Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT01586 (G418)
 2,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The complete suppression of tumorigenicity of a human cervical cancer cell (HeLa) and a Wilms' tumor cell line (G401) following the introduction via microcell fusion of a single chromosome t(X;11) has been demonstrated by Stanbridge and co-workers. To determine whether other tumor cell lines are suppressed by chromosome 11, we performed chromosome transfer experiments via microcell fusion into various human tumor cell lines, including a uterine cervical carcinoma (SiHa), a rhabdomyosarcoma (A204), a uterine endometrial carcinoma (HHUA), a renal cell carcinoma (YCR-1), and a rat ENU-induced nephroblastoma (ENU-T1). We first isolated a mouse A9 cell containing a single human chromosome 11 with integrated pSV2-neo plasmid DNA. Following microcell fusion of the neo-marked chromosome 11 with the various tumors mentioned above, we isolated clones that were resistant to G418 and performed karyotypic analyses and chromosomal in situ hybridization to ensure the transfer of the marked chromosome. Whereas the parental cells of each cell line were highly tumorigenic, SiHa and A204 microcell hybrid clones at early passages were nontumorigenic in nude mice and HHUA was moderately tumorigenic. On the other hand, YCR-1 and ENU-T1 microcell hybrid clones were still highly tumorigenic following the introduction of chromosome 11. Thus, the introduction of a normal chromosome 11 suppresses the tumorigenicity of some but not all tumors, suggesting that the function of the putative suppressor gene(s) on chromosome 11 is effective only in specific tumors.
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PMID:Transfer of a normal human chromosome 11 suppresses tumorigenicity of some but not all tumor cell lines. 231 11

Two kinds of clones were isolated successfully from the HHUA 95 cells that were derived from a human well-differentiated adenocarcinoma of endometrium, with 6-thioguanine (6-TG) selection and transfection with plasmid containing the neo gene (pSV2 neo). One clone was resistant to the 6-TG (6-TGr 95) and the other to both the 6-TG and the G418 (6-TGr-neor 95). Karyotypes of these three kinds of cells were normal, even though random chromosome abnormalities were observed in some cells. Two types of cell fusion were performed: one consisted of the hybridization between 6-TGr 95 cells and normal human fibroblasts (HF), and the other, between 6-TGr-neor 95 and human choriocarcinoma cells (CC1). Tumorigenicity of both hybrid cell types was completely suppressed. Complementation for genetic lesions given by cell hybridization was assumed to be responsible for the suppression of tumorigenicity. These results suggest that genetic losses played an essential role in the evolution of the malignant phenotype of endometrial carcinoma cells. The data obtained from the endometrial carcinoma could not be used directly for the understanding of suppression mechanisms of choriocarcinoma.
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PMID:Isolation of clones resistant to 6-thioguanine and G418 from HHUA endometrial carcinoma cells and their application to cell hybridization. 239 65

Mouse spleen cells transfected with pSV2 neo by CaPO4 precipitation were fused with highly metastatic cell clone (PLA801-D95) from human large cell lung cancer cell line. Hybrid cell clone PMS-2 was obtained after G418(400/ml)selection. After injection of 7 x 10(6) PMS-2 cells into nude mice, there was a tumor nodule developed, but the metastatic foci could not be found while 3 x 10(6) PLA801-D95 cells would metastasize to lung and lymph nodes after they were injected into nude mice. It might indicate that sometime mouse spleen cells could not suppress tumor formation but the metastatic potential could be suppressed by the fusion of mouse spleen cells with the lung cancer cells. The results of growth curve, serum independence and incorporation rates of H-thymidine all showed that the growth rates of parental cells were higher than those of PMS-2. Our data suggest that suppression of tumorigenicity and metastatic potential could be controlled by different kinds of genes, and the cloning of metastasis suppressor gene by subtractive hybridization is ongoing in our laboratory.
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PMID:[A primary observation on the effect of cell fusion on metastatic potential of tumor cells]. 870 58