Breast adenocarcinoma

The test system was considerably less sensitive to endosulfan when mouse ER, rather than human ER, was used to mediate (3-gal activity (Ramamoorthy et al. 1997). In similar assays, endosulfan at 10 jM had no effect on (3-gal activity in yeast Saccharomyces) transfected with either the human or rainbow trout ER (Andersen et al. 1999). In addition, no effect was observed on transcriptional activation of HeLa cells transfected with plasmids containing an estrogen receptor as a responsive element (Shelby et al. 1996). Endosulfan also did not induce transient reporter gene expression in MCF-7 human breast cancer cells at an incubation concentration of 2.5 pM (Andersen et al. 1999). Maximum endosulfan-induced ER-mediated luciferase reporter gene expression occurred in vitro in a T47D human breast adenocarcinoma cell line at approximately 10 pM, while 50% expression of luciferase occurred at about 5.9 pM the maximum expression was approximately 59% of the effect from exposure to 0.03 nM estradiol (0.00003 pM) (Legler et al. 1999). Luciferase expression from combined treatment with endosulfan and dieldrin was additive over concentrations ranging from 3 to 8 pM. 

Goldberg-Bittman L, Neumark E, Sagi-Assif O, et al. The expression of the chemokine receptor CXCR3 and its ligand, CXCL10, in human breast adenocarcinoma cell lines. Immunol Lett 2004 92 171-178. 

A 50- year-old female had a radical mastectomy three years ago for hormone-dependent breast adenocarcinoma. She is now complaining of shortness of breath, and chest X-ray shows diffuse lung metastases. As part of her therapeutic regimen, she is given intramuscular hormone replacement therapy (1IRT). 

In MDR cells, a significant fraction of P-gp is found associated with caveolin-rich membranes, and there is a substantial increase in the number of caveolae and caveolin-1 protein level. For example, both multidrug resistant human colon adenocarcinoma HT-29 cells and adriamycin-resistant breast adenocarcinoma MCF-7 cells display about a 12-fold increase in caveolin expression, which correlates with an approximate fivefold increase in morphologically identifiable caveolae [55], In addition, these cells exhibit increased amounts of phospholipase D and lipids such as cholesterol, glucosylceramide, and sphingomyelin [56, 57], Similarly, taxol-resistant A549 cells display both increased caveolin expression and caveolae numbers [58], While these correlations track with MDR, they do not suggest a simple mechanism for the role of... 

Ferrying of molecules into cells via entry through caveolae may represent a way to traffic specifically cytotoxic molecules to specific action sites. For example, elevating the intracellular level of the sphingolipid ceramide is known to exert antimitogenic and proapoptotic effects. While ceramide is cell-permeable and displays antiapoptotic properties in vitro, systemic in vivo use of ceramide is hampered by its hydrophobicity. Using a C6-ceramide formulation in pegylated liposomes was shown to elicit a sixfold reduction in solid phase tumors, when compared to unloaded liposomes in a mouse model of breast adenocarcinoma [68],... 

C. Cai and J. Chen. Overexpression of caveolin-1 induces alteration of multidrug resistance in Hs578T breast adenocarcinoma cells. Int. J. Cancer 111 317-323 (2004). 

T. C. Stover, A. Sharma, G. P. Robertson, and M. Kester. Systemic delivery of liposomal short-chain ceramide limits solid tumor growth in murine models of breast adenocarcinoma. Clin. Cancer Res. 11 3465-3474 (2005). 

CuvUlier, O., Nava, V.E., Murthy, S.K., Edsall, L.C., Levade, T, MUstien, S. and Spiegel, S., 2001, Sphingosine generation, cytochrome c release, and activation ofcaspase-7 in doxorubidn-induced apoptosis of MCF7 breast adenocarcinoma cells. Cell Death Differ 8 162-171. 

S. M. Scholl, C. Pallud, F. Beuvon, K. Hacene, E. R. Stanley, L. Rohrschneider, R. Tang, P. Pouillart, and R. Lidereau, Anti-colony-stimulating factor-1 antibody staining in primaiy breast adenocarcinomas correlates with marked inflammatory cell infdtrates and prognosis, J.Natl. Cancer Inst. 86(2), 120-126 (1994). 

It is indicated in leukaemias, lymphogranulomatosis, lymphosarcoma, reticulum cell sarcoma, Hodgkin s disease, multiple myeloma, retinoblastoma, carcinoma of the breast, adenocarcinoma of the ovary, inoperable solid malignancies. It is used in combination with surgery, radiation and other therapeutic measures. 

