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

The antitumor activity of recombinant human tumor necrosis factor (rTNF-alpha) was examined on murine tumors in mice and in cultured cells in vitro. Mice were implanted intradermally with Meth A fibrosarcoma (Meth A) on day 0. rTNF-alpha caused tumor necrosis and inhibited the tumor growth when given i.v. on day 7 or 10, but not when given on day 3. When rTNF-alpha was given i.v. in doses of 0.1-3.2 micrograms/mouse twice a week for 3 weeks beginning on day 7 or 11, the growth of solid Meth A, Colon 26 adenocarcinoma, Colon 38 carcinoma, Sarcoma-180, and M5076 reticulum cell sarcoma tumors implanted s.c. or intradermally was markedly inhibited, and the life of the mice bearing these tumors, except M5076 reticulum cell sarcoma, was prolonged. The growth of Meth A implanted i.m. was also markedly inhibited by rTNF-alpha given i.v. However, the life of mice bearing i.p. Colon 26 adenocarcinoma, MH134 hepatoma, Sarcoma-180, and Ehrlich carcinoma was not prolonged by rTNF-alpha given i.p. nine times (days 1-9) in doses up to 1.0 or 3.2 micrograms/mouse. Only in the case of mice bearing i.p. Meth A, the life was slightly prolonged by i.p. treatment with rTNF-alpha but not by i.v. treatment. In experiments against in vitro cultured cells, rTNF-alpha did not show any direct cytotoxicity against mouse tumor cells: Meth A, Colon 26 adenocarcinoma, Colon 38 carcinoma, and Sarcoma-180, but had a cytotoxic effect against L929 mouse fibroblast. The results suggest that rTNF-alpha is a unique antitumor drug with potent necrotizing activity against solid tumors in mice, and that this activity may derive from indirect mechanisms related to the growth of tumors and not to the direct cytotoxicity of the drug.
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PMID:Recombinant human tumor necrosis factor-alpha: evidence of an indirect mode of antitumor activity. 359 35

The 1H NMR spin-lattice relaxation time (T1), spin-spin relaxation time (T2), and spin-lattice relaxation time in the rotating frame (T1rho) were determined for Novikoff hepatoma, Walker-256 Carcinosarcoma, Sarcoma-180 and Ehrlich Ascites tumor as well as for 7 normal tissues in the rat at 2.18 MHz. T1 values yielded improved discrimination of normal and malignant tissue compared to previous results at higher frequencies.
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PMID:Improved discrimination of normal and malignant tissue using 1H NMR relaxation time measurements at 2.18 MHz. 654 47

The spin-labeled derivative of podophyllotoxin, N'-podophyllic acid-N-[3-(2,2,5,5-tetramethyl pyrrolinenyloxy)] semicarbazide (GP-11), was synthesized and tested for its antitumor activity against mouse transplantable tumors, Sarcoma-180, Hepatoma-A, P388 leukemia and Ehrlich ascites carcinoma. At an equitoxic dose, the antitumor activity of GP-11 was similar to that of etoposide (VP-16). However, the immunosuppressive effects of GP-11 were weaker than that of VP-16. In vitro, GP-11 and VP-16 inhibited the proliferation of human lymphoid leukemia Molt 4B cells and suppressed DNA and protein syntheses, but the effect of GP-11 and VP-16 on cell cycle progression was different. The mitotic index was increased by GP-11 and reduced by VP-16. On the basis of flow cytometric bromodeoxyuridine (BrdU)/DNA analysis, GP-11 and VP-16 resulted in the accumulation of cells in the S and G2/M phases. G2/M arrest by GP-11 on cell cycle progression was stronger than that of VP-16, while S arrest was weaker than that of VP-16. After the removal of drugs, the arrest by GP-11 and VP-16 still existed and was irreversible. These results may provide insights into the structure-activity relationships and the design of novel derivatives of podophyllotoxin useful in cancer chemotherapy.
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PMID:Antitumor activity of a new low immunosuppressive derivative of podophyllotoxin (GP-11) and its mechanisms. 851 13

Chitosan nanoparticles have been synthesized as potential anticancer agents, and evaluated, in vitro, against various cancer cell lines. In this study, in vivo antitumor activity of chitosan nanoparticles against Sarcoma-180 and mouse hepatoma H22 was investigated. Chitosan nanoparticles showed significant antitumor activity in vivo. The doses and particle size made a great effect on their efficacy.
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PMID:In vivo antitumor activity of chitosan nanoparticles. 1675 59

Primary malignant neoplasms of the liver are some of the most uncommon malignancies in many parts of the world. They include hepatocellular carcinoma and stromal tumors such as hepatic angiosarcoma. It is a lethal tumor with life expectancy of less than six months. Once discovered, it is often too late for surgical intervention. Like other vascular tumors of the liver and spleen, intraperitoneal hemorrhage is a well-documented finding of angiosarcoma which can be lethal if not diagnosed and treated immediately. As in our case, intraperitoneal hemorrhage from primary tumor rupture was the only clinical presentation of this neoplasm. Approximately 15% of patients present with acute hemoperitoneum from either tumor rupture or peritoneal metastasis. Although several therapeutic options are available, we describe apalliative therapy for hepatic angiosarcoma utilizing transcatheter arterial chemoembolization (TACE) techniques incorporating the newer embolization agent Embospheres to locally target and treat this aggressive tumor.
Sarcoma 2007
PMID:Hepatic angiosarcoma presenting as an acute intraabdominal hemorrhage treated with transarterial chemoembolization. 1828 42

