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Domenico Rotilio - One of the best experts on this subject based on the ideXlab platform.
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inhibition of gelatinase a mmp 2 by batimastat and Captopril reduces tumor growth and lung metastases in mice bearing lewis lung carcinoma
International Journal of Cancer, 1999Co-Authors: Cesaria Prontera, Cosmo Rossi, Barbara Mariani, Andreina Poggi, Domenico RotilioAbstract:We have examined the effects of the synthetic matrix metalloproteinase inhibitor, batimastat (BB-94) and the angiotensin-converting enzyme inhibitor, Captopril, on metalloproteinase activity of murine Lewis-lung-carcinoma cells (3LL) in vitro, and on local growth and lung metastasis of the same tumor implanted intramuscularly in syngeneic C57BL/6 mice. The effect of BB-94 and Captopril on the survival of the 3LL-tumor-bearing mice was also examined. Here we report that Captopril treatment resulted in decreased transcription and protein levels of gelatinase A by 3LL cells. Both BB-94 and Captopril also prevented substrate degradation by gelatinase A and B released in conditioned medium by cultured cells. Treatment of tumor-bearing animals with BB-94 (i.p.) or Captopril (in drinking water) resulted in significant inhibition of the mean tumor volume (25 and 33% respectively) and of the mean lung metastasis number (26 and 29% respectively). When both agents were given, they acted in synergy, resulting in 51 and 80% inhibition of tumor growth and metastasis. The survival time of the mice treated with both BB-94 and Captopril was also significantly longer compared with the groups treated with each agent alone or with the vehicle. Our data support the hypothesis of an essential role of metalloproteinase(s) in the metastatic process. Moreover, blockade of invasion, angiogenesis and other processes mediated by metalloproteinases may underlie the anti-tumor and anti-metastatic effect of BB-94 and Captopril and their combination. It is conceivable that this combination could be tested in selected clinical conditions as an adjuvant modality to cytotoxic therapy.
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inhibition of gelatinase a mmp 2 by batimastat and Captopril reduces tumor growth and lung metastases in mice bearing lewis lung carcinoma
International Journal of Cancer, 1999Co-Authors: Cesaria Prontera, Cosmo Rossi, Barbara Mariani, Andreina Poggi, Domenico RotilioAbstract:We have examined the effects of the synthetic matrix metalloproteinase inhibitor, batimastat (BB-94) and the angiotensin-converting enzyme inhibitor, Captopril, on metalloproteinase activity of murine Lewis-lung-carcinoma cells (3LL) in vitro, and on local growth and lung metastasis of the same tumor implanted intramuscularly in syngeneic C57BL/6 mice. The effect of BB-94 and Captopril on the survival of the 3LL-tumor-bearing mice was also examined. Here we report that Captopril treatment resulted in decreased transcription and protein levels of gelatinase A by 3LL cells. Both BB-94 and Captopril also prevented substrate degradation by gelatinase A and B released in conditioned medium by cultured cells. Treatment of tumor-bearing animals with BB-94 (i.p.) or Captopril (in drinking water) resulted in significant inhibition of the mean tumor volume (25 and 33% respectively) and of the mean lung metastasis number (26 and 29% respectively). When both agents were given, they acted in synergy, resulting in 51 and 80% inhibition of tumor growth and metastasis. The survival time of the mice treated with both BB-94 and Captopril was also significantly longer compared with the groups treated with each agent alone or with the vehicle. Our data support the hypothesis of an essential role of metalloproteinase(s) in the metastatic process. Moreover, blockade of invasion, angiogenesis and other processes mediated by metalloproteinases may underlie the anti-tumor and anti-metastatic effect of BB-94 and Captopril and their combination. It is conceivable that this combination could be tested in selected clinical conditions as an adjuvant modality to cytotoxic therapy. Int. J. Cancer 81:761–766, 1999. © 1999 Wiley-Liss, Inc.
Cesaria Prontera - One of the best experts on this subject based on the ideXlab platform.
