Acute Promyelocytic LeukemiaNCT02991066
Role of Microparticles in the Coagulopathy of Acute Promyelocytic Leukemia
An observational study of Acute Promyelocytic Leukemia, run by First Affiliated Hospital of Harbin Medical University at 1 site in China.
Trial summary
Although the clinical application of differentiation therapy has made great success in the treatment of acute promyelocytic leukemia (APL), early fatal bleeding remains an unsolved problem which accounts for the main reason of induction failure in APL patients. Read more about this study
- Who is it for?
- Ages 18 years and olderHealthy volunteers can take part
- Conditions the study is for
- Acute Promyelocytic Leukemia
- How many people
- 20 participants
- Where
- 1 siteChina
- Study dates
- Oct 2014to Dec 2020
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Study population: patients with acute promyelocytic leukemia
Who may be able to join
- Patients with de novo APL accompanied by hemorrhage.
- The diagnosis was confirmed by the presence of t(15;17) and/or the PML (promyelocytic leukemia)/RARa(retinoic acid receptor alpha) fusion gene.
- Patients should receive single-agent arsenic trioxide (ATO) for induction therapy.
Who cannot join
- Patients with relapsed acute promyelocytic leukemia.
- Patients without evidence of bleeding.
- Patients younger than 18 years.
Trial locations and contacts
1 site in 1 country.
China1 site, 1 recruiting
- Recruiting
the First Affiliated Hospital of Harbin Medical University
Harbin, Heilongjiang, 150001
Jin Zhou, MD, PhD, 008645185555951, zhoujin1111@126.com
About this study
Although the clinical application of differentiation therapy has made great success in the treatment of acute promyelocytic leukemia (APL), early fatal bleeding remains an unsolved problem which accounts for the main reason of induction failure in APL patients. The clinical manifestation of both serious bleeding and thrombosis illustrate the complexity of the pathogenesis of coagulopathy in APL. Despite extensive research, the pathogenesis of coagulopathy in APL is still unclear. Microparticles, 0.11μm in diameter, are small membrane vesicles released to circulation by blood cells and vascular endothelial cells during activation or apoptosis. Microparticles (MPs) derived from different cells types all exert procoagulant activity mediated by phosphatidylserine (PS) and carry some basic substances derived from their origin cells. Also, the biological activity of microparticles is often significantly higher than that of the cells they come from. According to these problems and background knowledge, our project aims to observe the roles of microparticles derived from APL cells and the procoagulant or profibrinolytic activating factors resided on these microparticles in the pathogenesis of coagulopathy in APL, and the effects of different induction therapies, chemotherapeutic drugs or differentiation agents on these microparticles and their procoagulant or profibrinolytic activating factors. To carry out this study, microparticles are obtained from patients who undergo different induction therapies at different time points or from primary bone marrow APL cells which are treated by different drugs in vitro at different time points, the expressions and activities of five procoagulant or profibrinolytic activating factors, which are highly expressed in APL cells, PS exposure and the functional state of these microparticles, will be dynamically monitored. Further study of the pathogenesis of coagulopathy in APL can provide clues and help for deep understanding of clinical manifestations, guiding clinical treatment as well as judging prognosis, and establishing theoretical basis for exploring new treatment.
Read the detailed description
The investigators plan to measure routine laboratory parameters of coagulation and fibrinolysis, the procoagulant or profibrinolytic activity of microparticles (MPs), and explore the role of the procoagulant and profibrinolytic activating factor of MPs in the pathogenesis of coagulopathy in patients with APL.
