suramin has been researched along with Cell Transformation, Neoplastic in 21 studies
Suramin: A polyanionic compound with an unknown mechanism of action. It is used parenterally in the treatment of African trypanosomiasis and it has been used clinically with diethylcarbamazine to kill the adult Onchocerca. (From AMA Drug Evaluations Annual, 1992, p1643) It has also been shown to have potent antineoplastic properties.
suramin : A member of the class of phenylureas that is urea in which each of the amino groups has been substituted by a 3-({2-methyl-5-[(4,6,8-trisulfo-1-naphthyl)carbamoyl]phenyl}carbamoyl)phenyl group. An activator of both the rabbit skeletal muscle RyR1 and sheep cardiac RyR2 isoform ryanodine receptor channels, it has been used for the treatment of human African trypanosomiasis for over 100 years.
Cell Transformation, Neoplastic: Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.
Excerpt | Relevance | Reference |
---|---|---|
"Treatment with suramin, a polyanionic compound that disrupts ligand/receptor interactions at the cell surface, was able to revert the transformed phenotype induced by the mutant sis-E1 constructs described here." | 1.29 | The v-sis oncoprotein loses transforming activity when targeted to the early Golgi complex. ( Donoghue, DJ; Hart, KC; Lee, BA; Meyer, AN; Xu, YF, 1994) |
"Suramin is an anti-helminthic drug that has been shown to antagonize the effects of a variety of growth factors including EGF, PDGF and TGF beta." | 1.28 | [Suramin inhibits the proliferation and stimulates the differentiation of tumoral cell lines HT29-D4 and C6]. ( Baghdiguian, S; Fantini, J; Marvaldi, J; Pichon, J, 1991) |
"Suramin treatment resulted in a marked reduction in tyrosine phosphorylated cell surface PDGF receptors but had no effect on the level of tyrosine phosphorylation of intracellular receptor species." | 1.28 | Autocrine mechanism for v-sis transformation requires cell surface localization of internally activated growth factor receptors. ( Aaronson, SA; Fleming, TP; Matsui, T; Molloy, CJ; Robbins, KC, 1989) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 5 (23.81) | 18.7374 |
1990's | 14 (66.67) | 18.2507 |
2000's | 2 (9.52) | 29.6817 |
2010's | 0 (0.00) | 24.3611 |
2020's | 0 (0.00) | 2.80 |
Authors | Studies |
---|---|
Radhika, V | 1 |
Hee Ha, J | 1 |
Jayaraman, M | 1 |
Tsim, ST | 1 |
Dhanasekaran, N | 1 |
Hart, KC | 1 |
Xu, YF | 1 |
Meyer, AN | 1 |
Lee, BA | 2 |
Donoghue, DJ | 2 |
Yang, D | 1 |
Kohler, SK | 1 |
Maher, VM | 1 |
McCormick, JJ | 1 |
Arnold, HH | 1 |
Salminen, A | 1 |
Chan, AM | 1 |
Fleming, TP | 2 |
McGovern, ES | 1 |
Chedid, M | 1 |
Miki, T | 1 |
Aaronson, SA | 2 |
Huang, SS | 2 |
Koh, HA | 1 |
Huang, JS | 2 |
Myers, CE | 1 |
Rosenmüller, T | 1 |
Rydh, K | 1 |
Nånberg, E | 1 |
Baghdiguian, S | 3 |
Boudier, JA | 1 |
Verrier, B | 1 |
Zappitelli, JP | 1 |
Fantini, J | 4 |
Fuller-Pace, F | 1 |
Peters, G | 1 |
Dickson, C | 1 |
Pichon, J | 1 |
Marvaldi, J | 2 |
Myers, C | 1 |
Rognoni, JB | 1 |
Theveniau, M | 1 |
Pommier, G | 1 |
Yayon, A | 1 |
Klagsbrun, M | 1 |
De Clercq, E | 1 |
Balzarini, J | 1 |
Buchou, T | 1 |
Charollais, RH | 1 |
Fagot, D | 1 |
Mester, J | 1 |
Moscatelli, D | 1 |
Quarto, N | 1 |
Matsui, T | 1 |
Molloy, CJ | 1 |
Robbins, KC | 1 |
Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
Observational Study on the Carcinogenesis of Gα12 in Oral Cancer, and Chemopreventive Possibility for the Treatment of Oral Cancer Using Ga12 Inhibitor.[NCT01919580] | 255 participants (Anticipated) | Observational | 2012-12-31 | Recruiting | |||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |
2 reviews available for suramin and Cell Transformation, Neoplastic
Article | Year |
---|---|
Differentiating agents and nontoxic therapies.
Topics: Antineoplastic Agents; Cell Transformation, Neoplastic; Fatty Acids; Humans; Male; Phenylacetates; P | 1999 |
Peptide growth factors: the parallel between fetal development and malignant transformation.
Topics: Antibodies, Monoclonal; Cell Transformation, Neoplastic; Embryonic and Fetal Development; Fibroblast | 1991 |
19 other studies available for suramin and Cell Transformation, Neoplastic
Article | Year |
---|---|
Mitogenic signaling by lysophosphatidic acid (LPA) involves Galpha12.