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inhibition of gelatinase a mmp 2 by batimastat and Captopril reduces tumor growth and lung metastases in mice bearing lewis lung carcinoma
International Journal of Cancer, 1999Co-Authors: Cesaria Prontera, Cosmo Rossi, Barbara Mariani, Andreina Poggi, Domenico RotilioAbstract:We have examined the effects of the synthetic matrix metalloproteinase inhibitor, batimastat (BB-94) and the angiotensin-converting enzyme inhibitor, Captopril, on metalloproteinase activity of murine Lewis-lung-carcinoma cells (3LL) in vitro, and on local growth and lung metastasis of the same tumor implanted intramuscularly in syngeneic C57BL/6 mice. The effect of BB-94 and Captopril on the survival of the 3LL-tumor-bearing mice was also examined. Here we report that Captopril treatment resulted in decreased transcription and protein levels of gelatinase A by 3LL cells. Both BB-94 and Captopril also prevented substrate degradation by gelatinase A and B released in conditioned medium by cultured cells. Treatment of tumor-bearing animals with BB-94 (i.p.) or Captopril (in drinking water) resulted in significant inhibition of the mean tumor volume (25 and 33% respectively) and of the mean lung metastasis number (26 and 29% respectively). When both agents were given, they acted in synergy, resulting in 51 and 80% inhibition of tumor growth and metastasis. The survival time of the mice treated with both BB-94 and Captopril was also significantly longer compared with the groups treated with each agent alone or with the vehicle. Our data support the hypothesis of an essential role of metalloproteinase(s) in the metastatic process. Moreover, blockade of invasion, angiogenesis and other processes mediated by metalloproteinases may underlie the anti-tumor and anti-metastatic effect of BB-94 and Captopril and their combination. It is conceivable that this combination could be tested in selected clinical conditions as an adjuvant modality to cytotoxic therapy.
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inhibition of gelatinase a mmp 2 by batimastat and Captopril reduces tumor growth and lung metastases in mice bearing lewis lung carcinoma
International Journal of Cancer, 1999Co-Authors: Cesaria Prontera, Cosmo Rossi, Barbara Mariani, Andreina Poggi, Domenico RotilioAbstract:We have examined the effects of the synthetic matrix metalloproteinase inhibitor, batimastat (BB-94) and the angiotensin-converting enzyme inhibitor, Captopril, on metalloproteinase activity of murine Lewis-lung-carcinoma cells (3LL) in vitro, and on local growth and lung metastasis of the same tumor implanted intramuscularly in syngeneic C57BL/6 mice. The effect of BB-94 and Captopril on the survival of the 3LL-tumor-bearing mice was also examined. Here we report that Captopril treatment resulted in decreased transcription and protein levels of gelatinase A by 3LL cells. Both BB-94 and Captopril also prevented substrate degradation by gelatinase A and B released in conditioned medium by cultured cells. Treatment of tumor-bearing animals with BB-94 (i.p.) or Captopril (in drinking water) resulted in significant inhibition of the mean tumor volume (25 and 33% respectively) and of the mean lung metastasis number (26 and 29% respectively). When both agents were given, they acted in synergy, resulting in 51 and 80% inhibition of tumor growth and metastasis. The survival time of the mice treated with both BB-94 and Captopril was also significantly longer compared with the groups treated with each agent alone or with the vehicle. Our data support the hypothesis of an essential role of metalloproteinase(s) in the metastatic process. Moreover, blockade of invasion, angiogenesis and other processes mediated by metalloproteinases may underlie the anti-tumor and anti-metastatic effect of BB-94 and Captopril and their combination. It is conceivable that this combination could be tested in selected clinical conditions as an adjuvant modality to cytotoxic therapy. Int. J. Cancer 81:761–766, 1999. © 1999 Wiley-Liss, Inc.
Daniel J Gans - One of the best experts on this subject based on the ideXlab platform.
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the beneficial effect of angiotensin converting enzyme inhibition with Captopril on diabetic nephropathy in normotensive iddm patients with microalbuminuria
The American Journal of Medicine, 1995Co-Authors: Lori M Laffel, Janet B Mcgill, Daniel J GansAbstract:Purpose To determine whether angiotensin-converting enzyme (ACE) inhibition with Captopril reduces the progression of microalbuminuria to overt proteinuria in normotensive patients with insulin-dependent diabetes mellitus (IDDM). Patients and methods This study was a prospective randomized, double-blind, placebo-controlled trial involving 26 centers in the United States and Canada. One hundred forty-three subjects, 14 to 57 years of age, with IDDM for 4 to 33 years, blood pressure Results Within 24 months, 6.0% (4/67) of Captopril-treated subjects and 18.6% (13/70) of placebo-treated subjects progressed to clinical proteinuria, defined as AER > 200 micrograms/min and at least 30% above baseline (risk reduction = 67.8%, P = 0.037). AER increased at an annual rate of 11.8% (95% confidence interval [CI] -3.3% to 29.1%) in the placebo group, while it declined by 17.9% (CI -29.6% to -4.3%) in the Captopril group (P = 0.004). CrCl decreased by 4.9 mL/min per 1.73 m2 per year in the placebo group, while it remained stable in the Captopril group (0.9 mL/min per 1.73 m2 per year, P = 0.039 between groups). Ten subjects required treatment for hypertension; 8 in the placebo group and 2 in the Captopril group. There was little correlation between the 24-month changes in mean arterial blood pressure and AER in either group. Glycohemoglobin and urinary urea excretion did not differ between groups. Conclusions After 24 months of therapy with Captopril, compared with placebo, normotensive subjects with IDDM experienced significantly less progression of microalbuminuria to clinical proteinuria, reduced albumin excretion, and preserved CrCl rate. The ACE inhibitor, Captopril, was well tolerated.