Hepatocellular carcinoma (HCC) is the most common primary cancer of the liver with high mortality and frequent recurrence. Although various therapies provide potential cure for HCC patients, unfortunately the five-year survival rate of advanced HCC remains dismal. It is critical to explore the pathogenesis of HCC and identify novel biomarkers for early HCC diagnosis. PSMD4 is a major receptor of the 26S proteasome involved in ubiquitindependent and proteasome-mediated protein degradation. In our study, PSMD4 was overexpressed in HCC tissues and cell lines determined by Northern blot, western blot and immunohistochemistry. The silencing of PSMD4 blocked cell proliferation and tumor growth, induced cell apoptosis and inhibited the proteasome activity. Western blot results showed that the knockdown of PSMD4 blocked the expression of cyclooxygenase 2 (COX2), phosphorylated Sarcoma tyrosine kinase (P-SRC) and Bcl-2, but improved the levels of p53 and Bax in HCC, lung cancer, colorectal cancer, breast cancer and endometrial cancer cell lines. Taken together, these findings indicated that the subunit of 26S proteasome PSMD4 exerts as an oncogene in HCC and other cancers via regulating the expression p53, Bcl-2 and Bax. These findings enriched the pathogenesis of HCC, and provided a new biomarker for cancers diagnosis and a new target for cancers therapy.
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PMID:Inhibition of PSMD4 blocks the tumorigenesis of hepatocellular carcinoma. 3093 Feb 24

Non-coding RNAs occupy a significant fraction of the human genome. Their biological significance is backed up by a plethora of emerging evidence. One of the most robust approaches to demonstrate non-coding RNA's biological relevance is through their prognostic value. Using the rich gene expression data from The Cancer Genome Altas (TCGA), we designed Advanced Expression Survival Analysis (AESA), a web tool which provides several novel survival analysis approaches not offered by previous tools. In addition to the common single-gene approach, AESA computes the gene expression composite score of a set of genes for survival analysis and utilizes permutation test or cross-validation to assess the significance of log-rank statistic and the degree of over-fitting. AESA offers survival feature selection with post-selection inference and utilizes expanded TCGA clinical data including overall, disease-specific, disease-free, and progression-free survival information. Users can analyse either protein-coding or non-coding regions of the transcriptome. We demonstrated the effectiveness of AESA using several empirical examples. Our analyses showed that non-coding RNAs perform as well as messenger RNAs in predicting survival of cancer patients. These results reinforce the potential prognostic value of non-coding RNAs. AESA is developed as a module in the freely accessible analysis suite MutEx. Abbreviation: ACC: Adrenocortical Carcinoma (n = 92); BLCA: Bladder Urothelial Carcinoma (n = 412); BRCA: Breast Invasive Carcinoma (n = 1098); CESC: Cervical Squamous Cell Carcinoma and Endocervical Adenocarcinoma (n = 307); CHOL: Cholangiocarcinoma (n = 51); COAD: Colon Adenocarcinoma (n = 461); DLBC: Lymphoid Neoplasm Diffuse Large B-cell Lymphoma (n = 58); ESCA: Oesophageal Carcinoma (n = 185); GBM: Glioblastoma Multiforme (n = 617); HNSC: Head and Neck Squamous Cell Carcinoma (n = 528); KICH: Kidney Chromophobe (n = 113); KIRC: Kidney Renal Clear Cell Carcinoma (n = 537); KIRP: Kidney Renal Papillary Cell Carcinoma (n = 291); LAML: Acute Myeloid Leukaemia (n = 200); LGG: Brain Lower Grade Glioma (n = 516); LIHC: Liver Hepatocellular Carcinoma (n = 377); LUAD: Lung Adenocarcinoma (n = 585); LUSC: Lung Squamous Cell Carcinoma (n = 504); MESO: Mesothelioma (n = 87); OV: Ovarian Serous Cystadenocarcinoma (n = 608) PAAD: Pancreatic Adenocarcinoma (n = 185); PCPG: Pheochromocytoma and Paraganglioma (n = 179); PRAD: Prostate Adenocarcinoma (n = 500); READ: Rectum Adenocarcinoma (n = 172); SARC: Sarcoma (n = 261); SKCM: Skin Cutaneous Melanoma (n = 470); STAD: Stomach Adenocarcinoma (n = 443); TGCT: Testicular Germ Cell Tumours (n = 150); THCA: Thyroid Carcinoma (n = 507) THYM: Thymoma (n = 124); UCEC: Uterine Corpus Endometrial Carcinoma (n = 560); UCS: Uterine Carcinosarcoma (n = 57); UVM: Uveal Melanoma (n = 80).
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PMID:Advancing Pan-cancer Gene Expression Survial Analysis by Inclusion of Non-coding RNA. 3160 16