- Dynamic turbidimetry of plasma clot formation. The effects of MPs on the kinetics of fibrin formation and on the optical properties of clots are studied using dynamic turbidimetry of re-calcified plasma samples (platelet-free plasma and microparticle-depleted plasma) without adding any clotting activator. Clotting of plasma samples induced by Ca2+ is followed by monitoring the optical density at λ = 405 nm at 37 °C. ii. Thrombin generation assay. The amount of thrombin formed in plasma upon re-calcification is measured directly using a modified thrombin generation test . Because fibrin interferes with colorimetric measurements, plasma samples are first defibrinated by adding reptilase followed by incubation at 37 °C. The clots are removed. Then a chromogenic substrate for thrombin is added to the plasma samples. Thrombin generation is started by adding CaCl2 with simultaneous recording of the absorbance at λ = 405 nm. iii. Thrombin generating capacity of the MPs. MPs are reconstituted in defibrinated (reptilase treated), normal pooled microparticle-depleted plasma. Then a chromogenic substrate for thrombin is added to the samples. Thrombin generation is started by adding CaCl2 with simultaneous recording of the absorbance at λ = 405 nm. iv. Thrombin generation inhibitory experiments. The following inhibitors are pre-incubated with the microparticles: Annexin V, anti-human tissue factor (TF) and irrelevant control immunoglobulin G (IgG). Then repeats the experiment iii.
- Fibrinolytic activity. Incubate a fixed concentration of plasminogen with the plasma samples in the presence of a chromogenic substrate selective for plasmin. Plasmin formed from plasminogen bound at the surface of microparticles cleaves the chromogenic substrate and the released p-nitroaniline is detected by measuring A405nm as a function of time. vi. Determination of fibrinolytic activity on microparticles. The capacity of microparticles to activate plasminogen is determined by incubating a fixed concentration of plasminogen (1mM) with the microparticles with or without t-PA and/or u-PA in the presence of a chromogenic substrate selective for plasmin. Plasmin formed from plasminogen bound at the surface of microparticles cleaves the chromogenic substrate and the released p-nitroaniline is detected by measuring A405nm. vii. Fibrinolytic activity inhibitory experiments. The following inhibitors are pre-incubated with the microparticles: anti-human tissue type plasminogen activator (tPA) , anti-human urokinase type plasminogen activator (uPA), and respective irrelevant control IgGs; ε-aminocaproic acid and plasminogen activator inhibitor-1 (PAI-1).Then repeat the experiment vi.
- Conditions
- Acute Promyelocytic Leukemia
- Keywords
- Acute promyelocytic leukemia, Coagulopathy, Microparticles, Mechanism
- Medical subject headings
- Leukemia, Promyelocytic, Acute, Hemostatic Disorders
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| Patients | patients with de novo acute promyelocytic leukemia with hemorrhage. | |
| Control | healthy volunteers. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Change From Baseline in the Levels and Cellular Origin of MPs at 5 Weeks
Demonstration that the some procoagulant or profibrinolytic activating factors expressed on MP in APL patients' plasma associate with the thrombin generating capacity and fibrinolytic activity of patients' plasma.
Measured: 5 weeks
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted13 Dec 2016 (estimated)
- Study startOct 2014
- Primary completionDec 2019 (estimated)
- Study completionDec 2020 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (14)Papers the sponsor has linked to this study.
- Other trials for Acute Promyelocytic LeukemiaStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Case-control
- Time perspective
- Prospective
- Enrolment
- 20 participants (estimated)
Sponsor and investigators
- Lead sponsor
- First Affiliated Hospital of Harbin Medical University
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Jin Zhou, MD, PhD, Study chair, First Affiliated Hospital of Harbin Medical University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02991066
- Sponsor's protocol ID
- 1309
- Status last verified
- Apr 2018
- First submitted
- 2 Mar 2016
- Last updated
- 24 Apr 2018
- Results posted
- No
- Data monitoring committee
- No
- Individual data sharing
- Yes
Publications
de la Serna J, Montesinos P, Vellenga E, Rayon C, Parody R, Leon A, Esteve J, Bergua JM, Milone G, Deben G, Rivas C, Gonzalez M, Tormo M, Diaz-Mediavilla J, Gonzalez JD, Negri S, Amutio E, Brunet S, Lowenberg B, Sanz MA. Causes and prognostic factors of remission induction failure in patients with acute promyelocytic leukemia treated with all-trans retinoic acid and idarubicin. Blood. 2008 Apr 1;111(7):3395-402. doi: 10.1182/blood-2007-07-100669. Epub 2008 Jan 14.
