HAEM5:Myelodysplastic neoplasm with increased blasts: Difference between revisions
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<blockquote class='blockedit'>{{Box-round|title=v4:Clinical Features|The content below was from the old template. Please incorporate above.}} | <blockquote class='blockedit'>{{Box-round|title=v4:Clinical Features|The content below was from the old template. Please incorporate above.}}</blockquote> | ||
The clinical features are often nonspecific and are generally related to the corresponding cytopenias such as anemia, thrombocytopenia and neutropenia. The recommended thresholds for cytopenia suggested by International Prognostic Scoring System (IPSS) (PMID: 22740453) include: | The clinical features are often nonspecific and are generally related to the corresponding cytopenias such as anemia, thrombocytopenia and neutropenia. The recommended thresholds for cytopenia suggested by International Prognostic Scoring System (IPSS) (PMID: 22740453) include: | ||
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*Platelet count: <100 x10<sup>9</sup>/L | *Platelet count: <100 x10<sup>9</sup>/L | ||
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==Sites of Involvement== | ==Sites of Involvement== | ||
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None | None | ||
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* Individual Region Genomic Gain/Loss/LOH | * Individual Region Genomic Gain/Loss/LOH | ||
* Characteristic Chromosomal Patterns | * Characteristic Chromosomal Patterns | ||
* Gene Mutations (SNV/INDEL)}} | * Gene Mutations (SNV/INDEL)}}</blockquote> | ||
*Diagnosis: 2-19% blasts in peripheral blood or 5-19% myeloblasts in bone marrow | *Diagnosis: 2-19% blasts in peripheral blood or 5-19% myeloblasts in bone marrow | ||
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*Therapeutic: Hematopoietic stem cell transplantation (HSCT) is the therapy of choice for MDS-EB in childhood with the best available donor<ref>{{Cite journal|last=Hasle|first=Henrik|date=2016-12-02|title=Myelodysplastic and myeloproliferative disorders of childhood|url=https://pubmed.ncbi.nlm.nih.gov/27913534|journal=Hematology. American Society of Hematology. Education Program|volume=2016|issue=1|pages=598–604|doi=10.1182/asheducation-2016.1.598|issn=1520-4383|pmc=6142519|pmid=27913534}}</ref>. Azacitidine, a DNA methyltransferase-inhibitor, has been reported to increase the overall survival for adult patients with high-risk MDS (MDS-REB) in comparison with conventional care<ref>{{Cite journal|last=Gore|first=Steven D.|last2=Fenaux|first2=Pierre|last3=Santini|first3=Valeria|last4=Bennett|first4=John M.|last5=Silverman|first5=Lewis R.|last6=Seymour|first6=John F.|last7=Hellström-Lindberg|first7=Eva|last8=Swern|first8=Arlene S.|last9=Beach|first9=Charles L.|date=2013-07|title=A multivariate analysis of the relationship between response and survival among patients with higher-risk myelodysplastic syndromes treated within azacitidine or conventional care regimens in the randomized AZA-001 trial|url=https://pubmed.ncbi.nlm.nih.gov/23585522|journal=Haematologica|volume=98|issue=7|pages=1067–1072|doi=10.3324/haematol.2012.074831|issn=1592-8721|pmc=3696610|pmid=23585522}}</ref>. | *Therapeutic: Hematopoietic stem cell transplantation (HSCT) is the therapy of choice for MDS-EB in childhood with the best available donor<ref>{{Cite journal|last=Hasle|first=Henrik|date=2016-12-02|title=Myelodysplastic and myeloproliferative disorders of childhood|url=https://pubmed.ncbi.nlm.nih.gov/27913534|journal=Hematology. American Society of Hematology. Education Program|volume=2016|issue=1|pages=598–604|doi=10.1182/asheducation-2016.1.598|issn=1520-4383|pmc=6142519|pmid=27913534}}</ref>. Azacitidine, a DNA methyltransferase-inhibitor, has been reported to increase the overall survival for adult patients with high-risk MDS (MDS-REB) in comparison with conventional care<ref>{{Cite journal|last=Gore|first=Steven D.