Topics: 3T3 Cells; Animals; Cell Proliferation; Cell Transformation, Neoplastic; Enzyme Activation; GTP-Bind | 2005 |
The v-sis oncoprotein loses transforming activity when targeted to the early Golgi complex.
Topics: 3T3 Cells; Amino Acid Sequence; Animals; Base Sequence; Biological Transport; Biomarkers; Cell Compa | 1994 |
v-sis oncogene-induced transformation of human fibroblasts into cells capable of forming benign tumors.
Topics: Animals; Base Sequence; Cell Adhesion; Cell Division; Cell Transformation, Neoplastic; Down-Regulati | 1994 |
Differentiation of BA-HAN-1C rhabdomyosarcoma cells is controlled by a pertussis toxin sensitive signaling pathway.
Topics: Adenosine Diphosphate; Animals; Cell Differentiation; Cell Transformation, Neoplastic; Cyclic AMP; F | 1993 |
Expression cDNA cloning of a transforming gene encoding the wild-type G alpha 12 gene product.
Topics: 3T3 Cells; Amino Acid Sequence; Animals; Blotting, Northern; Cell Transformation, Neoplastic; Clonin | 1993 |
Suramin enters and accumulates in low pH intracellular compartments of v-sis-transformed NIH 3T3 cells.
Topics: 3T3 Cells; Acridine Orange; Animals; Cell Line; Cell Line, Transformed; Cell Transformation, Neoplas | 1997 |
Role of phosphoinositide 3OH-kinase in autocrine transformation by PDGF-BB.
Topics: Animals; Autocrine Communication; Becaplermin; Cell Line; Cell Movement; Cell Surface Extensions; Ce | 2001 |
Intracellular retention of membrane-anchored v-sis protein abrogates autocrine signal transduction.
Topics: 3T3 Cells; Amino Acid Sequence; Animals; Base Sequence; Cell Membrane; Cell Transformation, Neoplast | 1992 |
[Suramin induces lysosomal storage disorder in HT29-D4 cells during a mechanism of polarized endocytosis].
Topics: Adenocarcinoma; Cell Line, Transformed; Cell Transformation, Neoplastic; Clone Cells; Colonic Neopla | 1992 |
Cell transformation by kFGF requires secretion but not glycosylation.
Topics: Animals; Asparagine; Base Sequence; Cell Line; Cell Transformation, Neoplastic; DNA Replication; Ele | 1991 |
[Suramin inhibits the proliferation and stimulates the differentiation of tumoral cell lines HT29-D4 and C6].
Topics: Adenocarcinoma; Animals; Cell Division; Cell Line, Transformed; Cell Transformation, Neoplastic; Col | 1991 |
[The in vitro differentiation of cancer cells of the human colon (HT29-D4) is associated with the presence of annulate lamellae in the basal part of the cytoplasm].
Topics: Cell Transformation, Neoplastic; Colonic Neoplasms; Cytoplasm; Epithelium; Humans; In Vitro Techniqu | 1990 |
Impaired carcinoembryonic antigen release during the process of suramin-induced differentiation of the human colonic adenocarcinoma cell clone HT29-D4.
Topics: Adenocarcinoma; Carcinoembryonic Antigen; Cell Membrane; Cell Transformation, Neoplastic; Colonic Ne | 1990 |
Autocrine transformation by chimeric signal peptide-basic fibroblast growth factor: reversal by suramin.
Topics: Animals; Cell Adhesion; Cell Division; Cell Transformation, Neoplastic; Cells, Cultured; Chimera; Fi | 1990 |
In search of specific inhibitors of retrovirus replication.
Topics: Acquired Immunodeficiency Syndrome; Amidines; Animals; Antiviral Agents; Cell Transformation, Neopla | 1985 |
Mitogenic activity of phorbol esters and insulin-like growth factor 1 in chemically transformed mouse fibroblasts BP-A31: independent effects and differential sensitivity to inhibition by 3-isobutyl-1-methyl xanthine.
Topics: 1-Methyl-3-isobutylxanthine; Animals; Blotting, Northern; Cell Division; Cell Transformation, Neopla | 1989 |
Transformation of NIH 3T3 cells with basic fibroblast growth factor or the hst/K-fgf oncogene causes downregulation of the fibroblast growth factor receptor: reversal of morphological transformation and restoration of receptor number by suramin.
Topics: Animals; Cell Transformation, Neoplastic; Cells, Cultured; DNA; Down-Regulation; Fibroblast Growth F | 1989 |
Autocrine mechanism for v-sis transformation requires cell surface localization of internally activated growth factor receptors.
Topics: Animals; Cell Division; Cell Transformation, Neoplastic; Cells, Cultured; DNA Replication; Kinetics; | 1989 |
Rapid turnover of the platelet-derived growth factor receptor in sis-transformed cells and reversal by suramin. Implications for the mechanism of autocrine transformation.
Topics: Cell Line, Transformed; Cell Membrane; Cell Transformation, Neoplastic; Hexosaminidases; Humans; Imm | 1988 |