphogenous peritoneal cancer dissemination: migration of fluorescent-labelled tumor cells in a rat model of mesenteric lymph vessel obstruction. 1096 21

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 levels of macrophage migration inhibitory factor (MIF), a proinflammatory and carcinogenic cytokine, were significantly higher in the sera from patients with hepatocellular carcinoma (HCC; 25.6+/-15.3 ng/ml, n=55) and liver cirrhosis (LC; 18.9+/-10.7 ng/ml, n=26) compared with sera from patients with gastrointestinal cancer (6.8+/-7.5 ng/ml, n=29) and normal controls (5.6+/-1.2 ng/ml, n=45; P<0.01). Hepatocytes from patients with LC and HCC, but not from chronic hepatitis, expressed very high levels of MIF. A possible association between overexpression of MIF and hepatocarcinogenesis is suggested.
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PMID:Macrophage migration inhibitory factor in hepatocellular carcinoma and liver cirrhosis; relevance to pathogenesis. 1152 May 95

beta-tubulin (beta-TUB), Bcl-XL, and additionally glutathione S-transferase pi (GSTpi) were found to participate in sensitivity to docetaxel (TXT) in 7 human gastrointestinal cancer cell lines. The gene expression level of beta-TUB, Bcl-XL, and GSTpi was closely correlated with the IC50 for TXT. beta-TUB amount related to TXT resistance, and GST activity was correlated with IC50 for TXT in the 30-min treatment setting. Bcl-XL transfection increased TXT resistance of COLO201 cells, whereas GST inhibition by ethacrynic acid enhanced TXT cytotoxicity. Continuous TXT treatment increased beta-TUB and GSTpi expression, but the increased GSTpi mRNA was observed in TXT-resistant HCC-48 cells alone.
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PMID:Cellular sensitivity determinants to docetaxel in human gastrointestinal cancers. 1178 97

This review is concerned with the usefulness and the problem of biomarkers for cancer of digestive organs. Carcinoembryonic antigen (CEA) is a most popular and useful tumor marker for cancer of digestive organs. Squamous cell carcinoma (SCC) antigen and CYFRA have been reported as a useful tumor marker for esophageal cancer. CEA and CA 19-9 are a good prognostic factor in gastric cancer patients. The post-operative increase of serum CEA can be a predictive marker for the patients of colorectal cancer. Development of a radioimmunoassay for highly sensitive detection of tumor markers, they are considered to be useful for monitoring after treatment. But are not useful for the early diagnosis. The diagnosis of hepatocellular carcinoma (HCC) is based mainly on serological markers, such as alpha-fetoprotein and PIVKA-II. The two are useful complementary markers of HCC because they do not correlate with each other. But the problem of the false-positive rate for the patients with chronic hepatitis or liver cirrhosis is still remained. A typical marker of pancreatic and bile duct cancer is carbohydrate antigen, but the sensitivity of these markers is only 50%. Recent molecular biological analysis may be used as effective biomarkers in the diagnosis, prognosis, therapy, and risk assessment of digestive cancer.
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PMID:[Biomarkers for neoplasmas in digestive organs]. 1527 78

Abnormal Savda Munziq (ASMq) is a traditional Uighur medicinal herbal preparation commonly used to treat diseases such as diabetes, cardiovascular diseases, chronic asthma and especially digestive cancer. Earlier studies have shown that ASMq is a free radical scavenger and could prevent mitochondrial and DNA oxidative damage. In this study, we tested the effects of aqueous extract of ASMq on human hepatoma cells (HepG2) to explore the possible mechanism of its putative anticancer properties. Aqueous extract of ASMq was tested on HepG2 proliferation (MTT assay) at 72 h, cell viability at 48 h (neutral red assay), lactate dehydrogenase release over 48 or 72 h as a measure of cytoplasmic leakage, lipid peroxidation (malondialdehyde-thiobarbituric acid adducts) at 48 h, and incorporation of [3H]-leucine, [3H]-thymidine and [3H]-uridine into cellular protein, DNA and RNA, respectively, at 24 or 48 h to assess the inhibition effects to cellular macromolecule synthesis. Our results showed a significant (P < 0.05) time- and concentration-dependent inhibition of HepG2 proliferation and viability, with increased cytoplasmic leakage, and time- and concentration-dependent inhibition of protein, DNA and RNA synthesis. No lipid peroxidation was found at these concentrations. The results of the present study suggest that the putative anticancer mechanisms of ASMq may at least involve cytotoxicity.
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PMID:Cytotoxicity of abnormal Savda Munziq aqueous extract in human hepatoma (HepG2) cells. 1601 34

Technologic advances have provided the means to deliver tumoricidal doses of radiation therapy (RT) to patients with unresectable hepatocellular carcinoma (HCC) while avoiding critical normal tissues, providing the opportunity to use RT for curative intent treatment of HCC. For the current report, the expanded role of external beam RT in the setting of HCC from palliation to cure was reviewed. A systematic literature search was undertaken using the MEDLINE data base and secondary references to identify peer-reviewed, English-language articles that reported clinical outcomes after external beam RT alone or in combination with other treatments for HCC. Abstracts from the 2005 American Society of Clinical Oncology, American Society for Therapeutic Radiology and Oncology, American Gastrointestinal Association, and Society of Surgical Oncology Gastrointestinal Cancer Symposium also were included in the search. More than 60 articles reporting on clinical outcomes among patients who received RT for HCC have been published since 1990, including 20 articles that described unique sets of at least 15 patients. RT was used for palliation, to improve local control, and with curative intent in a wide spectrum of patients who most often were unsuitable for surgery and other treatments. Pain reduction following RT was noted in approximately 75% of patients with bone metastases from HCC who received RT. For patients with liver-confined disease treated with conformal RT, proton beam RT, and/or image guided RT with or without transarterial chemoembolization (TACE), local control response rates ranged from 40% to 90%, and the median survival ranges from 10 months to 25 months. For patients with HCC who had portal vein thrombus, the median survival after RT to treat the thrombus and/or the hepatic tumor with or without TACE ranged from 5.3 months to 9.7 months. Although outcomes after high-dose conformal RT for liver-confined HCC were excellent, the potential survival benefit of RT should be tested in randomized controlled trials that require international collaboration.
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PMID:Radiation therapy for hepatocellular carcinoma: from palliation to cure. 1654 31


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