PubMed 18195095Jacomo RH, Melo RA, Souto FR, de Mattos ER, de Oliveira CT, Fagundes EM, Bittencourt HN, Bittencourt RI, Bortolheiro TC, Paton EJ, Bendlin R, Ismael S, Chauffaille Mde L, Silva D, Pagnano KB, Ribeiro R, Rego EM. Clinical features and outcomes of 134 Brazilians with acute promyelocytic leukemia who received ATRA and anthracyclines. Haematologica. 2007 Oct;92(10):1431-2. doi: 10.3324/haematol.10874.
PubMed 18024380Dally N, Hoffman R, Haddad N, Sarig G, Rowe JM, Brenner B. Predictive factors of bleeding and thrombosis during induction therapy in acute promyelocytic leukemia-a single center experience in 34 patients. Thromb Res. 2005;116(2):109-14. doi: 10.1016/j.thromres.2004.11.001. Epub 2005 Jan 12.
PubMed 15907524Breccia M, Avvisati G, Latagliata R, Carmosino I, Guarini A, De Propris MS, Gentilini F, Petti MC, Cimino G, Mandelli F, Lo-Coco F. Occurrence of thrombotic events in acute promyelocytic leukemia correlates with consistent immunophenotypic and molecular features. Leukemia. 2007 Jan;21(1):79-83. doi: 10.1038/sj.leu.2404377. Epub 2006 Aug 24.
PubMed 16932337Tapiovaara H, Alitalo R, Stephens R, Myohanen H, Ruutu T, Vaheri A. Abundant urokinase activity on the surface of mononuclear cells from blood and bone marrow of acute leukemia patients. Blood. 1993 Aug 1;82(3):914-9.
PubMed 8338954Menell JS, Cesarman GM, Jacovina AT, McLaughlin MA, Lev EA, Hajjar KA. Annexin II and bleeding in acute promyelocytic leukemia. N Engl J Med. 1999 Apr 1;340(13):994-1004. doi: 10.1056/NEJM199904013401303.
PubMed 10099141Liu Y, Wang Z, Jiang M, Dai L, Zhang W, Wu D, Ruan C. The expression of annexin II and its role in the fibrinolytic activity in acute promyelocytic leukemia. Leuk Res. 2011 Jul;35(7):879-84. doi: 10.1016/j.leukres.2010.11.008. Epub 2010 Dec 10.
PubMed 21146216Sinauridze EI, Kireev DA, Popenko NY, Pichugin AV, Panteleev MA, Krymskaya OV, Ataullakhanov FI. Platelet microparticle membranes have 50- to 100-fold higher specific procoagulant activity than activated platelets. Thromb Haemost. 2007 Mar;97(3):425-34.
PubMed 17334510Bach RR. Tissue factor encryption. Arterioscler Thromb Vasc Biol. 2006 Mar;26(3):456-61. doi: 10.1161/01.ATV.0000202656.53964.04. Epub 2006 Jan 5.
PubMed 16397140Hron G, Kollars M, Weber H, Sagaster V, Quehenberger P, Eichinger S, Kyrle PA, Weltermann A. Tissue factor-positive microparticles: cellular origin and association with coagulation activation in patients with colorectal cancer. Thromb Haemost. 2007 Jan;97(1):119-23.
PubMed 17200778Tesselaar ME, Romijn FP, Van Der Linden IK, Prins FA, Bertina RM, Osanto S. Microparticle-associated tissue factor activity: a link between cancer and thrombosis? J Thromb Haemost. 2007 Mar;5(3):520-7. doi: 10.1111/j.1538-7836.2007.02369.x. Epub 2006 Dec 13.
PubMed 17166244Biro E, Sturk-Maquelin KN, Vogel GM, Meuleman DG, Smit MJ, Hack CE, Sturk A, Nieuwland R. Human cell-derived microparticles promote thrombus formation in vivo in a tissue factor-dependent manner. J Thromb Haemost. 2003 Dec;1(12):2561-8. doi: 10.1046/j.1538-7836.2003.00456.x.
