Trials / Unknown
UnknownNCT04991532
Dasatinib Down-regulates the Expression of PD-1 and Enhances Killing pH + Leukemia Stem Cells
Research on the Mechanism of Dasatinib Down-regulates the Expression of PD-1 in CMV-activated NKG2C+NK Cells and Enhances Killing pH + Leukemia Stem Cells.
- Status
- Unknown
- Phase
- —
- Study type
- Observational
- Enrollment
- 324 (estimated)
- Sponsor
- Nanfang Hospital, Southern Medical University · Academic / Other
- Sex
- All
- Age
- 18 Years – 65 Years
- Healthy volunteers
- Not accepted
Summary
Research on the mechanism of dasatinib down-regulates the expression of PD-1 in CMV-activated NKG2C+NK cells and enhances killing pH + leukemia stem cells.
Detailed description
Some patients with CML can withdraw from TKIs after treatment, and the mechanism might be related to the effect of memory NK cells on anti-Ph+ leukemic stem cells (LSCs). Dasatinib affects immune through several pathways including the expression of PD1 in immune cells. Our previous work showed increased NKG2C+ NK cells were found in cases with CMV-DNA+ who suffered Ph+ leukemia and received Dasatinib, and these memory NK cells have anti-LSCs activity. We hypothesize that: CMV infection activates NKG2C+ memory NK cells proliferation; Dasatinib down-regulates the expression of PD1 in PD1+NKG2C+ NK cell subsets and then enhances anti-LSCs activity of these cells. In this study, the effect of Dasatinib on CMV-activated NKG2C+ cell subsets and its mechanism will be studies. Besides, the different NKG2C+ cell subsets on LSCs will be compared. This study might be helpful to clarify the mechanism of TKI withdrawal and to offer foundation for CMV and Ph+ ALL treatment strategies
Conditions
Interventions
| Type | Name | Description |
|---|---|---|
| OTHER | — |
Timeline
- Start date
- 2021-06-20
- Primary completion
- 2022-10-01
- Completion
- 2022-12-01
- First posted
- 2021-08-05
- Last updated
- 2021-08-05
Locations
1 site across 1 country: China
Source: ClinicalTrials.gov record NCT04991532. Inclusion in this directory is not an endorsement.