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the beneficial effect of angiotensin converting enzyme inhibition with Captopril on diabetic nephropathy in normotensive iddm patients with microalbuminuria
The American Journal of Medicine, 1995Co-Authors: Lori M Laffel, Janet B Mcgill, Daniel J GansAbstract:PURPOSE: To determine whether angiotensin-converting enzyme (ACE) inhibition with Captopril reduces the progression of microalbuminuria to overt proteinuria in normotensive patients with insulin-dependent diabetes mellitus (IDDM). PATIENTS AND METHODS: This study was a prospective randomized, double-blind, placebo-controlled trial involving 26 centers in the United States and Canada. One hundred forty-three subjects, 14 to 57 years of age, with IDDM for 4 to 33 years, blood pressure 200 micrograms/min and at least 30% above baseline (risk reduction = 67.8%, P = 0.037). AER increased at an annual rate of 11.8% (95% confidence interval [CI] -3.3% to 29.1%) in the placebo group, while it declined by 17.9% (CI -29.6% to -4.3%) in the Captopril group (P = 0.004). CrCl decreased by 4.9 mL/min per 1.73 m2 per year in the placebo group, while it remained stable in the Captopril group (0.9 mL/min per 1.73 m2 per year, P = 0.039 between groups). Ten subjects required treatment for hypertension; 8 in the placebo group and 2 in the Captopril group. There was little correlation between the 24-month changes in mean arterial blood pressure and AER in either group. Glycohemoglobin and urinary urea excretion did not differ between groups. CONCLUSIONS: After 24 months of therapy with Captopril, compared with placebo, normotensive subjects with IDDM experienced significantly less progression of microalbuminuria to clinical proteinuria, reduced albumin excretion, and preserved CrCl rate. The ACE inhibitor, Captopril, was well tolerated.
Cosmo Rossi - One of the best experts on this subject based on the ideXlab platform.
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inhibition of gelatinase a mmp 2 by batimastat and Captopril reduces tumor growth and lung metastases in mice bearing lewis lung carcinoma
International Journal of Cancer, 1999Co-Authors: Cesaria Prontera, Cosmo Rossi, Barbara Mariani, Andreina Poggi, Domenico RotilioAbstract:We have examined the effects of the synthetic matrix metalloproteinase inhibitor, batimastat (BB-94) and the angiotensin-converting enzyme inhibitor, Captopril, on metalloproteinase activity of murine Lewis-lung-carcinoma cells (3LL) in vitro, and on local growth and lung metastasis of the same tumor implanted intramuscularly in syngeneic C57BL/6 mice. The effect of BB-94 and Captopril on the survival of the 3LL-tumor-bearing mice was also examined. Here we report that Captopril treatment resulted in decreased transcription and protein levels of gelatinase A by 3LL cells. Both BB-94 and Captopril also prevented substrate degradation by gelatinase A and B released in conditioned medium by cultured cells. Treatment of tumor-bearing animals with BB-94 (i.p.) or Captopril (in drinking water) resulted in significant inhibition of the mean tumor volume (25 and 33% respectively) and of the mean lung metastasis number (26 and 29% respectively). When both agents were given, they acted in synergy, resulting in 51 and 80% inhibition of tumor growth and metastasis. The survival time of the mice treated with both BB-94 and Captopril was also significantly longer compared with the groups treated with each agent alone or with the vehicle. Our data support the hypothesis of an essential role of metalloproteinase(s) in the metastatic process. Moreover, blockade of invasion, angiogenesis and other processes mediated by metalloproteinases may underlie the anti-tumor and anti-metastatic effect of BB-94 and Captopril and their combination. It is conceivable that this combination could be tested in selected clinical conditions as an adjuvant modality to cytotoxic therapy.
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inhibition of gelatinase a mmp 2 by batimastat and Captopril reduces tumor growth and lung metastases in mice bearing lewis lung carcinoma
International Journal of Cancer, 1999Co-Authors: Cesaria Prontera, Cosmo Rossi, Barbara Mariani, Andreina Poggi, Domenico RotilioAbstract:We have examined the effects of the synthetic matrix metalloproteinase inhibitor, batimastat (BB-94) and the angiotensin-converting enzyme inhibitor, Captopril, on metalloproteinase activity of murine Lewis-lung-carcinoma cells (3LL) in vitro, and on local growth and lung metastasis of the same tumor implanted intramuscularly in syngeneic C57BL/6 mice. The effect of BB-94 and Captopril on the survival of the 3LL-tumor-bearing mice was also examined. Here we report that Captopril treatment resulted in decreased transcription and protein levels of gelatinase A by 3LL cells. Both BB-94 and Captopril also prevented substrate degradation by gelatinase A and B released in conditioned medium by cultured cells. Treatment of tumor-bearing animals with BB-94 (i.p.) or Captopril (in drinking water) resulted in significant inhibition of the mean tumor volume (25 and 33% respectively) and of the mean lung metastasis number (26 and 29% respectively). When both agents were given, they acted in synergy, resulting in 51 and 80% inhibition of tumor growth and metastasis. The survival time of the mice treated with both BB-94 and Captopril was also significantly longer compared with the groups treated with each agent alone or with the vehicle. Our data support the hypothesis of an essential role of metalloproteinase(s) in the metastatic process. Moreover, blockade of invasion, angiogenesis and other processes mediated by metalloproteinases may underlie the anti-tumor and anti-metastatic effect of BB-94 and Captopril and their combination. It is conceivable that this combination could be tested in selected clinical conditions as an adjuvant modality to cytotoxic therapy. Int. J. Cancer 81:761–766, 1999. © 1999 Wiley-Liss, Inc.