PubMed 14738565Pereira J, Alfaro G, Goycoolea M, Quiroga T, Ocqueteau M, Massardo L, Perez C, Saez C, Panes O, Matus V, Mezzano D. Circulating platelet-derived microparticles in systemic lupus erythematosus. Association with increased thrombin generation and procoagulant state. Thromb Haemost. 2006 Jan;95(1):94-9.
PubMed 16543967Kwaan HC, Rego EM. Role of microparticles in the hemostatic dysfunction in acute promyelocytic leukemia. Semin Thromb Hemost. 2010 Nov;36(8):917-24. doi: 10.1055/s-0030-1267045. Epub 2010 Nov 3.
PubMed 21049391
Study at a glance
From the registry record, last updated by the sponsor on 24 Apr 2018. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Role of Microparticles in the Coagulopathy of Acute Promyelocytic Leukemia
- ClinicalTrials.gov ID
- NCT02991066
- Acronym / sponsor ID
- 1309
- Conditions
- Acute Promyelocytic Leukemia
- Keywords
- Acute promyelocytic leukemia, Coagulopathy, Microparticles, Mechanism
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 20 participants (estimated)
- Lead sponsor
- First Affiliated Hospital of Harbin Medical UniversityUniversity, hospital or other
- Study start
- Oct 2014
- Primary completion
- Dec 2019 (estimated)
- Study completion
- Dec 2020 (estimated)
- First posted
- 13 Dec 2016 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Although the clinical application of differentiation therapy has made great success in the treatment of acute promyelocytic leukemia (APL), early fatal bleeding remains an unsolved problem which accounts for the main reason of induction failure in APL patients. The clinical manifestation of both serious bleeding and thrombosis illustrate the complexity of the pathogenesis of coagulopathy in APL. Despite extensive research, the pathogenesis of coagulopathy in APL is still unclear. Microparticles, 0.11μm in diameter, are small membrane vesicles released to circulation by blood cells and vascular endothelial cells during activation or apoptosis. Microparticles (MPs) derived from different cells types all exert procoagulant activity mediated by phosphatidylserine (PS) and carry some basic substances derived from their origin cells. Also, the biological activity of microparticles is often significantly higher than that of the cells they come from. According to these problems and background knowledge, our project aims to observe the roles of microparticles derived from APL cells and the procoagulant or profibrinolytic activating factors resided on these microparticles in the pathogenesis of coagulopathy in APL, and the effects of different induction therapies, chemotherapeutic drugs or differentiation agents on these microparticles and their procoagulant or profibrinolytic activating factors. To carry out this study, microparticles are obtained from patients who undergo different induction therapies at different time points or from primary bone marrow APL cells which are treated by different drugs in vitro at different time points, the expressions and activities of five procoagulant or profibrinolytic activating factors, which are highly expressed in APL cells, PS exposure and the functional state of these microparticles, will be dynamically monitored. Further study of the pathogenesis of coagulopathy in APL can provide clues and help for deep understanding of clinical manifestations, guiding clinical treatment as well as judging prognosis, and establishing theoretical basis for exploring new treatment.
Detailed description
The investigators plan to measure routine laboratory parameters of coagulation and fibrinolysis, the procoagulant or profibrinolytic activity of microparticles (MPs), and explore the role of the procoagulant and profibrinolytic activating factor of MPs in the pathogenesis of coagulopathy in patients with APL.
- Dynamic turbidimetry of plasma clot formation. The effects of MPs on the kinetics of fibrin formation and on the optical properties of clots are studied using dynamic turbidimetry of re-calcified plasma samples (platelet-free plasma and microparticle-depleted plasma) without adding any clotting activator. Clotting of plasma samples induced by Ca2+ is followed by monitoring the optical density at λ = 405 nm at 37 °C. ii. Thrombin generation assay. The amount of thrombin formed in plasma upon re-calcification is measured directly using a modified thrombin generation test . Because fibrin interferes with colorimetric measurements, plasma samples are first defibrinated by adding reptilase followed by incubation at 37 °C. The clots are removed. Then a chromogenic substrate for thrombin is added to the plasma samples. Thrombin generation is started by adding CaCl2 with simultaneous recording of the absorbance at λ = 405 nm. iii. Thrombin generating capacity of the MPs. MPs are reconstituted in defibrinated (reptilase treated), normal pooled microparticle-depleted plasma. Then a chromogenic substrate for thrombin is added to the samples. Thrombin generation is started by adding CaCl2 with simultaneous recording of the absorbance at λ = 405 nm. iv. Thrombin generation inhibitory experiments. The following inhibitors are pre-incubated with the microparticles: Annexin V, anti-human tissue factor (TF) and irrelevant control immunoglobulin G (IgG). Then repeats the experiment iii.
