Epigenetic Reprogramming in Relapse/Refractory AML

  • STATUS
    Recruiting
  • participants needed
    24
  • sponsor
    Therapeutic Advances in Childhood Leukemia Consortium
Updated on 7 May 2021
remission
graft versus host disease
fludarabine
tacrolimus
cyclosporine
hydroxyurea
cytarabine
filgrastim
ejection fraction
granulocyte colony stimulating factor
decitabine
direct bilirubin
minimal residual disease
residual tumor
refractory acute myeloid leukemia (aml)
secondary acute myeloid leukemia
gemtuzumab
blast cells
colony stimulating factor
hematopoietic growth factors

Summary

This is a pilot study using decitabine and vorinostat before and during chemotherapy with fludarabine, cytarabine and G-CSF (FLAG).

Description

Decitabine is a demethylating agent and vorinostat is a HDAC inhibitor. The use of demethylating agents and HDAC inhibitors in combination have been previously shown to have synergistic effects in altering neoplastic pathways of cancer cells and be well tolerated in human clinical studies. With the ability of decitabine and vorinostat to alter the abnormal cellular pathways of leukemic blasts and essentially turn off anti-apoptotic proteins, the leukemia cells have become primed for cytotoxic cell kill via chemotherapeutic agents. This study will ask the question as to whether or not the combination of decitabine and vorinostat followed by chemotherapy is feasible and whether it can positively impact outcome in patients with relapsed or refractory acute myelogenous leukemia.

Details
Condition Acute myeloid leukemia, Acute Myelogenous Leukemia (AML), acute myelogenous leukemia, anll, acute myeloblastic leukemia
Treatment cytarabine, Fludarabine, Decitabine, Vorinostat, Filgrastim (G-CSF)
Clinical Study IdentifierNCT03263936
SponsorTherapeutic Advances in Childhood Leukemia Consortium
Last Modified on7 May 2021

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