Disease relevance of NCI60_000547

• Estradiol decreased sensitivity to ADM, MMC, and TXL in MCF-7 and MDA-MB-231 breast cancer cells, and this was associated in part with an increase in the amount of Bcl-2 protein, and decreases in levels of Bax and cytochrome c leading to apoptosis [1].
• CONCLUSION: We suggest that interactions between NO and apoptosis are important in the pathogenesis of the ADR-induced nephrosis [2].
• On the contrary, only ADM and MMC induced chromosomal aberrations in mouse spermatogonia [3].
• On the other hand, body weight was significantly smaller in group ADR-H than in group ADR in more than half of the observation period [4].
• TYK-R10 is a cisplatin resistant human ovarian carcinoma cell line and showed a cross resistance to various anti-cancer drugs including adriamycin (ADR), vincristine (VCR) and etoposide, despite a lack of multidrug phenotype [5].

High impact information on NCI60_000547

• The effect on cultured cells suggested that KW2152 was not cross-resistant to Adriamycin (ADM) but was cross-resistant to mitomycin C (MMC); however, KW2152 caused prolongation of life span against mice bearing P388/ADM or P388/MMC [6].
• It was previously shown that a decreased uptake accounts for the cross-resistance of these cells to AD and ADM which then suggested that the 9-OH-E-resistant cells might display some of the properties usually associated with the multidrug resistance phenotype [7].
• 9-OH-Ellipticine (9-OH-E)-resistant cells are not only resistant to the DNA topoisomerase II inhibitors, but also to some other antitumor agents, such as actinomycin D (AD), adriamycin (ADM), daunorubicin and vincristine [7].
• The correlations of the chemosensitivity results were 73.9% for ADM, 73.9% for MMC, 82.6% for DDP and 60.9% for 5-FU [8].
• However, the percentages of apoptotic cells were 5.6% (medium alone), 75.9% (CDDP), 20.0% (CPM), 22.2% (ADM), 20.5% (VCR) and 13.1% (MTX) [9].

Chemical compound and disease context of NCI60_000547

• Genistein enhanced cytotoxic effect of ADR at low doses less than IC50 against the human breast cancer cell [10].

Biological context of NCI60_000547

• Estradiol in MDA-MB-231 cells similarly increased the IC50 values for ADM (9.5-fold), MMC (15.6-fold), and TXL (2.4-fold) [1].
• The results obtained indicate that ADM, CH and EDTA are able to induce micronuclei at meiosis [3].
• The upregulation of iNOS gene and protein may be somehow correlated with morphological changes seen in heart of rat treated with ADR [11].
• In rabbits with VX2 tumor in the liver we compared plasmatic and cellular pharmacokinetics of ADM and THP after i.v. and IAH therapy [12].
• These results suggest that genistein enhances necrotic-like cell death of the breast cancer cells through the inactivation of HER-2 receptor and Akt in combination with ADR [10].

Anatomical context of NCI60_000547

• In a clonogenic assay it was observed that TAM (1-10 microM) significantly enhanced the activity of MXN in the MCF-7/ADR but not in the drug-sensitive cell line [13].
• Myocardium exhibited intensive morphological changes after 8 weeks of ADR treatment [11].

Associations of NCI60_000547 with other chemical compounds

• The effect of mitomycin C (MMC), adriamycin (ADM), cyclophosphamide (CTX), cisplatinum (cis-DDP) and bleomycin (BLM) on the aerobic and hypoxic cells of a C3H mammary carcinoma in CDF1 mice was investigated using the tumor control assay [14].
• Serum creatinine and blood urea nitrogen were significantly lower in either group ADR-H or ADR-M than in group ADR at week 34 [4].
• The triplet states of adriamycin (Ad), daunomycin (D) and two daunomycin analogues, daunomycinone (Dc) and daunomycin N-trifluoroacetamide (DAc), have been studied using laser flash photolysis and pulse radiolysis techniques [15].
• The MD-mediated NADPH oxidation was inhibited in the presence of NAD(P)H:quinone oxidoreductase (QR), but Mit C- and Adr-mediated NADPH oxidations were not [16].

Gene context of NCI60_000547

• MMC, ADM and CTX had a significant enhancing effect on the unclamped TCD50 [14].
• For ADM, there were no differences in plasma and heart concentrations, with only a slight increase in tumoral levels after IAH compared to i.v. administration; on the other hand, with IAH THP, there was important reduction in systemic exposure with a major increase in tumoral drug distribution [12].

Analytical, diagnostic and therapeutic context of NCI60_000547

• Rats were stratified into control groups and ADR-induced nephropathy groups [2].
• Intra-arterial hepatic chemotherapy (IAHC) with adriamycin (ADM) has not increased its therapeutic index [12].

References