Myelodysplastic Syndrome With Excess Blasts

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Retrieved

2022-04-26

Source

Gard

Trials

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Genes

TET2, FANCB, CD34, RUNX1, CCR7, MECOM, KMT2A, EPO, GATA2, HPSE2, ACSL5, SF3B1, ACSL6, AKAP12, DLK1, CIP2A, IGHV1-12, ACHE, NSD1, VEGFA, DERL1, ATAD1, ASXL1, ILDR1, MIR29B1, MIR29B2, VIM2P, MOGS, SRSF2, U2AF1, THY1, BCL2, BCR, CBL, CDKN2B, CHEK1, CSF3, ETV6, FLT3, HLA-DRB1, ITGA2B, MCL1, NCAM1, NRAS, RARS1, BCHE, SPN, THPO, U2AF1L5

Drugs

2-hydroxymethyl-2-methoxymethyl-1-azabicyclo[2,2,2]octan-3-one, Allogeneic ex vivo expanded umbilical cord blood cells, Allogeneic multi-virus specific T lymphocytes targeting BK virus, cytomegalovirus, human herpesvirus-6, Epstein Barr virus and adenovirus, Arsenic trioxide ( Arsenic Trioxide Accord, Arsenic trioxide Mylan, Arsenic trioxide medac, TRISENOX ), Asunercept, Azacitidine ( AZACITIDINE ACCORD, AZACITIDINE BETAPHARM, AZACITIDINE CELGENE, AZACITIDINE MYLAN, VIDAZA ), Decitabine ( DACOGEN ), Fully human IgG1 antibody specific for CD33, Humanised IgG4 monoclonal antibody to the human toll-like receptor type 2, Imatinib mesilate ( GLEEVEC, GLIVEC, IMATINIB TEVA, IMATINIB TEVA B.V. ), Lenalidomide ( LENALIDOMIDE ACCORD, REVLIMID ), Lintuzumab, Luspatercept ( REBLOZYL ), Magrolimab, Mocetinostat, NEDD8-activating enzyme (NAE) inhibitor, Rigosertib, Sapacitabine, Sotatercept, Stem/progenitor cells derived from ex vivo expanded allogeneic umbilical cord blood cells, Thalidomide ( THALIDOMIDE CELGENE, THALOMID ), Val-Leu-Gln-Glu-Leu-Asn-Val-Thr-Val (Pr1 nanopeptide, sequence 169-177, of proteinase 3), haematopoietic stem cells and blood progenitors umbilical cord-derived expanded with (1R, 4R)-N1-(2-benzyl-7-(2-methyl-2H-tetrazol-5-yl)-9H-pyrimido[4,5-b]indol-4-yl)cyclohexane-1,4-diamine dihydrobromide dihydrate

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Myelodysplastic syndrome with excess blasts is a rare type of syndromes" target="_blank">myelodysplastic syndrome (MDS). In this type of MDS, the number of very early forms of blood cells (blasts) are increased in the bone marrow and/or blood. There is also a low numbers of at least one type of blood cell. The early forms of cell types in the bone marrow (red blood cells, white blood cells, or platelets) may or may not look abnormal (dysplasia) under the microscope. Signs and symptoms may include a very hard to treat and persistent anemia (refractory anemia), frequent infections (due to low numbers of neutrophils), easy bruising and bleeding (due to low number or abnormal platelets). MDS with excess blasts is one of the MDS most likely to turn into acute myeloid leukemia (AML). It is classified into 2 types, based on how many of the cells in the bone marrow or blood are blasts:

MDS-EB1: blasts make up 5% to 9% of the cells in the bone marrow, or 2% to 4% of the cells in the blood
MDS-EB2: blasts make up 10% to 19% of the cells in the bone marrow, or 5% to 19% of the cells in the blood; this type has a higher risk to become AML.

Some cases of MDS are linked to known risk factors (such as smoking, chemotherapy, having a genetic syndrome that increases the chance of developing MDS and other). These factors lead to changes in the DNA in bone marrow cells may cause MDS to develop, but most often, the cause is unknown. Treatment may include blood transfusions, supportive care, chemotherapy, radiotherapy and bone marrow transplant.[ 14773]