View clinical trials related to Neoplasm, Residual.
Filter by:The AML-03 regimen investigates the addition of G-CSF priming to both induction and consolidation chemotherapies administrated in the previous AML-99 trial (NCT01716793) refines risk-stratification based on biological characterization also the AML-03 trial incorporates novel approaches for hematopoietic stem cell transplantation: such as Mylotarg™ "in vivo purging" in autografts, extends unrelated volunteers donors for allotransplants in high-risk patients, and introduces reduced intensity conditioning in patients with elder age (more than 50 years old). The aims of these modifications are to analyse eficacy and toxicity of this induction and consolidation therapy and to analyse the disease free survival in patients who achieved complete response following a risk adjusted therapy.
RATIONALE: Testing for minimal residual disease in blood samples from patients with acute lymphoblastic leukemia may help doctors plan better treatment. PURPOSE: This research trial studies a genetic test in detecting minimal residual disease in samples from younger patients registered on COG-AALL08B1 trial.
It is the study hypothesis that hypo-fractionated image-guided radiosurgery significantly improves pain relief compared to historic data of conventionally fractionated radiotherapy. Primary endpoint is pain response 3 months after radiosurgery, which is defined as pain reduction of ≥2 points at the treated vertebral site on the 0 to 10 Visual Analogue Scale. 60 patients will be included into this II trial.
RATIONALE: Testing for minimal residual disease in cell samples from patients with acute lymphoblastic leukemia may help doctors plan better treatment. PURPOSE: This research trial studies a genetic test in identifying previously undetectable minimal residual disease in cell samples from younger patients with acute lymphoblastic leukemia.
This is a 2 part study. The goal of the first part of this clinical research study is to find the highest tolerable dose of azacitidine that can be given with a TKI that you are already taking (such as Gleevec, Sprycel, or Tasigna). The safety of this drug will also be studied. The goal of the second part is to see if this combination may improve your response to the TKI you are already taking. Azacitidine is designed to change genes that are thought to cause leukemia. By changing these genes, the drug may help to stop them from causing the disease to grow.
Ceplene/IL-2 remission maintenance therapy has been shown to significantly prolong Leukemia Free Survival in patients with Acute Myeloid Leukemia (AML) in first complete remission. This is an international, multicenter, open-label study to evaluate the effects of remission maintenance therapy with Ceplene/IL-2 in adult patients with AML in CR1 on specific immune system cells (T and NK cells) and prospectively defined markers of immune response that are known to reflect T and NK cell ability to combat AML.
The purpose of this study is to study the MRD status after VELCADE based induction therapy (VELCADE, lenalidomide, dexamethasone or VELCADE, liposomal doxorubicin, dexamethasone) in patients with previously untreated multiple myeloma and study the impact of HDC and ASCT on MRD status post‐transplant. Our hypothesis is that MRD‐status will continue to increase significantly at 3 months post‐transplant and will validate that HDC and ASCT needs to be performed even when patients have achieved major response after induction therapy with novel agents.
The purpose of this study is to confirm whether the bispecific T cell engager blinatumomab (MT103) is effective, safe and tolerable in the treatment of ALL patients with minimal residual disease.
To determine if MRD (minimal residual disease) can be found in the blood (only) as opposed to bone marrow in children with ALL (acute lymphoblastic leukemia).
Although allogeneic stem cell transplantation is curative in CML, evidence of the BCR-ABL oncogene at low levels is still found in long-term follow-up of survivors. Such low levels of BCR-ABL post-transplant which do not fulfill criteria for molecular relapse are monitored regularly and considered to be suppressed by the GVL effect. Treatment with donor lymphocyte infusions is only instituted when quantifiable BCR-ABL transcript levels rise steadily, indicative of a true molecular relapse . Similarly, BCR-ABL is still detectable in the majority of CML patients treated with imatinib who achieve complete cytogenetic response, although the amount of BCR-ABL transcripts seem to decline with longer follow-up. With 5 years follow-up of CML patients at CP who received imatinib, the estimated cumulative best rates of complete hematologic response and complete cytogenetic response were 98 percent and 87 percent, respectively10. For the minority of CP-CML patients who do not respond satisfactorily to imatinib, second-generation tyrosine kinase inhibitors are now the recommended next line of treatment. A major question facing clinicians is whether imatinib and the other more pharmacologically potent second-generation tyrosine kinase inhibitors;can suppress the CML clone at the leukemic stem cell level as effectively as allogeneic stem cell transplantation. This protocol is designed to scientifically compare the treatment responses of patients who are treated with allogeneic stem cell transplantation with patients who receive imatinib or second generation tyrosine kinase inhibitors. The primary endpoint of this trial will be the proportion of patients who have detected minimal residual disease (DMRD) in primitive CD34 plus progenitor subpopulations no earlier than 60 days from the onset of their respective treatments.