|last2=Fenaux|first2=Pierre|last3=Santini|first3=Valeria|last4=Bennett|first4=John M.|last5=Silverman|first5=Lewis R.|last6=Seymour|first6=John F.|last7=Hellström-Lindberg|first7=Eva|last8=Swern|first8=Arlene S.|last9=Beach|first9=Charles L.|date=2013-07|title=A multivariate analysis of the relationship between response and survival among patients with higher-risk myelodysplastic syndromes treated within azacitidine or conventional care regimens in the randomized AZA-001 trial|url=https://pubmed.ncbi.nlm.nih.gov/23585522|journal=Haematologica|volume=98|issue=7|pages=1067–1072|doi=10.3324/haematol.2012.074831|issn=1592-8721|pmc=3696610|pmid=23585522}}</ref>. | ||
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==Individual Region Genomic Gain / Loss / LOH== | ==Individual Region Genomic Gain / Loss / LOH== | ||
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*Nonspecific cytogenetic abnormalities have been observed in 30-50% of MDS-EB cases. | *Nonspecific cytogenetic abnormalities have been observed in 30-50% of MDS-EB cases. | ||
*Gain of chromosome 8, del(5q) or t(5q), monosomy 7, del(7q), del(20q), complex karyotype<ref>{{Cite journal|last=Germing|first=Ulrich|last2=Strupp|first2=Corinna|last3=Kuendgen|first3=Andrea|last4=Isa|first4=Shadi|last5=Knipp|first5=Sabine|last6=Hildebrandt|first6=Barbara|last7=Giagounidis|first7=Aristoteles|last8=Aul|first8=Carlo|last9=Gattermann|first9=Norbert|date=2006-12|title=Prospective validation of the WHO proposals for the classification of myelodysplastic syndromes|url=https://pubmed.ncbi.nlm.nih.gov/17145595|journal=Haematologica|volume=91|issue=12|pages=1596–1604|issn=1592-8721|pmid=17145595}}</ref>. | *Gain of chromosome 8, del(5q) or t(5q), monosomy 7, del(7q), del(20q), complex karyotype<ref>{{Cite journal|last=Germing|first=Ulrich|last2=Strupp|first2=Corinna|last3=Kuendgen|first3=Andrea|last4=Isa|first4=Shadi|last5=Knipp|first5=Sabine|last6=Hildebrandt|first6=Barbara|last7=Giagounidis|first7=Aristoteles|last8=Aul|first8=Carlo|last9=Gattermann|first9=Norbert|date=2006-12|title=Prospective validation of the WHO proposals for the classification of myelodysplastic syndromes|url=https://pubmed.ncbi.nlm.nih.gov/17145595|journal=Haematologica|volume=91|issue=12|pages=1596–1604|issn=1592-8721|pmid=17145595}}</ref>. | ||
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==Characteristic Chromosomal Patterns== | ==Characteristic Chromosomal Patterns== | ||
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Gain of chromosome 8, del(5q) or t(5q), monosomy 7, del(7q), del(20q), complex karyotype | Gain of chromosome 8, del(5q) or t(5q), monosomy 7, del(7q), del(20q), complex karyotype | ||
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==Gene Mutations (SNV / INDEL)== | ==Gene Mutations (SNV / INDEL)== | ||
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Most frequent mutations: ''SRSF2, IDH1, IDH2, ASXL1, CBL, RUNX1, RAS'' | Most frequent mutations: ''SRSF2, IDH1, IDH2, ASXL1, CBL, RUNX1, RAS'' | ||
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None | None | ||
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==Epigenomic Alterations== | ==Epigenomic Alterations== | ||
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*''SRSF2'': involved in pre-mRNA splicing | *''SRSF2'': involved in pre-mRNA splicing | ||
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*''RAS'': involved in RAS/MAPK pathway | *''RAS'': involved in RAS/MAPK pathway | ||
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==Genetic Diagnostic Testing Methods== | ==Genetic Diagnostic Testing Methods== | ||
Revision as of 13:25, 10 February 2025
Haematolymphoid Tumours (WHO Classification, 5th ed.)
 | This page is under construction |
editContent Update To WHO 5th Edition Classification Is In Process; Content Below is Based on WHO 4th Edition ClassificationThis page was converted to the new template on 2023-12-07. The original page can be found at HAEM4:Myelodysplastic Syndrome (MDS) with Excess Blasts.