Karamanakos P, Mitsiades CS, Lembessis P, Kontos M, Trafalis D, Koutsilieris M. Male breast adenocarcinoma in a prostate cancer patient following prolonged anti-androgen monotherapy. Anticancer Res 2004 24 1077-81. 

Dasgupta P, Singh A, Mukherjee R (2002) N-terminal acylation of somatostatin analog with long chain fatty acids enhances its stability and anti-proliferative activity in human breast adenocarcinoma cells. Biol Pharm Bull 25 29-36 Delgado C, Francis GE, D. F (1992) The uses and properties of PEG-linked proteins. Crit Rev Ther Drug Carrier Syst 9 249-304... 

Moongkarndi, P., Kosem, N., Luanratana, O., Jongsomboonkusol, S. and Pongpan, N. (2004b) Antiproliferative activity of Thai medicinal plant extracts on human breast adenocarcinoma cell line. Fitoterapia 75(3—4), 375-377. 

The antiproliferative and antitubulin activities of libraries of pyranopyridones and pyranoquinolones 147 (Scheme 28) derived from aldehydes, malononitrile and pyridones 146 have been examined [65]. The compounds were evaluated for their ability to reduce cell viability by 50% after 48 h of treatment relative to control. The HeLa and MCE-7 cell fines were used as models for human cervical and breast adenocarcinoma, respectively. Numerous compounds exhibited submicromolar antiproliferative activities with the quinolones being more potent than their pyridine counterparts (Eig. 20). Because of the structural similarity of pyranopyridones with chromene scaffolds known to inhibit tubulin polymerization, compounds 149 and 150 were further evaluated in Jurkat cells for their apoptotic... 

Leveque J, Eoucher E, Havouis R, Desury D, Grail J-Y, Mouli-noux J-P. Benefits of complete polyamine deprivation in hormone responsive and hormone resistant MCF-7 human breast adenocarcinoma in vivo. Anticancer Res. 2000 20(1A) 97-101. 

Noel, A., de Pauw-Gillet, M. C., Purnell, G., Nusgens, B., Lapiere, C. M. and Foidart, J. M. (1993). Enhancement of tumorigenicity of human breast adenocarcinoma cells in nude mice by matrigel and fibroblasts. Br. J. Cancer 68, 909-915. 

Krajewski, S., Blomqvist, C., Franssila, K., Krajewska, M., Wasenius, V-M., Niskanen, E., Nordling, S., and Reed, J. C. (1995) Reduced expression of proapoptotic gene Bax is associated with poor response rates to combination chemotherapy and shorter survival in women with metastatic breast adenocarcinoma. Cancer Res. 55,4471 1478. 

Fig. 1. Binding of Rh-PE-iabeied Gd-DTPA-PLL-NGPE-containing PEGyiated piain and immunoiiposomes to murine Lewis iung carcinoma (EEC) and human mammary adenocarcinoma (BT-20) and breast adenocarcinoma (MCE-7) ceiis (With permission from (21))...

Human breast adenocarcinoma MCF-7 cells were incubated for different time intervals with deuterated LIP and TATp-LIP at a Upid concentration of 2 mg ml" . After incubation, the cells were fixed in a phosphate-buffered formalin solution and subsequently washed and submerged in phosphate-buffered saline, to maintain the cell shape within the aqueous environment. 

Toth B. 1969. Lung tumor induction and inhibition of breast adenocarcinomas by hydrazine sulfate in mice. J Natl Cancer Inst 42 469-475. 

Kramer VJ, Helferich WG, Bergman A, et al. 1997. Hydroxylated polychlorinated biphenyl metabolites are anti-estrogenic in a stably transfected human breast adenocarcinoma (MCF7) cell line. Toxicol Appl Pharmacol 144 363-374. 

We confirmed that this assay could be used to quantify active caspase-3 and active caspase-7 in other cell types. Active caspase-3 and active caspase-7 were quantified in the extracts from STS-treated human neuroblastoma (CHP-100 and SH-SY5Y) and promyelocytic leukemia (HL60) cells (Table 1). The amount of active caspase-3 was found to be much higher than the amount of active caspase-7 in these cell types. Very low or no amounts of active caspases were detected in control cells (cells not treated with STS). Active caspase-3 and active caspase-7 were also quantified in human breast adenocarcinoma (MCF-7) cells that do not express caspase-3 (28,38). No... 

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