| Type I Receptor Kinase Inhibitors - A Novel Treatment for Breast Cancer |
JUN 2002 |
9 pages |
| Authors:
Michael Reiss; CANCER INST OF NEW JERSEY NEW BRUNSWICK
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 | Transforming Growth Factor-Betas (TGF beta) are polypeptides that are constitutively secreted and activated by many breast carcinomas. They contribute to the tumor's ability to invade and metastasize, to induce angiogenesis and to escape from immune destruction. These circumstances raise the question whether blocking the effects of tumor-derived TGF beta on normal tissue (stroma, bloodvessels and immune cells) could be developed as a novel approach to the treatment of breast cancer. ... |
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| TGFbeta Type I Receptor Kinase Inhibitors - A Novel Treatment for Breast Cancer |
APR 2001 |
8 pages |
| Authors:
Michael Reiss; CANCER INST OF NEW JERSEY PISCATAWAY
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| Transforming Growth Factor-Bs (TGFBeta)are polypeptides that are constitutively secreted and activated by many breast carcinomas. They contribute to the tumor's ability to invade and metastasize, to induce angiogenesis and to escape from immune destruction. These circumstances raise the question whether blocking the effects of tumor-derived TGFBeta on normal tissue (stroma, bloodvessels and immune cells) could be developed as a novel approach to the treatment of breast cancer. We propose to ... |
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| Transforming Growth Factor-B Receptors in Humans |
JAN 2001 |
15 pages |
| Authors:
Michael Reiss; YALE UNIV NEW HAVEN CT
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| Transforming Growth Factor-Beta (TGF-Beta) is the most potent known inhibitor of cell cycle progression of normal mammary epithelial cells. In general, advanced breast cancers are refractory to TGF-Beta-mediated growth inhibition. The TGF-Beta type I and type II receptors (T-Beta-R-I and -II) are the primary transducers of TGF-Beta's antiproliferative effects. It is our working hypothesis that TGF-Beta-resistance is caused by lesions in the T-Beta-R genes. Using touch preps of primary breast ... |
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| Transforming Growth Factor-B Receptors in Human Breast Cancer |
MAY 2000 |
35 pages |
| Authors:
Michael Reiss; YALE UNIV NEW HAVEN CT
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| Transforming Growth Factor-Beta (TGFBeta) is the most potent known inhibitor of cell cycle progression of normal mammary epithelial cells. In general, advanced breast cancers are refractory to TGFBeta-mediated growth inhibition. The TGFBeta type I and type II receptors (TBetaR-l and -11) are the primary transducers of TGFBeta's antiproliferative effects. It is our working hypothesis that TGFBeta-resistance is caused by lesions in the TBetaR genes. ... |
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| Transforming Growth Factor-B Receptors in Human Breast Cancer |
MAY 1999 |
60 pages |
| Authors:
Michael Reiss; YALE UNIV NEW HAVEN CT
|
| Transforming Growth Factor-B (TGFBeta) is the most potent known inhibitor of cell cycle progression of normal mammary epithelial cells. In general, advanced breast cancers are refractory to TGFBeta-mediated growth inhibition. The TGFBeta type I and -II receptors (TBetaR-I and -II) are the primary transducer of TGFBeta's growth inhibitory effect. It is our working hypothesis that TGFBeta-resistance is caused by molecular lesions in the TBetaR ... |
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| Transforming Growth Factor-B Receptors in Human Breast Cancer |
MAY 1998 |
47 pages |
| Authors:
Michael Reiss; YALE UNIV NEW HAVEN CT SCHOOL OF MEDICINE
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| This project addresses the question whether and, if so, how molecular lesions of the genes involved in the TGFB signaling pathway contribute to the origin and/or progression of breast cancer. We have cloned and determined the intron-exon structure of the TGFB type I receptor (TBR-I). This has allowed us to study this gene in a series of primary breast cancer specimens. Our most important finding is a much higher frequency ... |
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| Transforming Growth Factor-beta Receptors in Human Breast Cancer |
MAY 97 |
10 pages |
| Authors:
Michael Reiss; YALE UNIV NEW HAVEN CT SCHOOL OF MEDICINE
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| This project addresses three fundamental research issues. The first question is whether or not molecular lesions of the genes involved in the TGFB signaling pathway contribute to the origin and/or progression of breast cancer. We expect changes in these genes to be relatively late events, perhaps characteristic of metastatic cancer. Secondly, we propose to determine how molecular lesions in the TGFB receptor and/or Smad genes affect receptor function, and how ... |
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