Molecular therapy for Inflammation-mediated cancers: ING1b increases the expression of oncogenic suppressor PTX3 and inhibits complement-dependent inflammation via down regulation of its target gene, 13/March/2015, 12.25 pm

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A recent study from the Humanitas Clinical and Research Center, Rozzano (Milan) 20089, Italy shows that “PTX3 Is an Extrinsic Oncosuppressor Regulating Complement-Dependent Inflammation in Cancer.” This study was published in the 12 February  2015 issue of the Journal “Cell” [I.F:33] by Drs. Alberto Mantovani , Eduardo Bonavita and others.

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Molecular therapy for Inflammation-mediated cancers: ING1b increases the expression of oncogenic suppressor PTX3 and inhibits complement-dependent inflammation via down regulation of its target gene. Thus, pharmacological formulations encompassing “ING1b activators” may be used to treat patients suffering from inflammation-mediated tumorigenesis.

Idea Proposed/Formulated byDr L Boominathan Ph.D.

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To citeBoominathan,  Molecular therapy for Inflammation-mediated cancers: ING1b increases the expression of oncogenic suppressor PTX3 and inhibits complement-dependent inflammation via down regulation of its target gene, 13/March/2015,  12.25 pm,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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Undisclosed information: How ING1b increases the expression of PTX3

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