|1.||Poznyak, Vladimir: 1 article (01/2008)|
|2.||Orozco, Ricardo: 1 article (01/2008)|
|3.||Cherpitel, Cheryl: 1 article (01/2008)|
|4.||Cremonte, Mariana: 1 article (01/2008)|
|5.||Borges, Guilherme: 1 article (01/2008)|
|6.||Buzi-Figlie, Neliana: 1 article (01/2008)|
05/04/1988 - "The favorable therapeutic ratio, the non-cross-resistance with DOX, and the previously described lack of cardiac toxicity all make MRA-CN an attractive candidate for clinical trials in patients with acute leukemia."
05/04/1988 - "There was a lack of correlation between MRA-CN and DOX at a drug concentration at which the colony formation is inhibited by 50% in the leukemia cell lines (correlation coefficient = 0.38), which supported the previous reports of non-cross-resistance between these two agents. "
05/04/1988 - "In addition, the therapeutic ratio was uniformly greater than 1, indicating that each leukemia cell line tested was more sensitive than CFU-GM to MRA-CN in vitro. "
05/04/1988 - "MRA-CN was found to be 100 times more potent than DOX against normal myeloid progenitors--colony-forming units, granulocyte-macrophage (CFU-GM)--and 40-240 times more potent than DOX against leukemia cell lines. "
05/04/1988 - "The effect of MRA-CN on the leukemia cells was compared to its toxicity on normal myeloid progenitors (therapeutic ratio) and to the effect of DOX on the leukemia and normal cells. "
01/01/1992 - "We have developed an ovarian carcinoma cell line ES-2R that is 4-fold resistant to MRA-CN, compared to the parental ES-2 cells. "
10/01/1991 - "To further examine mechanisms of action and resistance to MRA-CN, a cell line resistant to MRA-CN, ES-2R, was established by growing a human ovarian carcinoma cell line, ES-2, in increasing concentrations of the drug. "
10/01/1991 - "Multifactorial mechanisms associated with broad cross-resistance of ovarian carcinoma cells selected by cyanomorpholino doxorubicin."
07/01/1990 - "A human ovarian carcinoma cell line, ES-2, was grown in increasing concentrations of MRA-CN from 0.1 to 0.5 nM. The resultant resistant subline, ES-2R, was 4-fold resistant to MRA-CN. "
08/01/1987 - "Cellular pharmacology of 3'-(3-cyano-4-morpholinyl)-3'-deaminoadriamycin and structural analogues in human colon carcinoma HT-29 cells in vitro."
01/15/1994 - "Thus, MRA-CN induces apoptosis in L5178Y cells, and this effect may be important for the anti-tumor activity of this agent. "
09/01/1991 - "In view of the potential of MRA-CN in cancer treatment, these results need to be confirmed and extended."
11/15/1987 - "The potent Adriamycin (ADR) analogue, 3'-(3-cyano-4-morpholinyl)-3'-deaminoadriamycin (CMA), produces DNA-DNA cross-links in human and murine tumor cells. "
03/01/1987 - "Induction of malignant transformation in vitro and mammary tumors in rats by two new potent anthracycline antitumor antibiotics, morpholinodaunomycin and cyanomorpholinoadriamycin."
|4.||Small Cell Lung Carcinoma (Small Cell Lung Cancer)
01/01/1995 - "The cytotoxic action of two morpholino anthracyclines, methoxymorpholino anthracycline (MRA-MT, FCE 23,762) and cyanomorpholino anthracycline (MRA-CN), was compared with the cytotoxicity of doxorubicin (DOX), the topoisomerase II inhibitor etoposide (VP-16), the topoisomerase I inhibitor camptothecin, methotrexate, and cisplatin in GLC4, a human small-cell lung-cancer cell line, in GLC4-Adr, its P-glycoprotein (Pgp)-negative, multidrug-resistant (MDR; 100-fold DOX-resistant) subline with overexpression of the MDR-associated protein (MRP) and a lowered topoisomerase II activity, and in GLC4-CDDP, its cisplatin-resistant subline. "
|5.||Precursor Cell Lymphoblastic Leukemia-Lymphoma (Acute Lymphoblastic Leukemia)
|2.||DNA (Deoxyribonucleic Acid)
|3.||3'- deamino- 3'- (3- cyano- 4- morpholinyl)doxorubicin
|4.||Anti-Bacterial Agents (Antibiotics)
|5.||3'- (4- morpholinyl)- 3'- deaminodaunorubicin
|9.||DNA-Directed RNA Polymerases (RNA Polymerase)
|10.||RNA (Ribonucleic Acid)
|1.||Heterologous Transplantation (Xenotransplantation)