Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Teniposide”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources
PubMedDate not supplied

The inhibitory effects of teniposide and homoharringtonine on the growth of pancreatic carcinoma cells in vitro.

The inhibitory effect of VM-26 and Homoharringtonine (HHT) on the in vitro growth of a human pancreatic cell line (MIA PaCa-2) was tested. The ID50 of VM-26 and HHT was 6 x 10(-7) M and 2 x 10(-5) M respectively. Increasing time exposure from 1 hr to continuous exposure for 5 days resulted in a 30-fold decrease in ID50 for VM-26 and a 2,000-fold decrease for HHT. 14C-labelled thymidine and leucine studies revealed that VM-26 inhibited DNA synthesis, while HHT inhibited both DNA and protein synthesis.

Alkaloids↗
PubMed1987

Atypical multiple drug resistance in a human leukemic cell line selected for resistance to teniposide (VM-26).

Resistance to the cytotoxic effects of many natural product drugs after exposure to a single agent is a common observation. The classes of drugs included in the "classic" multiple drug resistance phenotype are Vinca alkaloids, anthracyclines, epipodophyllotoxins, and antibiotics. We report here the characterization of a human leukemic cell line (CEM/VM-1) with "atypical" multiple drug resistance: despite resistance and cross-resistance to etoposide, anthracyclines, mitoxantrone, and 4'-[(9-acridinyl)amino]methanesulphon-m-anisidide (mAMSA), these cells retain sensitivity to the Vinca alkaloids. Further, even though this cell line is approximately equal to 40-fold cross-resistant to the cytotoxic effect of etoposide (VP-16), it is similar to drug-sensitive CEM cells in the cellular pharmacology of [3H]VP-16 as determined by zero time binding, initial influx rate, steady state drug concentration, and unidirectional efflux. Our studies suggest that the resistance of CEM/VM-1 cells to epipodophyllotoxins is due to an altered interaction between drug and its cellular target(s) by a mechanism unrelated to the decreased cellular concentration of drug associated with the "classic" multiple drug resistance phenotype.

Cell Line↗
PubMed1993

Dissociation between bulk damage to DNA and the antiproliferative activity of teniposide (VM-26) in the MCF-7 breast tumor cell line: evidence for induction of gene-specific damage and alterations in gene expression.

In the MCF-7 breast tumor cell line, induction of bulk damage to DNA (measured either as total strand breaks or as double-strand breaks) fails to correspond with the antiproliferative activity of the demethylepipodo-phyllotoxin derivative, VM-26. In contrast, VM-26 produces an early (within 2-3 h) concentration-dependent reduction in c-myc expression (and of DNA synthesis) which parallels inhibition of cell growth, suggesting the possibility of effects of VM-26 at the level of genomic regions which regulate DNA replicative function. Although VM-26 also produces a reduction in c-myc expression in K562 human leukemic cells, these alterations fail to correspond with the concentration-dependent effects on cell growth in this cell line. Utilizing the newly developed alkaline unwinding/Southern blotting assay in the MCF-7 breast tumor cell line, it was determined that VM-26 induces damage within regions surrounding the c-myc gene and the beta-globin gene which exceeds that induced in both alpha-satellite DNA and in L1 repeat sequences; damage within c-myc and beta-globin also exceeds that observed throughout the genome as a whole. These findings indicate that certain genomic regions incur preferential damage in MCF-7 cells exposed to VM-26. It appears possible that damage within such genomic regions could lead to alterations in expression of select genes associated with regulation of cellular proliferation, resulting in reduced DNA synthesis, compromised cell growth, and, ultimately, cell death.

Blotting, Southern↗