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Chemical Compound Review

AC1L9HAR     1-[(2R,4S)-4-[(2S,4S,5S,6S)- 4-amino-5...

Synonyms: 1i1e
 
 
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Disease relevance of Adriamycin

  • ADM was more effective than was THP-ADM against colon adenocarcinoma 26 [1].
  • Cytofluorographic analysis of cellular ADR content and labeling studies with [3H]daunomycin demonstrated that hemin decreases the intracellular accumulation of these anthracyclines by more than 50% in K562 erythroleukemia cells [2].
  • THP-ADM administered i.p. five times, every other day starting from Day 1, was more effective than ADM was against Lewis lung carcinoma, B16 melanoma, and colon adenocarcinoma 38 inoculated s.c. In the study with Lewis lung carcinoma, metastasis to the lungs was well suppressed by THP-ADM [1].
  • When mice with P388 leukemia were given i.p. injections of THP-ADM or ADM daily for 9 consecutive days, the maximum increases in life span (ILSs) of the mice were 190 and 175%, respectively [1].
  • Hemin did protect human neuroblastoma IMP-32 cells from ADR cytotoxicity; however, this nonhemopoietic cell line undergoes dendrite formation in response to hemin induction [2].
 

High impact information on Adriamycin

 

Chemical compound and disease context of Adriamycin

 

Biological context of Adriamycin

 

Anatomical context of Adriamycin

  • While MA and ADR produced DNA strand breaks in HT-29 cells, this damage was not observed with CMA and ICMA [16].
  • Agents known to increase the permeability of the plasma membrane did not alter ADR accumulation or its efflux in HCT-8 cells unless these same agents were also capable of interacting with the lysosome [17].
  • Because THP-ADM was more cytotoxic than or almost equally as cytotoxic as ADM against the established cell lines from the above mouse tumors, we suggest that THP-ADM is more efficiently transported into cultured cells [1].
  • However, incubation of isolated nuclei in ADR (1 microgram/ml) showed that bone marrow and heart nuclei had greater amounts of ADR fluorescence (2- to 3-fold) than did spleen or liver nuclei similarly treated [18].
  • [3H]VCR bound to the plasma membrane prepared from K562/ADM cells, but not from parental K562 cells, depending on the concentrations of ATP and Mg2+ [7].
 

Associations of Adriamycin with other chemical compounds

 

Gene context of Adriamycin

  • However, SF did not cause significant changes in the cell cycle distribution of ADR-treated cells [20].
  • In PAN and ADR nephropathy, the phosphorylation of p38 MAPK and ERK was marked but transient, preceding overt proteinuria [21].
  • Different resistance mechanisms emerge sequentially as cells become more resistant to ADR; the mechanisms are retained during the development of multidrug resistance (MDR) [22].
  • In addition, the two cell lines displaying the pure classical MDR phenotype, linked exclusively to the P-glycoprotein (P-gp) overexpression (P388/VCR-20 and S1/tMDR), were as sensitive to S16020-2 as their sensitive parental counterparts, although they were resistant to ADR [23].
  • After ADR treatment, high molecular weight (Mr hyperphosphorylated) BRCA1 decreased more rapidly than the low Mr species [24].
 

Analytical, diagnostic and therapeutic context of Adriamycin

  • Further, acetylated p53 (Lys382) was found in chemically cross-linked complexes at all promoter sites examined after treatment of cells with ADR [25].
  • Northern blot analysis indicates that this defect in AdrR MCF-7 cells involves a regulatory defect at the level of P-450IA1 RNA [15].
  • Mean tumor volume (cm3) was unaffected by MTX, while significant tumor inhibition (p less than 0.01) was evident for ADR-treated TB animals [26].
  • Although transfection of the sFv did not result in the down-regulation of P-gp expression in P-gp positive MDR cells as determined by flow cytometry analysis, Adriamycin (ADM) uptake and Rhodamine123 (Rh123) retention were increased by the C219 intra-cellular sFv transfection [27].
  • Microspheres containing ADR (100 or 200 micrograms) were randomly administered to one eye [28].