(General Instructions – The main focus of these pages is the clinically significant genetic alterations in each disease type. Use HUGO-approved gene names and symbols (italicized when appropriate), HGVS-based nomenclature for variants, as well as generic names of drugs and testing platforms or assays if applicable. Please complete tables whenever possible and do not delete them (add N/A if not applicable in the table and delete the examples); to add (or move) a row or column to a table, click within the table and select the > symbol that appears to be given options. Please do not delete or alter the section headings. The use of bullet points alongside short blocks of text rather than only large paragraphs is encouraged. Additional instructions below in italicized blue text should not be included in the final page content. Please also see Author_Instructions and FAQs as well as contact your Associate Editor or Technical Support)
Primary Author(s)*
Xiaoli Du, Ph.D; Teresa A. Smolarek, Ph.D, FACMG
Division of Human Genetics, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH, 45229, USA.
WHO Classification of Disease
| Structure | Disease |
|---|---|
| Book | Haematolymphoid Tumours (5th ed.) |
| Category | Myeloid proliferations and neoplasms |
| Family | Myelodysplastic neoplasms |
| Type | Myelodysplastic neoplasms, morphologically defined |
| Subtype(s) | Myelodysplastic neoplasm with increased blasts |
Definition / Description of Disease
Myelodysplastic syndrome (MDS) with excess blasts (EB) is a category of MDS characterized by <20% blasts in both peripheral blood and bone marrow. MDS-EB type 1 (MDS-EB-1) is classified as <5% blasts in the blood and <10% blasts in the bone marrow. MDS-EB type 2 (MDS-EB-2) is classified as 5-19% blasts in the blood and 10-19% blasts in the bone marrow with the presence of Auer rods[1][2]. The category of erythroid/myeloid-type acute erythroid leukemia in the 2008 WHO classification is now categorized as MDS-EB[3]. In addition, the majority of myelodysplastic syndrome with marrow fibrosis (MDS-F) belongs to myelodysplastic syndrome with excess blasts and fibrosis (MDS-EB-F)[4][5][6].
Synonyms / Terminology
Refractory anemia with excess blasts, erythroid/myeloid-type acute erythroid leukemia
Epidemiology / Prevalence
MDS-EB accounts for 40% of all cases of MDS (Arber DA, et al., (2016).)
- Occurs mainly in patients aged greater than 50 years old
Clinical Features
Put your text here and fill in the table (Instruction: Can include references in the table. Do not delete table.)
| Signs and Symptoms | EXAMPLE: Asymptomatic (incidental finding on complete blood counts)
EXAMPLE: B-symptoms (weight loss, fever, night sweats) EXAMPLE: Fatigue EXAMPLE: Lymphadenopathy (uncommon) |
| Laboratory Findings | EXAMPLE: Cytopenias
EXAMPLE: Lymphocytosis (low level) |
editv4:Clinical FeaturesThe content below was from the old template. Please incorporate above.
The clinical features are often nonspecific and are generally related to the corresponding cytopenias such as anemia, thrombocytopenia and neutropenia. The recommended thresholds for cytopenia suggested by International Prognostic Scoring System (IPSS) (PMID: 22740453) include:
- Hemoglobin concentration: <10 g/dL
- Absolute neutrophil count: <1.8 x109/L AND
- Platelet count: <100 x109/L
End of V4 Section
Sites of Involvement
Peripheral blood and bone marrow
Morphologic Features
The morphologic features of the peripheral blood and bone marrow are currently the gold standard for the diagnosis of MDS[3].
