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By selectively targeting caPCNA, it may be possible to kill cancer cells without affecting healthy tissues. [5] 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.
The p53 upregulated modulator of apoptosis (PUMA) also known as Bcl-2-binding component 3 (BBC3), is a pro-apoptotic protein, member of the Bcl-2 protein family. [5] [6] In humans, the Bcl-2-binding component 3 protein is encoded by the BBC3 gene. [5] [6] The expression of PUMA is regulated by the tumor suppressor p53.
Aspartate transaminase (AST) or aspartate aminotransferase, also known as AspAT/ASAT/AAT or (serum) glutamic oxaloacetic transaminase (GOT, SGOT), is a pyridoxal phosphate (PLP)-dependent transaminase enzyme (EC 2.6.1.1) that was first described by Arthur Karmen and colleagues in 1954.
Cancer gene therapy was introduced in 1992/93 (Trojan et al. 1993). [167] The treatment of glioblastoma multiforme, the malignant brain tumor whose outcome is always fatal, was done using a vector expressing antisense IGF-I RNA (clinical trial approved by NIH protocol no.1602 24 November 1993, [168] and by the FDA in 1994). This therapy also ...
The precise mechanism by which altretamine exerts its anti-cancer effect is unknown but it is classified by MeSH as an alkylating antineoplastic agent. [ 5 ] This unique structure is believed to damage tumor cells through the production of the weakly alkylating species formaldehyde , a product of CYP450 -mediated N -demethylation .
It has been the perfect cure in this case. [2] The active component responsible for the tumoricidal activity was found in 2000 and found to be a complex of alpha-lactalbumin and oleic acid. [3] Endogenous human alpha-lactalbumin is complexed with a calcium ion and serves as a cofactor in lactose synthesis, but has no tumoricidal properties. The ...
However, favorable results in studies with monkeys and in vitro human cells allowed testing to continue in humans. [ 47 ] [ 48 ] [ 49 ] The first clinical trial of Gleevec took place in 1998, after Novartis reluctantly synthesized and released a few grams of the drug for Druker, enough for him to run a trial using a hundred or so patients. [ 50 ]
In another study, Yamanaka reported that one can create iPSCs without the oncogene c-Myc. The process took longer and was not as efficient, but the resulting chimeras did not develop cancer. [39] Inactivation or deletion of the tumor suppressor p53, which is a key regulator of cancer, significantly increases reprogramming efficiency. [40]