References

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  2. Prevention of anthracycline-induced cytotoxicity in hemopoietic cells by hemin. Tsiftsoglou, A.S., Wong, W., Wheeler, C., Steinberg, H.N., Robinson, S.H. Cancer Res. (1986) [Pubmed]
  3. Serial micropuncture analysis of glomerular function in two rat models of glomerular sclerosis. Fogo, A., Yoshida, Y., Glick, A.D., Homma, T., Ichikawa, I. J. Clin. Invest. (1988) [Pubmed]
  4. Characterization of a cell line derived from the ascites of a patient with papillary serous cystadenocarcinoma of the ovary. Wilson, A.P. J. Natl. Cancer Inst. (1984) [Pubmed]
  5. Cycle-dependent anticancer drug cytotoxicity in mammalian cells synchronized by centrifugal elutriation. Meyn, R.E., Meistrich, M.L., White, R.A. J. Natl. Cancer Inst. (1980) [Pubmed]
  6. Chemotherapy of pancreatic adenocarcinoma: initial report on two transplantable models in the Syrian hamster. Chang, B.K., Gutman, R. Cancer Res. (1982) [Pubmed]
  7. ATP/Mg2+-dependent binding of vincristine to the plasma membrane of multidrug-resistant K562 cells. Naito, M., Hamada, H., Tsuruo, T. J. Biol. Chem. (1988) [Pubmed]
  8. Cytotoxic effect in vivo of selected chemotherapeutic agents on synchronized murine fibrosarcoma cells. Grdina, D.J., Sigdestad, C.P., Peters, L.J. Br. J. Cancer (1980) [Pubmed]
  9. Immunomorphometric studies of proteinuria in individual deep and superficial nephrons of rats. Hoyer, J.R., Fogo, A.B., Terrell, C.H., Delaney, M.M. Lab. Invest. (2000) [Pubmed]
  10. In vitro and in vivo circumvention of multidrug resistance by Servier 9788, a novel triazinoaminopiperidine derivative. Pierré, A., Dunn, T.A., Kraus-Berthier, L., Léonce, S., Saint-Dizier, D., Régnier, G., Dhainaut, A., Berlion, M., Bizzari, J.P., Atassi, G. Investigational new drugs. (1992) [Pubmed]
  11. Supramolecular complex formation between Rad6 and proteins of the p53 pathway during DNA damage-induced response. Lyakhovich, A., Shekhar, M.P. Mol. Cell. Biol. (2003) [Pubmed]
  12. Cellular pharmacology of MX2, a new morpholino anthracycline, in human pleiotropic drug-resistant cells. Watanabe, M., Komeshima, N., Naito, M., Isoe, T., Otake, N., Tsuruo, T. Cancer Res. (1991) [Pubmed]
  13. Flow cytometric localization within the cell cycle and isolation of viable cells following exposure to cytotoxic agents. Crissman, H.A., Wilder, M.E., Tobey, R.A. Cancer Res. (1988) [Pubmed]
  14. ERK activation mediates cell cycle arrest and apoptosis after DNA damage independently of p53. Tang, D., Wu, D., Hirao, A., Lahti, J.M., Liu, L., Mazza, B., Kidd, V.J., Mak, T.W., Ingram, A.J. J. Biol. Chem. (2002) [Pubmed]
  15. Altered regulation of P-450IA1 expression in a multidrug-resistant MCF-7 human breast cancer cell line. Ivy, S.P., Tulpule, A., Fairchild, C.R., Averbuch, S.D., Myers, C.E., Nebert, D.W., Baird, W.M., Cowan, K.H. J. Biol. Chem. (1988) [Pubmed]
  16. Effects of 3'-(3-cyano-4-morpholinyl)-3'-deaminoadriamycin and structural analogues on DNA in HT-29 human colon carcinoma cells. Jesson, M.I., Johnston, J.B., Anhalt, C.D., Begleiter, A. Cancer Res. (1987) [Pubmed]
  17. Possible link between the intrinsic drug resistance of colon tumors and a detoxification mechanism of intestinal cells. Klohs, W.D., Steinkampf, R.W. Cancer Res. (1988) [Pubmed]
  18. Laser flow cytometric studies on the intracellular fluorescence of anthracyclines. Krishan, A., Ganapathi, R. Cancer Res. (1980) [Pubmed]
  19. Cardiotoxicity and comparative pharmacokinetics of six anthracyclines in the rabbit. Jaenke, R.S., Deprez-DeCampeneere, D., Trouet, A. Cancer Res. (1980) [Pubmed]
  20. Scatter factor protects epithelial and carcinoma cells against apoptosis induced by DNA-damaging agents. Fan, S., Wang, J.A., Yuan, R.Q., Rockwell, S., Andres, J., Zlatapolskiy, A., Goldberg, I.D., Rosen, E.M. Oncogene (1998) [Pubmed]
  21. Role of p38 mitogen-activated protein kinase activation in podocyte injury and proteinuria in experimental nephrotic syndrome. Koshikawa, M., Mukoyama, M., Mori, K., Suganami, T., Sawai, K., Yoshioka, T., Nagae, T., Yokoi, H., Kawachi, H., Shimizu, F., Sugawara, A., Nakao, K. J. Am. Soc. Nephrol. (2005) [Pubmed]
  22. Emergence of different mechanisms of resistance in the evolution of multidrug resistance in murine erythroleukemia cell lines. Modrak, D.E., Draper, M.P., Levy, S.B. Biochem. Pharmacol. (1997) [Pubmed]
  23. In vitro cytotoxicity of S16020-2, a new olivacine derivative. Léonce, S., Perez, V., Casabianca-Pignede, M.R., Anstett, M., Bisagni, E., Pierré, A., Atassi, G. Investigational new drugs. (1996) [Pubmed]
  24. Coordinate alterations in the expression of BRCA1, BRCA2, p300, and Rad51 in response to genotoxic and other stresses in human prostate cancer cells. Yuan, R., Fan, S., Wang, J.A., Meng, Q., Ma, Y., Schreiber, D., Goldberg, I.D., Rosen, E.M. Prostate (1999) [Pubmed]
  25. Kinetics of p53 binding to promoter sites in vivo. Szak, S.T., Mays, D., Pietenpol, J.A. Mol. Cell. Biol. (2001) [Pubmed]
  26. Experimental and clinical observations of the effects of cytotoxic chemotherapeutic drugs on wound healing. Bland, K.I., Palin, W.E., von Fraunhofer, J.A., Morris, R.R., Adcock, R.A., Tobin, G.R. Ann. Surg. (1984) [Pubmed]
  27. Overcoming multi-drug resistance using an intracellular anti-MDR1 sFv. Heike, Y., Kasono, K., Kunisaki, C., Hama, S., Saijo, N., Tsuruo, T., Kuntz, D.A., Rose, D.R., Curiel, D.T. Int. J. Cancer (2001) [Pubmed]
  28. Injectable microspheres with controlled drug release for glaucoma filtering surgery. Kimura, H., Ogura, Y., Moritera, T., Honda, Y., Wada, R., Hyon, S.H., Ikada, Y. Invest. Ophthalmol. Vis. Sci. (1992) [Pubmed]
 
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