tretinoin has been researched along with Neuroectodermal-Tumors* in 3 studies
3 other study(ies) available for tretinoin and Neuroectodermal-Tumors
Article | Year |
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Treatment of therapy related acute promyelocytic leukemia with the combination of all trans retinoic acid and arsenic trioxide without chemotherapy: a series of three patients.
Topics: Adult; Antineoplastic Combined Chemotherapy Protocols; Arsenic Trioxide; Arsenicals; Choriocarcinoma; Female; Humans; Kidney Neoplasms; Leukemia, Promyelocytic, Acute; Male; Middle Aged; Neuroectodermal Tumors; Ovarian Neoplasms; Oxides; Prognosis; Tretinoin | 2010 |
A possible growth factor role of IL-6 in neuroectodermal tumours.
Preliminary data have shown that IL-6 may act as an autocrine growth factor to control proliferation. We further characterised the role of IL-6 in tumour growth as an autocrine/paracrine growth factor in neuroectodermal tumours. We evaluated the production and secretion of IL-6 by seven human melanoma, five neuroblastoma and one glioblastoma cell lines. Moreover, we determined their IL-6-dependent growth in serum free-medium or under minimal growth-supplement conditions: IL-6 dependent growth was observed in two non-IL-6 producing melanoma and in one neuroblastoma cell lines. In addition, expression of IL-6 mRNA and peptide was increased by retinoic acid. The data support the hypothesis that IL-6 contributes to neuroectodermal tumour growth, even though it shows a less potent effect than other reported growth factor such as IGF-II. Topics: Antineoplastic Agents; Blotting, Northern; Cell Division; Culture Media, Serum-Free; Gene Expression Regulation, Neoplastic; Glioblastoma; Growth Substances; Humans; Interleukin-6; Melanoma; Neuroblastoma; Neuroectodermal Tumors; Radioimmunoassay; RNA, Messenger; Tretinoin; Tumor Cells, Cultured | 1997 |
Neuroectodermal tumors expressing c-, L-, and N-myc in transgenic mice that carry the E1A/E1B gene of human adenovirus type 12.
Adenovirus early 1 (E1) region gene products, including E1A and E1B, are required for transformation of primary cultured rodent cells. In order to investigate in vivo action of the E1 region, we established a line of transgenic mice carrying the oncogenic E1A and E1B genes of human adenovirus type 12 under control of the human angiotensinogen promoter. Histopathological analyses indicated that transgenic mice heritably develop neuroectodermal tumors arising from the pelvic region with varying degrees of incidence. The transgene was expressed in the neuroectodermal tumors as well as in TNT-1 cells, a cell line established from the tumors, where the human angiotensinogen promoter was constitutively active. The high level expression of c-, L-, and N-myc without gene amplification was notable in the original tumors and TNT-1 cells, but not in another tissue examined. The co-expression of the three sets of myc family genes in both the original tumors and the established cell line provided the possibility that the target cells for transformation may belong to a specific cell type that expresses all these oncogenes during development. Topics: 3T3 Cells; Adenovirus E1A Proteins; Adenovirus E1B Proteins; Adenoviruses, Human; Angiotensinogen; Animals; Base Sequence; Cell Adhesion Molecules, Neuronal; Cell Division; Cells, Cultured; DNA Primers; Female; Gene Expression Regulation; Genes, myc; Male; Mice; Mice, Transgenic; Molecular Sequence Data; Neuroectodermal Tumors; Pedigree; Promoter Regions, Genetic; Tretinoin | 1994 |