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648 results on '"Hanahan D"'

5. A personalised approach for anti-GITR-based immunotherapy in pre-clinical models of pancreatic ductal adenocarcinoma

Author

Desai, K., primary, Ragulan, C., additional, Lawrence, P.V., additional, Wullschleger, S., additional, Tichet, M.L., additional, Box, G., additional, Fontana, E., additional, Young, K., additional, Larkin, J.M.J., additional, Hanahan, D., additional, Cunningham, D., additional, Starling, N., additional, and Sadanandam, A., additional

Published
2019
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8. Betacellulin: a mitogen from pancreatic beta cell tumors

Author

Shing, Y., Christofori, G., Hanahan, D., Sasada, R., Igarashi, K., and Folkman, J.

Subjects
Mitogens -- Research -- Physiological aspects, Pancreatic beta cells -- Physiological aspects -- Research, Science and technology, Physiological aspects, Research
Abstract

Betacellulin, a member of the epidermal growth factor family, has been identified in the Conditioned medium of cell lines derived from mouse pancreatic Β cell tumors. Betacellulin is a 32-kilodalton glyprotein that appears to be processed from a larger transmembrane precursor by proteolytic cleavage. The carboxyl-terminal domain of betacellulin has 50 percent sequence similarity with that of rat transforming growth factor [Alpha]. Betacellulin is a potent nitrogen for retinal pigment epithelial cells and vascular smooth muscle cells., It is increasingly evident that carcinogenesis involves a series of genetic and epigenetic changes that together produce a malignant phenotype. Many of these changes are implicated in the aberrant growth [...]

Published
1993

13. Evidence for Threshold Effects in Transformation of Pancreatic β Cells by SV40 T Antigen in Transgenic Mice

Author

Efrat, S., Hanahan, D., Compans, R. W., editor, Cooper, M., editor, Koprowski, H., editor, McConell, I., editor, Melchers, F., editor, Nussenzweig, V., editor, Oldstone, M., editor, Olsnes, S., editor, Saedler, H., editor, Vogt, P. K., editor, Wagner, H., editor, Wilson, I., editor, Knippers, Rolf, editor, and Levine, Arnold J., editor

Published
1989
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25. Antitumor effects in mice of low-dose (metronomic) cyclophosphamide administered continuously through the drinking water

Author

Man, S, Bocci, Guido, Francia, G, Green, Sk, Jothy, S, Hanahan, D, Bohlen, P, Hicklin, Dj, Bergers, G, and Kerbel, Rs

Subjects
Male, Drinking, Administration, Oral, Mice, Nude, Angiogenesis Inhibitors, Breast Neoplasms, Mice, SCID, Antibodies, angiogenesis, Mice, metronomic chemotherapy, Tumor Cells, Cultured, Animals, Humans, Receptors, Growth Factor, Antineoplastic Agents, Alkylating, Cyclophosphamide, Dose-Response Relationship, Drug, Prostatic Neoplasms, Receptor Protein-Tyrosine Kinases, Xenograft Model Antitumor Assays, Receptors, Vascular Endothelial Growth Factor, Female, HT29 Cells, Cell Division
Abstract

A number of recent preclinical studies have sparked interest in the concept of exploiting conventional chemotherapeutic drugs as antiangiogenics. Such antiangiogenic activity is achieved or optimized by metronomic-dosing protocols in which the drug is given at comparatively low doses using a frequent schedule of administration (e.g., once to three times per week) with no breaks, particularly when combined with an endothelial cell-specific antiangiogenic drug. The use of p.o. chemotherapeutic drugs is particularly suitable for this type of treatment strategy. We tested one such drug, cyclophosphamide (CTX), in a protocol wherein the drug was administered to mice at low doses, of approximately 10-40 mg/kg on a daily basis through the drinking water. CTX is typically given p.o. to patients, but it has almost always been injected when treating preclinical mouse tumor models. We found p.o. CTX to be a safe and convenient treatment with significant antitumor efficacy. Growth delays were observed for human orthotopic breast or ectopic colon cancer xenografts in nude or SCID mice. Established PC3 human prostate tumor xenografts could be induced to almost fully regress, remaining virtually nonpalpable foror =2 months of continuous therapy, after which tumors began to grow progressively. These re-emergent tumors were not found to be drug resistant when tested in new hosts, using the same treatment protocol. Regression of spontaneously arising, late-stage pancreatic islet cell carcinomas in Rip Tag transgenic mice was also observed. The effects of continuous p.o. CTX treatment were enhanced significantly in an orthotopic, metastatic breast cancer xenograft model when used in combination with an antivascular endothelial growth factor receptor-2 blocking antibody. Maximum tolerated dose levels established for other mouse strains proved highly toxic to SCID mice, whereas daily p.o. low-dose regimens of CTX were well tolerated. Taken together, the results demonstrate the feasibility of delivering CTX in a p.o. metronomic chemotherapy regimen, which proved safe, reasonably efficacious, and potentially applicable to chronic treatment. Such a regimen may be particularly well suited for integration with antiangiogenic drugs.

Published
2002

26. Mouse models for the study of telomerase

Author

Maria A. Blasco, Hw, Lee, Rizen M, Hanahan D, DePinho R, and Cw, Greider

Subjects
Enzyme Activation, Mice, Knockout, Mice, Models, Genetic, Disease Progression, Animals, RNA, Mice, Transgenic, Telomerase, Neoplasm Staging
Abstract

The ends of chromosomes, or telomeres, consist of short repeated sequences that are synthesized by a ribonucleoprotein-DNA polymerase called telomerase. The RNA component of telomerase is essential for enzyme activity. The maintenance of telomere length by telomerase has been proposed to be essential for cellular viability and to play an important role in cellular senescence and immortalization. We are interested in using the mouse as a model system for the study of telomerase. We studied telomerase activity and expression of the mouse telomerase RNA component (mTR) in two different transgenic mouse models of multistage tumorigenesis: models of islet cell carcinoma and squamous cell carcinoma. In both tumour models, telomerase activity was detected only in late-stage tumours, whereas the telomerase RNA was present at higher than normal levels in pre-neoplastic stages and increased further in late-stage tumours. However, the RNA levels did not parallel the amounts of telomerase activity detected, suggesting that regulation of telomerase activity does not correlate with the regulation of its RNA component. These results establish a direct correlation between progression to late-stage tumours and induction of telomerase activity, and suggest that the initial upregulation of telomerase RNA is an early event. To address the role of telomerase during normal mouse development and tumour formation, we have constructed a knockout mouse for the mouse telomerase RNA, mTR-/-. These mice and the cell lines derived from them are telomerase deficient.

Published
1997

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