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NCT07471074: SLP-rares-CSM
Phenotypic and Functional Study of Bone Marrow Mesenchymal Stem Cells in Waldenström Macroglobulinemia
NA trial testing sample of bone marrow cells in Waldenström Macroglobuloinemia in 50 participants. Currently enrolling.
1 March 2028
Quick facts
| Lead sponsor | Centre Hospitalier Universitaire, Amiens |
|---|---|
| Phase | NA |
| Status | Recruiting now |
| Study type | INTERVENTIONAL |
| Allocation | non randomized |
| Design | parallel |
| Masking | none |
| Primary purpose | screening |
| Enrollment | 50 |
| Start date | 10 February 2026 |
| Primary completion | 1 March 2028 |
| Estimated completion | 1 March 2028 |
| Sites | 1 location across France |
Drugs / interventions tested
- sample of bone marrow cells
Conditions studied
- Waldenström Macroglobuloinemia — all drugs for Waldenström Macroglobuloinemia →
Sponsor
Centre Hospitalier Universitaire, Amiens
Who can join
18 and older, any sex, with Waldenström Macroglobuloinemia. Healthy volunteers can join.
What's being measured
Primary outcomes are the specific endpoints the trial is designed to prove or disprove.
-
Variation of transcriptome between both groups
Time frame: 2 years
Comparison of the transcriptome of MSCs from patients with WM with that of MSCs from healthy subjects
Sponsor's own description
Waldenström disease (WM) is defined by the presence of bone marrow lymphoplasmocytes and monoclonal immunoglobulin M (IgM). Treatment should be initiated in cases of cytopenia, tumor syndrome or when the physicochemical or immunological properties of IgM explain the occurrence of amyloidosis, cryoglobulin or neurological manifestations, which have already been extensively studied. The disease is characterized by a MYD88 emutation found in 90% of patients. However, the molecular landscape is complex: the other most frequent anomaly is a mutation in CXCR4, found in 30% of patients. This is a chronic, relapsing-remitting disease involving cells of the B lymphoid lineage, whose behavior is normally influenced by the presence of their specific target and signals from their environment. Indeed, around WM tumor cells, numerous lymphocyte population abnormalities have been reported (excess of atypical extra follicular B lymphocytes, decrease in naive B, T or NK populations, increase in certain suppressive subpopulations (Treg, TFH). In a mouse model, excess Tregs cells appear to interact with WM cells via the CD40/CD40ligand axis. Mast cells may also promote proliferation of WM malignant cells via the same axis. Myeloid and monocytic populations have an inflammatory profile. Furthermore, increased angiogenesis may counteract the effects of bone marrow hypoxia (which itself prevents WM cell proliferation and adhesion to mesenchymal cells). In addition, several cytokines probably play an important role: CXCL12, highly expressed in the marrow of WM patients, may play a role due to the high frequency of CXCR4 activating mutations. CXCL12 is also involved in the adhesion of WM cells to fibronectin. WM cells have increased expression of Very late antigen-4 (VLA4), which co-interacts with CXCR4 and promotes WM cell adhesion to medullary mesenchymal stem cells (MSCs) and endothelial cells. The CCL5/GLI2/IL6 axis also appears to be important. Other factors have also been suggested: Interleukin 21, Blys and abnormal angiogenic factors. MSCs could play an important role in these multiple cellular \& extracellular factors via CCL5, then IL6. CXCL12, activation of the Eph-B2-(expressed by WM cells) Ephrin B2 (expressed by MSCs) pathway. The role of MSCs and abnormalities in these cells has already been recognized in certain leukemias, leading to therapeutic strategies that are now envisaged to target not the neoplastic cell but its microenvironment. However, in WM, the interactions between these cells and the clonal cells of the disease remain unknown today. cellular factors via CCL5, then IL6. CXCL12, activation of the Eph-B2-(expressed by WM cells) Ephrin B2 (expressed by MSCs) pathway.
Publications & conference data
No peer-reviewed publications indexed yet for this trial.
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Verify against primary sources
- ClinicalTrials.gov — authoritative US registry record
- WHO ICTRP — international registry index
- EU Clinical Trials Register
- Sponsor press releases (Google)
- Trial protocol + status: ClinicalTrials.gov NCT07471074 (US National Library of Medicine, public domain)
- Drug + disease cross-links: matched in real time against Drug Landscape's normalised drug + company + condition tables
- Sponsor: as reported to ClinicalTrials.gov by Centre Hospitalier Universitaire, Amiens
- Last refreshed: 10 March 2026
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