- Fibrinolytic activity. Incubate a fixed concentration of plasminogen with the plasma samples in the presence of a chromogenic substrate selective for plasmin. Plasmin formed from plasminogen bound at the surface of microparticles cleaves the chromogenic substrate and the released p-nitroaniline is detected by measuring A405nm as a function of time. vi. Determination of fibrinolytic activity on microparticles. The capacity of microparticles to activate plasminogen is determined by incubating a fixed concentration of plasminogen (1mM) with the microparticles with or without t-PA and/or u-PA in the presence of a chromogenic substrate selective for plasmin. Plasmin formed from plasminogen bound at the surface of microparticles cleaves the chromogenic substrate and the released p-nitroaniline is detected by measuring A405nm. vii. Fibrinolytic activity inhibitory experiments. The following inhibitors are pre-incubated with the microparticles: anti-human tissue type plasminogen activator (tPA) , anti-human urokinase type plasminogen activator (uPA), and respective irrelevant control IgGs; ε-aminocaproic acid and plasminogen activator inhibitor-1 (PAI-1).Then repeat the experiment vi.
Study design
- Observational model
- Case-control
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Patients | – | –patients with de novo acute promyelocytic leukemia with hemorrhage. |
| Control | – | –healthy volunteers. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
- Study population
- patients with acute promyelocytic leukemia
Key inclusion criteria (3 listed)
- Patients with de novo APL accompanied by hemorrhage.
- The diagnosis was confirmed by the presence of t(15;17) and/or the PML (promyelocytic leukemia)/RARa(retinoic acid receptor alpha) fusion gene.
- Patients should receive single-agent arsenic trioxide (ATO) for induction therapy.
Key exclusion criteria (3 listed)
- Patients with relapsed acute promyelocytic leukemia.
- Patients without evidence of bleeding.
- Patients younger than 18 years.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Change From Baseline in the Levels and Cellular Origin of MPs at 5 Weeks
Time frame: 5 weeks
Demonstration that the some procoagulant or profibrinolytic activating factors expressed on MP in APL patients' plasma associate with the thrombin generating capacity and fibrinolytic activity of patients' plasma.
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 24 Apr 2018.
- Background: PubMed 18195095de la Serna J, Montesinos P, Vellenga E, Rayon C, Parody R, Leon A, Esteve J, Bergua JM, Milone G, Deben G, Rivas C, Gonzalez M, Tormo M, Diaz-Mediavilla J, Gonzalez JD, Negri S, Amutio E, Brunet S, Lowenberg B, Sanz MA. Causes and prognostic factors of remission induction failure in patients with acute promyelocytic leukemia treated with all-trans retinoic acid and idarubicin. Blood. 2008 Apr 1;111(7):3395-402. doi: 10.1182/blood-2007-07-100669. Epub 2008 Jan 14.
- Background: PubMed 18024380Jacomo RH, Melo RA, Souto FR, de Mattos ER, de Oliveira CT, Fagundes EM, Bittencourt HN, Bittencourt RI, Bortolheiro TC, Paton EJ, Bendlin R, Ismael S, Chauffaille Mde L, Silva D, Pagnano KB, Ribeiro R, Rego EM. Clinical features and outcomes of 134 Brazilians with acute promyelocytic leukemia who received ATRA and anthracyclines. Haematologica. 2007 Oct;92(10):1431-2. doi: 10.3324/haematol.10874.