| Categories | Morphologic Features |
|---|---|
| Blood | Abnormalities in all three myeloid cell lines; blasts commonly present |
Bone marrow
|
Erythropoiesis: erythropoiesis increased, dyserythropoiesis: abnormally lobated nuclei, internuclear bridging |
| Granulopoiesis: dysplasia, nuclear hyposegmentation or hypersegmented nuclei or cytoplasmic hypogranularity | |
| Dysmegakaryopoiesis: micromegakaryocytes often seen; multiple widely separated nuclei also can occur |
Immunophenotype
Put your text here and/or fill in the table
| Finding | Marker |
|---|---|
| Positive (universal) | CD34 and/or KIT (CD117), CD38, HLA-DR and CD13 and/or CD33 |
| Positive (subset) | CD7 (20%), CD56 (10%) |
Chromosomal Rearrangements (Gene Fusions)
Put your text here and fill in the table
| Chromosomal Rearrangement | Genes in Fusion (5’ or 3’ Segments) | Pathogenic Derivative | Prevalence | Diagnostic Significance (Yes, No or Unknown) | Prognostic Significance (Yes, No or Unknown) | Therapeutic Significance (Yes, No or Unknown) | Notes |
|---|---|---|---|---|---|---|---|
| EXAMPLE: t(9;22)(q34;q11.2) | EXAMPLE: 3'ABL1 / 5'BCR | EXAMPLE: der(22) | EXAMPLE: 20% (COSMIC)
EXAMPLE: 30% (add reference) |
Yes | No | Yes | EXAMPLE:
The t(9;22) is diagnostic of CML in the appropriate morphology and clinical context (add reference). This fusion is responsive to targeted therapy such as Imatinib (Gleevec) (add reference). |
editv4:Chromosomal Rearrangements (Gene Fusions)The content below was from the old template. Please incorporate above.
None
End of V4 Section
editv4:Clinical Significance (Diagnosis, Prognosis and Therapeutic Implications).Please incorporate this section into the relevant tables found in:
- Chromosomal Rearrangements (Gene Fusions)
- Individual Region Genomic Gain/Loss/LOH
- Characteristic Chromosomal Patterns
- Gene Mutations (SNV/INDEL)
- Diagnosis: 2-19% blasts in peripheral blood or 5-19% myeloblasts in bone marrow
- Prognosis: Patients with MDS-EB-1 have a median survival of 16 months with 25% cases progressing to AML. While patients with MDS-EB-2 have a median survival of 9 months with 33% cases progressing to AML[7][8][9]. TP53, RUNX1 or ASXL1 mutations are associated with poor prognosis in MDS-EB with erythroid predominance[10][11].
- Therapeutic: Hematopoietic stem cell transplantation (HSCT) is the therapy of choice for MDS-EB in childhood with the best available donor[12]. Azacitidine, a DNA methyltransferase-inhibitor, has been reported to increase the overall survival for adult patients with high-risk MDS (MDS-REB) in comparison with conventional care[13].
End of V4 Section
Individual Region Genomic Gain / Loss / LOH
Put your text here and fill in the table (Instructions: Includes aberrations not involving gene fusions. Can include references in the table. Can refer to CGC workgroup tables as linked on the homepage if applicable. Do not delete table.)
| Chr # | Gain / Loss / Amp / LOH | Minimal Region Genomic Coordinates [Genome Build] | Minimal Region Cytoband | Diagnostic Significance (Yes, No or Unknown) | Prognostic Significance (Yes, No or Unknown) | Therapeutic Significance (Yes, No or Unknown) | Notes |
|---|---|---|---|---|---|---|---|
| EXAMPLE:
7 |
EXAMPLE: Loss | EXAMPLE:
chr7:1- 159,335,973 [hg38] |
EXAMPLE:
chr7 |
Yes | Yes | No | EXAMPLE:
Presence of monosomy 7 (or 7q deletion) is sufficient for a diagnosis of AML with MDS-related changes when there is ≥20% blasts and no prior therapy (add reference). Monosomy 7/7q deletion is associated with a poor prognosis in AML (add reference). |
| EXAMPLE:
8 |
EXAMPLE: Gain | EXAMPLE:
chr8:1-145,138,636 [hg38] |
EXAMPLE:
chr8 |
No | No | No | EXAMPLE:
Common recurrent secondary finding for t(8;21) (add reference). |
editv4:Genomic Gain/Loss/LOHThe content below was from the old template. Please incorporate above.
- Nonspecific cytogenetic abnormalities have been observed in 30-50% of MDS-EB cases.
