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Preclinical and clinical development of new progesterone receptor antagonists with high receptor specificity for breast cancer treatment
Published in A. R. Genazzani, Hormone Replacement Therapy and Cancer, 2020
J. Hoffmann, H. Hess-Stumpp, R. B. Lichtner, U. Fuhrmann, G. Siemeister, M. R. Schneider
In intact control animals, progressive tumor growth was observed, whereas ovariectomy caused a complete tumor regression in 90% of the animals. A dose of 0.5 mg/kg of the progesterone antagonist ZK 230211 administered subcutaneously led to an inhibition of tumor growth, although this was not statistically significant. A maximal statistically significant growth inhibition was achieved with doses ≥ 2 mg/kg (Figure 4). In the group treated with 2 mg/kg, 50% of the animals showed complete tumor regression. Higher doses of ZK 230211 (5 and 10 mg/kg) resulted in tumor growth inhibition comparable to that with the dose of 2 mg/kg. Onapristone, a pure progesterone receptor antagonist, also showed a growth-inhibitory effect, but with no statistical significance at the dose used (5 mg/kg). Taken together, in the DMBA-induced mammary tumor model in the rat, ZK 230211 completely suppressed tumor growth in intact animals. At equal doses, the newer investigational drug ZK 230211 was distinctly more potent than onapristone.
Tissue injury and repair
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
It is important to recognize that there are also signals that inhibit cell proliferation. This is an important form of regulation when healing has occurred, e.g. in compensatory liver hyperplasia after hepatectomy, it is important that proliferation does not get out of control and is kept in check by inhibitory signals. There is less known about growth inhibition than proliferation, although it appears to be regulated through autocrine and paracrine means by growth factors such as TGF-β.
Microorganisms, Plants, and Lower Animals
Published in Stephen P. Coburn, The Chemistry and Metabolism of 4′-Deoxypyridoxine, 2018
Most of the studies to be discussed in this section were simply gross tests for growth inhibition. However, they provide some perspective on the breadth of organisms affected by deoxypyridoxine and in a few cases permit some generalizations.
Bacterial death from treatment with fluoroquinolones and other lethal stressors
Published in Expert Review of Anti-infective Therapy, 2021
We begin by distinguishing growth inhibition from killing (Figure 1). Growth inhibition is assayed with the stressor present, as with determination of minimal inhibitory concentration (MIC); killing is measured as bacterial survival after stressor removal. Some killing, an irreversible process, may occur during growth-inhibition measurements, but in those measurements killing cannot be distinguished from growth inhibition, which is reversible. This consideration is important, because bacteriostasis assays, such as the efficiency-of-plating test, are commonly interpreted in terms of killing. The two processes are also mechanistically distinct – mutations and chemicals exist that affect only killing. For example, during norfloxacin treatment a deficiency in catalase has no effect on MIC, but the deficiency lowers survival by 10–20 fold [7].
Chemopreventive Properties of Extracts Obtained from Blueberry (Vaccinium myrtillus L.) and Jabuticaba (Myrciaria cauliflora Berg.) in Combination with Probiotics
Published in Nutrition and Cancer, 2021
Augusto Tasch Holkem, Valérie Robichaud, Carmen Silvia Favaro-Trindade, Monique Lacroix
To select the best extracts to add the probiotics the antiproliferative test was carried out. Hepa 1c1c7 and HT-29 cells were seeded at a concentration of 2 × 104 cells/well of medium in a 96 well plate and incubated for 24 h, at 37 °C in 5% CO2. Then, the medium was removed and 100 μL of fresh medium containing 10 μL of serial concentrations of extracts were incubated for 48 h, as mentioned above. The medium was then replaced with 225 μL of fresh medium containing 25 μL of a 0.5% (w/v) solution of Thiazolyl blue tetrazolium bromide (MTT) followed by incubation for 4 h, at 37 °C in 5% CO2. Finally, the medium was carefully removed and replaced with 225 μL of DMSO containing 25 μL of Sorensen buffer (0.1 mol/L glycine and 0.1 mol/L NaCl at pH of 10.5). The microplate was read at 562 nm. Negative control and blank were used PBS and cell-free medium, respectively. Growth inhibition was calculated according to Fortin et al. (37):
Current therapeutical strategies for allergic rhinitis
Published in Expert Opinion on Pharmacotherapy, 2019
Ludger Klimek, Annette Sperl, Sven Becker, Ralph Mösges, Peter Valentin Tomazic
With regard to clinical efficacy, GCSs can effectively improve all nasal symptoms, including the often difficult-to-treat nasal obstruction and reduced sense of smell [9,12]. These agents are generally well tolerated but may have local side effects such as epistaxis, nasal dryness, and throat irritation. Systemic side effects, such as those feared during oral or parenteral administration of GCSs, are extremely rare. Growth inhibition in children has so far been demonstrated only during treatment with beclomethasone dipropionate [26]. Other potential but rare risks of long-term GCS use include nasal bleeding, septal perforation, candidiasis, headache, cataract, and suppression of the hypothalamic-pituitary axis [27]. Nevertheless, children should be regularly monitored during long-term treatment [9]. In contrast to antihistamines, GCSs show maximal efficacy after an interval of up to 1–3 weeks. Therapy must therefore be started early and applied regularly, and it should not be used ‘as needed’ [9]. Due to their good efficacy profile, nasal GCSs are the first choice in the treatment of AR [9].