Vitro Study of Tigecycline to Treat Chronic Myeloid Leukemia
Changes of Mitochondrial Biogenesis and Metabolic Characteristics About Tigecycline to Treat Chronic Myeloid Leukemia in Vitro
1 other identifier
observational
100
1 country
1
Brief Summary
Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm companies with the BCR-ABL fusion gene encoded by the Philadelphia (Ph) chromosome. The BCR-ABL fusion protein(the formation of the chimeric gene BCR/ABL on chromosome 22 and a reciprocal ABL/BCR on chromosome 9,it has no expanded name) plays key role on CML leukemogenesis by activating its downstream signaling pathway of survival and proliferation. Imatinib, a targeted competitive inhibitor of a BCR-ABL tyrosine kinase, changed the clinical treatment and prognosis of CML. As its optimized generation, other tyrosine kinase inhibitors (TKIs), dasatinib and nilotinib have more potent anti-leukemic activity and less side-effect. However, acquired resistance to TKIs is one of the main obstacles to effective CML treatment and is involved in gene amplication of ABL tyrosine kinase point mutations. The outcomes of patients with these ABL tyrosine kinase point mutations have linked to worse prognosis and higher mortality generally. Metabolic adaptations are common in cancer cells, and cancer cells become more dependent on mitochondrial biogenesis. Tigecycline, as a broad-spectrum antibiotics, inhibits mitochondrial biogenesis as its an interesting "side-effect".In recent study,researchers indicated that tigecycline can eradicate cancer stem cells by targeting mitochondrial.Here, the investigators test tigecycline's anti-leukemic activity to chronic myeloid leukemia in vitro.
Trial Health
Trial Health Score
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participants targeted
Target at P50-P75 for all trials
1 active site
Health score is calculated from publicly available data and should be used for screening purposes only.
Trial Relationships
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Study Timeline
Key milestones and dates
First Submitted
Initial submission to the registry
August 19, 2016
CompletedFirst Posted
Study publicly available on registry
August 30, 2016
CompletedStudy Start
First participant enrolled
September 1, 2016
CompletedPrimary Completion
Last participant's last visit for primary outcome
September 1, 2021
CompletedAugust 30, 2016
August 1, 2016
5 years
August 19, 2016
August 24, 2016
Conditions
Keywords
Outcome Measures
Primary Outcomes (1)
mitochondrial biogenesis and metabolic characteristics of Bone Marrow(BM)/ Peripheral Blood(PB) mononuclear cells
Through study completion, an average of 1 year
Secondary Outcomes (3)
mitochondrial biogenesis and metabolic characteristics of BM/PB mononuclear cells after tigecycline stimulation
After Hour 24 and 48 tigecycline stimulation
cell viability and apoptosis of BM/PB mononuclear cells after tigecycline stimulation
After Hour 24 and 48 tigecycline stimulation
Patients' clinical characteristics and survival outcomes
Through study completion, an average of 1 year
Study Arms (2)
Patients with chronic myeloid leukemia
100 adult patients(age\>18 years),with chronic myeloid leukemia defined by the World Health Organization(WHO) criteria
Healthy volunteers
Healthy volunteers
Interventions
sampling after diagnosis and the mononuclear cells will be given tigecycline stimulation in vitro
Eligibility Criteria
100 adults patients with chronic myeloid leukemia
You may qualify if:
- Diagnosis of Philadelphia chromosome positive and/or BCR-ABL positive CML confirmed by cytogenetic and/or molecular analysis;
- Age \>18 years.
- Eligibility of patients receiving any medications or substances known to affect or determined following review of their case by the Principal Investigator
You may not qualify if:
- Patients may not receive any other antibiotics.
- Patients may not have received prior treatment with TKIs or hydroxyurea.
- Major cognitive deficits or psychiatric problems hampering a self-reported evaluation.
- No prior malignancies or any other cancer from which patient has been disease free for 5 years.
Contact the study team to confirm eligibility.
Sponsors & Collaborators
Study Sites (1)
Department of hematology,Nanfang Hospital
Guangzhou, Guangdong, 510515, China
Related Publications (2)
Lamb R, Ozsvari B, Lisanti CL, Tanowitz HB, Howell A, Martinez-Outschoorn UE, Sotgia F, Lisanti MP. Antibiotics that target mitochondria effectively eradicate cancer stem cells, across multiple tumor types: treating cancer like an infectious disease. Oncotarget. 2015 Mar 10;6(7):4569-84. doi: 10.18632/oncotarget.3174.
PMID: 25625193BACKGROUNDSkrtic M, Sriskanthadevan S, Jhas B, Gebbia M, Wang X, Wang Z, Hurren R, Jitkova Y, Gronda M, Maclean N, Lai CK, Eberhard Y, Bartoszko J, Spagnuolo P, Rutledge AC, Datti A, Ketela T, Moffat J, Robinson BH, Cameron JH, Wrana J, Eaves CJ, Minden MD, Wang JC, Dick JE, Humphries K, Nislow C, Giaever G, Schimmer AD. Inhibition of mitochondrial translation as a therapeutic strategy for human acute myeloid leukemia. Cancer Cell. 2011 Nov 15;20(5):674-88. doi: 10.1016/j.ccr.2011.10.015.
PMID: 22094260BACKGROUND
Biospecimen
mononuclear cells of bone marrow and/or peripheral blood
MeSH Terms
Conditions
Interventions
Condition Hierarchy (Ancestors)
Intervention Hierarchy (Ancestors)
Central Study Contacts
Study Design
- Study Type
- observational
- Observational Model
- COHORT
- Time Perspective
- PROSPECTIVE
- Sponsor Type
- OTHER
- Responsible Party
- PRINCIPAL INVESTIGATOR
- PI Title
- professor
Study Record Dates
First Submitted
August 19, 2016
First Posted
August 30, 2016
Study Start
September 1, 2016
Primary Completion
September 1, 2021
Last Updated
August 30, 2016
Record last verified: 2016-08