An interventional study of Monocytes signatures in myeloproliferative neoplasms at diagnosis in Myeloproliferative Neoplasm, Polycythemia Vera and Essential Thrombocythemia, sponsored by University Hospital, Angers. Recruiting at 3 sites in France. Open to participants aged 18 Years and older. Per ClinicalTrials.gov, last updated 2026-10-29.
Sponsored by University Hospital, Angers · Not applicable, Interventional, and Diagnostic
Prospective study for functional and phenotypic characterization of monocytes in philadelphia-negative myeloproliferative neoplasms
Philadelphia-negative myeloproliferative neoplasms (MPN) are clonal disorders of the hematopoietic stem cell characterized by an excessive production of mature myeloid cells. MPNs are characterized by the presence of somatic gain-of-function mutations present in more than 80% of cases and affecting JAK2, CALR or MPL genes. These mutations lead to a constitutive activation of the JAK-STAT signaling pathway at the origin of cell proliferation.
MPN include polycythemia vera (PV), essential thrombocythemia (ET), prefibrotic primary myelofibrosis (pre-PMF), and primary myelofibrosis (PMF). Despite the classification of MPNs into distinct subtypes based on clinical and pathological features, the precise mechanisms underlying the phenotypic diversity within these disorders remain poorly understood. One aspect that has received limited attention is the role of monocytes and macrophages, key components of the innate immune system, in MPN pathogenesis.
Monocytes, circulating precursors of tissue-resident macrophages, play essential roles in inflammation, immune surveillance, and tissue repair. Upon recruitment to tissues, monocytes differentiate into macrophages with diverse phenotypes and functions influenced by local microenvironmental cues. Macrophages, in turn, exhibit a spectrum of activation states ranging from pro-inflammatory (M1) to anti-inflammatory or pro-repair (M2), with implications for various physiological and pathological processes. Recent studies have implicated monocytes and macrophages in the pathogenesis of MPNs. Circulating monocytes in MPN patients display altered functional characteristics, including dysregulated cytokine production and enhanced fibrotic potential. Additionally, monocytosis, an elevated monocyte count, has been identified as an adverse prognostic factor in MPNs, particularly in PMF.
Based on these observations, investigator propose that monocytes and macrophages contribute to the phenotypic expression of MPNs and that distinct phenotypic and functional signatures of these cells may be associated with different MPN subtypes. By leveraging available techniques for genetic and functional analysis, study team aims to elucidate the role of monocytes and macrophages in MPN pathogenesis and identify potential biomarkers associated with disease phenotype and prognosis. Through comprehensive characterization of these immune cell populations, investigator seek to gain insights into the underlying mechanisms driving the heterogeneity of MPNs and identify novel therapeutic targets for precision medicine approaches.
667 studies on the registry are indexed under Myeloproliferative Disorders; 110 are open to participants now.
This study's planned enrollment of 70 is above the median of 47 across 462 interventional studies indexed under Myeloproliferative Disorders.
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Exclusion Criteria:
Diagnostic Test: Monocytes signatures in myeloproliferative neoplasms at diagnosis
The monocytes signatures will be perform from a peripheral blood sample. The signature will be derived from (i) surface marker expression, (ii) cytokines profiles, (iii) genes expression.
WHO 2016 criteria for polycythemia vera, prefibrotic myelofibrosis, essential thrombocytosis and overt myelofibrosis diagnosis
Assessment of the monocytic signature against the WHO diagnosis (AUC will be determined)
Time frame: Day 0
Identify correlation between the monocytic signature and driver mutations (mutation in JAK2, CALR or MPL gene).
The monocytic signature will be derived from surface marker expression, cytokines profile and genes expression using a principal component analysis
Time frame: 24 months
Identify correlation between the monocytic signature and the grade of fibrosis
The monocytic signature will be derived from surface marker expression, cytokines profile and genes expression using a principal component analysis The monocytic signature will be compared between the different stages of fibrosis (WHO definition for fibrosis grading)
Time frame: 24 months
prognostic value of the monocytic signature using a principal component analysis Response criteria according to Barosi et al., Leukemia, vol. 29,1 (2015): 20-6
Evaluate the prognostic value of the monocytic signature for treatment response The monocytic signature will be derived from surface marker expression, cytokines profile and genes expression using a principal component analysis Response criteria according to Barosi et al., Leukemia, vol. 29,1 (2015): 20-6 : * Complete response: normal blood counts * Partial response: platelets between 400 and 600 G/L * No response: absence of complete or partial response
Time frame: 12, 24 months
Prognostic value of the monocyte signature for disease worsening according to Sureau et al., Blood Cancer Journal, vol. 12,4, 56. 8 Apr. 2022
Evaluate the prognostic value of the monocyte signature for disease worsening The monocytic signature will be derived from surface marker expression, cytokines profile and genes expression using a principal component analysis Disease worsening criteria according to Sureau et al., Blood Cancer Journal, vol. 12,4, 56. 8 Apr. 2022): \- Worsening is defined by the presence of at least one of the following criteria: i) leukocytosis \>12 G/L or presence of immature granulocytes \>2% or erythroblasts \>1%; (ii) anemia (hemoglobin \<12 g/dL in a woman or \<13 g/dL in man) not related to treatment toxicity; (iii) thrombocytopenia (platelet count \<150G/L) not related to treatment toxicity; (iv) onset of splenomegaly or progression of pre-existing splenomegaly; (v) thrombocytosis despite cytoreductive therapy
Time frame: 24 months
leukemia-free survival
The monocytic signature will be derived from surface marker expression, cytokines profile and genes expression using a principal component analysis Outcome measure : leukemia-free survival and myelofibrosis-free survival Evaluate the prognostic value of the monocytic signature for hematological progression (acute myeloid leukemia or myelofibrosis)
Time frame: 24 months
myelofibrosis-free survival
The monocytic signature will be derived from surface marker expression, cytokines profile and genes expression using a principal component analysis Outcome measure : leukemia-free survival and myelofibrosis-free survival Evaluate the prognostic value of the monocytic signature for hematological progression (acute myeloid leukemia or myelofibrosis)
Time frame: 24 months
Monocytes parameters for hematological progression
Evaluate the prosnostic value of monocytes parameters for hematological progression Hematological free survival wil be evaluated by cox models
Time frame: 24 months
Plan to share: Undecided
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