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The concept of treatment personalization in cancer often means associating a drug with an actionable mutation.

Background: Currently approved therapies for myeloproliferative neoplasms (MPNs) are limited to cytoreductive agents such as hydroxyurea and the Jak1/2 inhibitor ruxolitinib.

The epitome of cancer treatment personalization is N=1 segmentation where a custom therapy is designed for every patient. 

Statins are potent competitive inhibitors of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase (HMGCR), a rate-limiting enzyme in the mevalonate pathway (cholesterol synthesis or isoprenoid pathway;

Ursolic acid (UA) is a pentacyclic triterpene acid present in many plants, including apples, basil, cranberries, and rosemary.

Background: The unique signature of a patient’s tumor implies that a one-size-fits-all treatment approach will likely fail. This necessitates a rationally designed personalized therapeutic approach employing N=1 segmentation.

Background: The Jak2-V617F mutation is frequently found in MPN. The bone marrow micro-environment of MPN patients constitutes high levels of TNFα, IFNγ and IL-6.

Glioblastoma (GBM) is an aggressive disease associated with poor survival.

Background: The unique signature of a patient’s tumor mandates the need to rationally design personalized therapies employing N=1 segmentation conceptually.

Recently, we developed an in silico simulation model to predict chemokine and cytokine responses of dendritic cells to pro-inflammatory stimulation.

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