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hydroquinone/sarcoma

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Protection of hydroquinone-induced apoptosis by downregulation of Fau is mediated by NQO1.

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The Fau gene (Finkel-Biskis-Reilly murine sarcoma virus (FBR-MuSV)-associated ubiquitously expressed gene) was identified as a potential tumor suppressor gene using a forward genetics approach. Downregulation of Fau by overexpression of its reverse sequence has been shown to inhibit apoptosis

Synthesis and antineoplastic activity of hydroquinone dialdehydes.

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A number of hydroquinone dialdehydes and structurally related compounds were synthesized and tested for antineoplastic efficacy against transplanted murine tumors. 3,6-Dihydroxy-4,5-dimethylphthalaldehyde,3,6-dihydroxy-4,5-dipropylphthalaldehyde, and 3,6-dihydroxy-4,5-dimethylphthalaldehyde
Our previous study shows that 6-O-acyl derivatives of L-ascorbic acid inhibits more markedly cell growth of mouse Ehrlich carcinoma than ascorbic acid. The present study shows that 6-O-palmitoyl ascorbic acid but not ascorbic acid prolongs the lifespan of mice into which tumors such as Meth A
An extract prepared from the fruit of Choerospondias axillaris exhibited differential cytotoxic effects when tested in a panel of pediatric cancer cell lines [Ewing sarcoma (A-673), rhabdomyosarcoma (SJCRH30), medulloblastoma (D283), and hepatoblastoma (Hep293TT)]. Bioassay-guided

Synthesis and antitumour activity of the Primin (2-methoxy-6-n-pentyl-1,4-benzoquinone) and analogues.

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Cancer is a serious worldwide health threat, killing almost seven million people per year. Quinones are an important class of antitumour agents that are activated by tumour hypoxia. Primin (2-methoxy-6-n-pentyl-1,4-benzo-quinone), a naturally-occurring product obtained from Primula obconica

Mode of action of the bioreductive alkylating agent, 2,3-bis(chloromethyl)-1,4-naphthoquinone.

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The bioreductive alkylating agent, 2,3-bis(chloromethyl)-1,4-napthoquinone (CMNQ), has been shown to inhibit the growth of Sarcoma 180 ascites cells in vivo. Evidence for the reductive activation of this agent via the mitochondrial respiratory chain was provided by CMNQ-induced oxidation of reduced
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