Sentence examples for most cytotoxic anticancer from inspiring English sources
Most cytotoxic anticancer therapies are encumbered by the development of acquired resistance of cancer cells.
Most cytotoxic anticancer drugs exert their effects under the involvement of p53 activation if the functional gene is expressed, which is the case in about 50% of all tumours.
While most cytotoxic anticancer drugs including alkylating agents such as TMZ have been shown to induce apoptosis [ 52], cancer cells could potentially be targeted by other death mechanisms such as necrosis, autophagy, senescence, or mitotic catastrophe [ 53].
Overexpression of antiapoptotic Bcl-2 or Bcl-xL probably occurs in more than half of all cancers [ 34], rendering tumor cells resistant to myriad apoptotic stimuli, including most cytotoxic anticancer drugs.
This impacts false positive selection when drugs are more effective in 2D than in 3D [ 13, 14], resulting in promising early drug leads failing to perform in animal models because most cytotoxic anticancer drugs are less effective in killing tumor cells within multicellular tissues than as grown as monolayer cultures [ 15].
Also, it is remarkable that most of the cytotoxic anticancer drugs belong to the BCS class IV which comprises substances with both low solubility in aqueous fluids and low apparent permeability [ 3].
Most of the presently available cytotoxic anticancer drugs mediate their effect via apoptosis in cancer cells [ 34].
One of these isolates, 10′(Z),13′(E),15′(E -heptadecatrienylhydroquinone [HQ17(3)], bE -heptadecatrienylhydroquinoneosen for studying the anticancer mechanism of these compounds.
Indeed, the vast majority of cytotoxic anticancer agents (including ionizing radiation, most chemotherapeutic agents, and some targeted therapies) work through the generation of ROS either directly or indirectly [ 34].
The enediyne natural products are the most cytotoxic molecules in existence today, and their use as anticancer drugs has been demonstrated clinically.
Because Bcl-2 antisense enhances sensitivity to cytotoxic anticancer drugs in vitro and in xenograft models, most clinical trials combine the antisense agent with conventional chemotherapy.
