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Clinical Trial Summary

Recent advances in hematology clearly illustrate that the simple "clonal" nature of various hematological malignancies may not really reflect the reality of malignant cells natural expansion. This has been nicely illustrated in recent works in AML for example where subclones coexists in the same patient at the same time, but could also differentially expand over time because of effects of therapeutics intervention, but also by oncogenic spontaneous events (1).

These observations have been done recently because of next generation sequencing that allows to discriminate in the same tumor samples, different subclones and to analyse the clonal architecture. Sequential analyses could help us to identify the first oncogenic event and to correlate disease progression to the emergence of subclones.

For all these reasons it is of a major interest to precisely understand the architecture of the clone in MPNs, especially to understand which is the initiating event and how from this initial event the clone develops.

In MPNs in which JAK2V617F is the initiating event, its targeting is expected to be extremely effective. If JAK2V617F is a secondary event its targeting might allow to alleviate the MPN, but may favor the development of other malignant hemopathies.


Clinical Trial Description

n/a


Study Design


Related Conditions & MeSH terms


NCT number NCT02260739
Study type Interventional
Source Gustave Roussy, Cancer Campus, Grand Paris
Contact Vincent RIBRAG, MD
Phone 0142114507
Email vincent.ribrag@gustaveroussy.fr
Status Recruiting
Phase N/A
Start date January 2014
Completion date January 2026

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