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The mechanism of action of acrylonitrile appears to involve oxidative stress and oxidative DNA damage. [21] Acrylonitrile increases cancer in high dose tests in male and female rats and mice [22] and induces apoptosis in human umbilical cord mesenchymal stem cells. [23]
As examples, DNA damaging effects have been reported for acrolein, [14] formaldehyde, [15] and acrylonitrile. [16] Breast cancer is the second most frequent cancer worldwide on a yearly basis [(1.38 million cases, 10.9% of all cancer cases), and ranks 5th as cause of death (458,000, 6.1% of all cancer deaths)]. [12]
Duvelisib is a Phosphoinositide 3-kinase inhibitor, specifically of the delta and gamma isoforms of PI3K. [9] This class of compounds works by preventing PI3K from playing its role in transducing signals from outside of cells into various intracellular pathways involved in cell cycle regulation, apoptosis, DNA repair, senescence, angiogenesis and cell metabolism, including the PI3K/AKT/mTOR ...
In vitro testing demonstrated that AOH1996 inhibited the growth and induced cell cycle arrest and apoptotic cell death in a wide variety of cancer cell lines, but had no effect on several normal, nonmalignant cell types. [6] [7] In mouse and dog animal models, there were no observed side effects or toxicity even at six times the effective dose. [3]
Nausea and vomiting are two of the most feared cancer treatment-related side effects for cancer patients and their families. In 1983, Coates et al. found that patients receiving chemotherapy ranked nausea and vomiting as the first and second most severe side effects, respectively.
Two distinct drug classes in which cardiotoxicity can occur are in anti-cancer and antiarrhythmic drugs. Anti-cancer drug classes that cause cardiotoxicity include anthracyclines, monoclonal antibodies, and antimetabolites. This form generally manifests as a progressive form of heart failure, but can also manifest as an harmful arrhythmia. [2]
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