- Background: PubMed 15907524Dally N, Hoffman R, Haddad N, Sarig G, Rowe JM, Brenner B. Predictive factors of bleeding and thrombosis during induction therapy in acute promyelocytic leukemia-a single center experience in 34 patients. Thromb Res. 2005;116(2):109-14. doi: 10.1016/j.thromres.2004.11.001. Epub 2005 Jan 12.
- Background: PubMed 16932337Breccia M, Avvisati G, Latagliata R, Carmosino I, Guarini A, De Propris MS, Gentilini F, Petti MC, Cimino G, Mandelli F, Lo-Coco F. Occurrence of thrombotic events in acute promyelocytic leukemia correlates with consistent immunophenotypic and molecular features. Leukemia. 2007 Jan;21(1):79-83. doi: 10.1038/sj.leu.2404377. Epub 2006 Aug 24.
- Background: PubMed 8338954Tapiovaara H, Alitalo R, Stephens R, Myohanen H, Ruutu T, Vaheri A. Abundant urokinase activity on the surface of mononuclear cells from blood and bone marrow of acute leukemia patients. Blood. 1993 Aug 1;82(3):914-9.
- Background: PubMed 10099141Menell JS, Cesarman GM, Jacovina AT, McLaughlin MA, Lev EA, Hajjar KA. Annexin II and bleeding in acute promyelocytic leukemia. N Engl J Med. 1999 Apr 1;340(13):994-1004. doi: 10.1056/NEJM199904013401303.
- Background: PubMed 21146216Liu Y, Wang Z, Jiang M, Dai L, Zhang W, Wu D, Ruan C. The expression of annexin II and its role in the fibrinolytic activity in acute promyelocytic leukemia. Leuk Res. 2011 Jul;35(7):879-84. doi: 10.1016/j.leukres.2010.11.008. Epub 2010 Dec 10.
- Background: PubMed 17334510Sinauridze EI, Kireev DA, Popenko NY, Pichugin AV, Panteleev MA, Krymskaya OV, Ataullakhanov FI. Platelet microparticle membranes have 50- to 100-fold higher specific procoagulant activity than activated platelets. Thromb Haemost. 2007 Mar;97(3):425-34.
- Background: PubMed 16397140Bach RR. Tissue factor encryption. Arterioscler Thromb Vasc Biol. 2006 Mar;26(3):456-61. doi: 10.1161/01.ATV.0000202656.53964.04. Epub 2006 Jan 5.
- Background: PubMed 17200778Hron G, Kollars M, Weber H, Sagaster V, Quehenberger P, Eichinger S, Kyrle PA, Weltermann A. Tissue factor-positive microparticles: cellular origin and association with coagulation activation in patients with colorectal cancer. Thromb Haemost. 2007 Jan;97(1):119-23.
- Background: PubMed 17166244Tesselaar ME, Romijn FP, Van Der Linden IK, Prins FA, Bertina RM, Osanto S. Microparticle-associated tissue factor activity: a link between cancer and thrombosis? J Thromb Haemost. 2007 Mar;5(3):520-7. doi: 10.1111/j.1538-7836.2007.02369.x. Epub 2006 Dec 13.
- Background: PubMed 14738565Biro E, Sturk-Maquelin KN, Vogel GM, Meuleman DG, Smit MJ, Hack CE, Sturk A, Nieuwland R. Human cell-derived microparticles promote thrombus formation in vivo in a tissue factor-dependent manner. J Thromb Haemost. 2003 Dec;1(12):2561-8. doi: 10.1046/j.1538-7836.2003.00456.x.
- Individual participant dataSharing planned: Yes
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Jin Zhou, MD, PhD study chair
First Affiliated Hospital of Harbin Medical University
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Acute Promyelocytic Leukemia, run by First Affiliated Hospital of Harbin Medical University at 1 site in China.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 3 inclusion and 3 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 24 Apr 2018. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in China. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Jin Zhou, MD, PhD (008645185555951, zhoujin1111@126.com), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Change From Baseline in the Levels and Cellular Origin of MPs at 5 Weeks (time frame: 5 weeks). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT02991066, which also lists 14 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 24 Apr 2018.