Establishment and characterization of new murine breast cancer cell lines.

The establishment of two new breast cancer cell lines, MXT+ and MXT-, derived from the murine breast cancer models MXT-M-3,2 MC (hormone-sensitive) and MXT-M-3,2 (ovex) MC (hormone-insensitive), is described. Characterization of the cell lines was performed by investigation of morphology, steroid hormone receptor state, growth kinetics, and drug response as well as by cytogenetic analysis. MXT+ contains estrogen receptors (ER; 6.

Establishment and Characterization of New Murine Breast Cancer Cell Lines.

The establishment of two new breast cancer cell lines, MXT(+) and MXT(-), derived from the murine breast cancer models MXT-M-3, 2 MC (hormone-sensitive) and MXT-M-3, 2 (ovex) MC (hormone-insensitive), is described. Characterization of the cell lines was performed by investigation of morphology, steroid hormone receptor state, growth kinetics, and drug response as well as by cytogenetic analysis. MXT(+) contains estrogen receptors (ER; 6.

Discrepancy between cytotoxicity, platinum accumulation, and DNA platination in MCF-7 breast cancer cells treated with diaqua (1,2-diphenylethylenediamine) platinum (II) sulfates and cisplatin.

Cisplatin (cis), raceme-diaqua[1,2-bis(4-fluorophenyl)ethylenediamine] platinum(II) sulfate (r-4F-PtSO4), meso-diaqua[1,2-bis(4-fluorophenyl)ethylenediamine]platinum(II) sulfate (m-4F-PtSO4), and meso-diaqua[1,2-bis(2,6-dichloro-4-hydroxyphenyl)ethylenediamine] platinum(II) sulfate (m-2,6Cl2-4OH-PtSO4) were compared with regard to their growth inhibitory effect on MCF-7 breast cancer cells. At concentrations of 5 microM, cis, r-4F-PtSO4, and m-4F-PtSO4 were essentially equiactive, whereas m-2,6Cl2-4OH-PtSO4 was ineffective. Platinum measurements by neutron activation analysis showed that a 24-h treatment of the MCF-7 cells with r-4F-PtSO4 and m-4F-PtSO4 caused a 22.

New antagonists of bombesin gastrin-releasing Peptide with C-terminal leu-psi-(ch2n)tac-nh2.

Several new pseudononapeptide bombesin/GRP analogs containing C-terminal Leu Psi(CH2N)Tac-NH2 with variations at the N-terminus, corresponding to position 6 of bombesin, have been synthesized in order to develop more potent Bn antagonists for the hormonal therapy of cancers. The biological activities of the new compounds were evaluated in vitro by investigating their ability to inhibit the binding of [I-125-Tyr(4)]Bn and to suppress the GRP(14-27)-stimulated DNA synthesis in quiescent Swiss 3T3 cells. All compounds investigated inhibited the binding of [I-125-Tyr(4)]Bn, suppressed the GRP(14-27)-induced proliferation of Swiss 3T3 cells in a dose-dependent manner and proved to act as Bn antagonists without agonistic activity.

Potent bombesin antagonists with C-terminal Leu-psi(CH2-N)-Tac-NH2 or its derivatives.

Various pseudononapeptide bombesin (BN)-(6-14) antagonists with a reduced peptide bond (CH2-NH) between positions 13 and 14 can suppress the mitogenic activity of BN or gastrin-releasing peptide in 3T3 fibroblast cells and small cell lung carcinoma. In the search for more potent BN antagonists, 10 modified nonapeptide BN antagonists containing N-terminal D-Phe, D-Cpa, and D- or L-Tpi and C-terminal Leu-psi(CH2-N)-Tac-NH2, Leu-psi(CH2-N)-MeTac-NH2, or Leu-psi(CH2-N)-Me2Tac-NH2 have been synthesized by incubating [13 psi 14,CH2-NH,Cys14]BN-(6-14) or [13 psi 14-CH2-NH,Pen14]BN-(6-14) with formaldehyde or acetaldehyde (Cpa = 4-chlorophenylalanine, Tac = thiazolidine-4-carboxylic acid, Tpi = 2,3,4,9-tetrahydro-1H- pyrido[3,4-b]indol-3-carboxylic acid, and Pen = penicillamine). The biological activities of these compounds were then evaluated.