Barbara Mariani - One of the best experts on this subject based on the ideXlab platform.
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inhibition of gelatinase a mmp 2 by batimastat and Captopril reduces tumor growth and lung metastases in mice bearing lewis lung carcinoma
International Journal of Cancer, 1999Co-Authors: Cesaria Prontera, Cosmo Rossi, Barbara Mariani, Andreina Poggi, Domenico RotilioAbstract:We have examined the effects of the synthetic matrix metalloproteinase inhibitor, batimastat (BB-94) and the angiotensin-converting enzyme inhibitor, Captopril, on metalloproteinase activity of murine Lewis-lung-carcinoma cells (3LL) in vitro, and on local growth and lung metastasis of the same tumor implanted intramuscularly in syngeneic C57BL/6 mice. The effect of BB-94 and Captopril on the survival of the 3LL-tumor-bearing mice was also examined. Here we report that Captopril treatment resulted in decreased transcription and protein levels of gelatinase A by 3LL cells. Both BB-94 and Captopril also prevented substrate degradation by gelatinase A and B released in conditioned medium by cultured cells. Treatment of tumor-bearing animals with BB-94 (i.p.) or Captopril (in drinking water) resulted in significant inhibition of the mean tumor volume (25 and 33% respectively) and of the mean lung metastasis number (26 and 29% respectively). When both agents were given, they acted in synergy, resulting in 51 and 80% inhibition of tumor growth and metastasis. The survival time of the mice treated with both BB-94 and Captopril was also significantly longer compared with the groups treated with each agent alone or with the vehicle. Our data support the hypothesis of an essential role of metalloproteinase(s) in the metastatic process. Moreover, blockade of invasion, angiogenesis and other processes mediated by metalloproteinases may underlie the anti-tumor and anti-metastatic effect of BB-94 and Captopril and their combination. It is conceivable that this combination could be tested in selected clinical conditions as an adjuvant modality to cytotoxic therapy.
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inhibition of gelatinase a mmp 2 by batimastat and Captopril reduces tumor growth and lung metastases in mice bearing lewis lung carcinoma
International Journal of Cancer, 1999Co-Authors: Cesaria Prontera, Cosmo Rossi, Barbara Mariani, Andreina Poggi, Domenico RotilioAbstract:We have examined the effects of the synthetic matrix metalloproteinase inhibitor, batimastat (BB-94) and the angiotensin-converting enzyme inhibitor, Captopril, on metalloproteinase activity of murine Lewis-lung-carcinoma cells (3LL) in vitro, and on local growth and lung metastasis of the same tumor implanted intramuscularly in syngeneic C57BL/6 mice. The effect of BB-94 and Captopril on the survival of the 3LL-tumor-bearing mice was also examined. Here we report that Captopril treatment resulted in decreased transcription and protein levels of gelatinase A by 3LL cells. Both BB-94 and Captopril also prevented substrate degradation by gelatinase A and B released in conditioned medium by cultured cells. Treatment of tumor-bearing animals with BB-94 (i.p.) or Captopril (in drinking water) resulted in significant inhibition of the mean tumor volume (25 and 33% respectively) and of the mean lung metastasis number (26 and 29% respectively). When both agents were given, they acted in synergy, resulting in 51 and 80% inhibition of tumor growth and metastasis. The survival time of the mice treated with both BB-94 and Captopril was also significantly longer compared with the groups treated with each agent alone or with the vehicle. Our data support the hypothesis of an essential role of metalloproteinase(s) in the metastatic process. Moreover, blockade of invasion, angiogenesis and other processes mediated by metalloproteinases may underlie the anti-tumor and anti-metastatic effect of BB-94 and Captopril and their combination. It is conceivable that this combination could be tested in selected clinical conditions as an adjuvant modality to cytotoxic therapy. Int. J. Cancer 81:761–766, 1999. © 1999 Wiley-Liss, Inc.