Abrogation of etoposide-mediated cytotoxicity by cycloheximide

Chow, Kuan‐Chih; King, Charles K.; Ross, Warren E.

doi:10.1016/0006-2952(88)90519-9

Cited by 27 publications

(1 citation statement)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The present results suggest a more complicated description of ErbB4, coupling extracellular signals for tissue growth and metabolism under favorable conditions, and DNA repair, cell-cycle arrest and/or suppression of growth under conditions of cellular or tissue stress. For example, recent studies suggest potential roles of p21WAF1/CIP1 that are independent of its function in cell cycle regulation [40], including actin cytoskeleton organization [41; 42; 43]. Thus ErbB4 dependent p53 activity may serve to regulate myocyte cytoarchitecture and/or growth via regulation of this and/or other pathways.…”

Section: Discussionmentioning

confidence: 99%

ErbB4 localization to cardiac myocyte nuclei, and its role in myocyte DNA damage response

Icli

Bharti

Pentassuglia

et al. 2012

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

The intracellular domain of ErbB4 receptor tyrosine kinase is known to translocate to the nucleus of cells where it can regulate p53 transcriptional activity. The purpose of this study was to examine whether ErbB4 can localize to the nucleus of adult rat ventricular myocytes (ARVM), and regulate p53 in these cells. We demonstrate that ErbB4 does locate to the nucleus of cardiac myocytes as a full-length protein, although nuclear location occurs as a full-length protein that does not require Protein Kinase C or γ-secretase activity. Consistent with this we found that only the non-cleavable JM-b isoform of ErbB4 is expressed in ARVM. Doxorubicin was used to examine ErbB4 role in regulation of a DNA damage response in ARVM. Doxorubicin induced p53 and p21 was suppressed by treatment with AG1478, an EGFR and ErbB4 kinase inhibitor, or suppression of ErbB4 expression with small interfering RNA. Thus ErbB4 localizes to the nucleus as a full-length protein, and plays a role in the DNA damage response induced by doxorubicin in cardiac myocytes.

show abstract

Section: Discussionmentioning

confidence: 99%

ErbB4 localization to cardiac myocyte nuclei, and its role in myocyte DNA damage response

Icli

Bharti

Pentassuglia

et al. 2012

Biochemical and Biophysical Research Communications

View full text Add to dashboard Cite

show abstract

Pre‐treatment of a human T‐lymphoblastoid cell line with L‐asparaginase reduces etoposide‐induced DNA strand breakage and cytotoxicity

Shimizu

Kubota

Adachi

et al. 1992

Intl Journal of Cancer

View full text Add to dashboard Cite

The effect of L-asparaginase (L-asp) pre-treatment on etoposide-induced DNA strand breakage and cytotoxicity was investigated. In a T-lymphoblastoid cell line, Molt 4, etoposide-induced DNA strand breaks, DNA-protein cross-links and cytotoxicity were reduced by pre-treatment with L-asp for 15 hr, but it did not cause these changes in a promyelocytic-leukemia cell line, HL-60, which is less sensitive than Molt 4 to L-asp. However, pre-treatment of Molt 4 cells with L-asp did not significantly alter the accumulation of [3H]-etoposide. Cell-cycle analyses showed an increase in G1-phase cells, a significant decrease in both S-phase cells and G2/M-phase cells pre-treated with L-asp in Molt 4 cells, but L-asp exposure did not result in any significant changes in HL-60 cells. On the other hand, L-asp pre-treatment did not affect topoisomerase-I (Topo-I) inhibitor, camptothecin (CPT)-induced DNA strand breaks or toxicity in Molt 4 cells. Our data imply that a decrease in S- and G2/M-phase cells following L-asp treatment may explain the reduction of etoposide-induced DNA lesions and cytotoxicity in Molt 4 cells, since topoisomerase-II (Topo-II) content or activity is a function of cellular proliferation status.

show abstract

Therapy‐related acute myeloid leukemia following treatment with epipodophyllotoxins: Estimating the risks

Smith

Rubinstein

Ungerleider

1994

Med. Pediatr. Oncol.

165

102

View full text Add to dashboard Cite

In the past decade, therapy-related acute myeloid leukemia (t-AML) following treatment with regimens that include inhibitors of topoisomerase-II (TOPO-II) has been reported with increasing frequency. These cases of t-AML generally have a shorter latency period than t-AML following alkylator therapy, are associated with chromosomal translocations (especially involving chromosome band 11q23), and usually present as M4 or M5 FAB subtype. Although the epipodophyllotoxins (etoposide and teniposide) have been most often implicated, similar cases of t-AML occur following therapy with other classes of Topo-II inhibitors (e.g., anthracyclines). There is wide variation in published studies in the estimates of risk of t-AML following epipodophyllotoxin therapy. These varying estimates may reflect a number of factors, including: small sample size leading to large confidence intervals around risk estimates; varying susceptibility of different patient populations; varying schedules of epipodophyllotoxin administration; different cumulative doses of epipodophyllotoxins; and administration of epopodophyllotoxins with additional agents that may alter the leukemogenic effect of the epipodophyllotoxins. Available data suggest that children with acute lymphocytic leukemia (ALL) treated with high cumulative doses of epipodophyllotoxins using either weekly or twice-weekly schedules of administration have a relatively high risk of developing t-AML (5-12% cumulative risk). On the other hand, germ cell patients treated with relatively low cumulative doses of etoposide (usually 1,500-2,500 mg/m2) appear to have a low risk for developing t-AML. There is inadequate experience at this time with higher cumulative doses of etoposide (e.g., 4,000-5,000 mg/m2 as used for pediatric solid tumors) given on a daily x 5 schedule to allow estimates of risk to be developed for this schedule and cumulative dose. The Cancer Therapy Evaluation Program (CTEP) of the National Cancer Institute (NCI) has developed a monitoring plan designed to obtain reliable estimates of the risk of t-AML following epipodophyllotoxin treatment. Twelve Cooperative Group clinical trials that use epipodophyllotoxins at either low (< 1,500 mg/m2), moderate (1,500-3,999 mg/m2), or higher cumulative doses (> 4,000 mg/m2) are being prospectively monitored for cases of t-AML occurring among patients entered onto the trials.

show abstract

Abrogation of etoposide-mediated cytotoxicity by cycloheximide

Cited by 27 publications

References 19 publications

ErbB4 localization to cardiac myocyte nuclei, and its role in myocyte DNA damage response

ErbB4 localization to cardiac myocyte nuclei, and its role in myocyte DNA damage response

Pre‐treatment of a human T‐lymphoblastoid cell line with L‐asparaginase reduces etoposide‐induced DNA strand breakage and cytotoxicity

Therapy‐related acute myeloid leukemia following treatment with epipodophyllotoxins: Estimating the risks

Contact Info

Product

Resources

About