- Gain of chromosome 8, del(5q) or t(5q), monosomy 7, del(7q), del(20q), complex karyotype[14].
End of V4 Section
Characteristic Chromosomal Patterns
Put your text here (EXAMPLE PATTERNS: hyperdiploid; gain of odd number chromosomes including typically chromosome 1, 3, 5, 7, 11, and 17; co-deletion of 1p and 19q; complex karyotypes without characteristic genetic findings; chromothripsis. Do not delete table.)
| Chromosomal Pattern | Diagnostic Significance (Yes, No or Unknown) | Prognostic Significance (Yes, No or Unknown) | Therapeutic Significance (Yes, No or Unknown) | Notes |
|---|---|---|---|---|
| EXAMPLE:
Co-deletion of 1p and 18q |
Yes | No | No | EXAMPLE:
See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference). |
editv4:Characteristic Chromosomal Aberrations / PatternsThe content below was from the old template. Please incorporate above.
Gain of chromosome 8, del(5q) or t(5q), monosomy 7, del(7q), del(20q), complex karyotype
End of V4 Section
Gene Mutations (SNV / INDEL)
Put your text here and fill in the table (Instructions: This table is not meant to be an exhaustive list; please include only genes/alterations that are recurrent and common as well as either disease defining and/or clinically significant. Can include references in the table. For clinical significance, denote associations with FDA-approved therapy (not an extensive list of applicable drugs) and NCCN or other national guidelines if applicable. Can also refer to CGC workgroup tables as linked on the homepage if applicable as well as any high impact papers or reviews of gene mutations in this entity. Do not delete table.)
| Gene; Genetic Alteration | Presumed Mechanism (Tumor Suppressor Gene [TSG] / Oncogene / Other) | Prevalence (COSMIC / TCGA / Other) | Concomitant Mutations | Mutually Exclusive Mutations | Diagnostic Significance (Yes, No or Unknown) | Prognostic Significance (Yes, No or Unknown) | Therapeutic Significance (Yes, No or Unknown) | Notes |
|---|---|---|---|---|---|---|---|---|
| EXAMPLE: TP53; Variable LOF mutations
EXAMPLE: EGFR; Exon 20 mutations EXAMPLE: BRAF; Activating mutations |
EXAMPLE: TSG | EXAMPLE: 20% (COSMIC)
EXAMPLE: 30% (add Reference) |
EXAMPLE: IDH1 R123H | EXAMPLE: EGFR amplification | EXAMPLE: Excludes hairy cell leukemia (HCL) (add reference).
|
Note: A more extensive list of mutations can be found in cBioportal (https://www.cbioportal.org/), COSMIC (https://cancer.sanger.ac.uk/cosmic), ICGC (https://dcc.icgc.org/) and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.
editv4:Gene Mutations (SNV/INDEL)The content below was from the old template. Please incorporate above.
Most frequent mutations: SRSF2, IDH1, IDH2, ASXL1, CBL, RUNX1, RAS
Other Mutations
None
End of V4 Section
Epigenomic Alterations
No
Genes and Main Pathways Involved
Put your text here and fill in the table (Instructions: Can include references in the table. Do not delete table.)
| Gene; Genetic Alteration | Pathway | Pathophysiologic Outcome |
|---|---|---|
| EXAMPLE: BRAF and MAP2K1; Activating mutations | EXAMPLE: MAPK signaling | EXAMPLE: Increased cell growth and proliferation |
| EXAMPLE: CDKN2A; Inactivating mutations | EXAMPLE: Cell cycle regulation | EXAMPLE: Unregulated cell division |
| EXAMPLE: KMT2C and ARID1A; Inactivating mutations | EXAMPLE: Histone modification, chromatin remodeling | EXAMPLE: Abnormal gene expression program |
editv4:Genes and Main Pathways InvolvedThe content below was from the old template. Please incorporate above.
- SRSF2: involved in pre-mRNA splicing
- IDH1/IDH2: involved in hypoxia pathways
- ASXL1: involved in chromatin remodeling
- CBL: involved in targeting substrates for degradation by the proteasome
- RUNX1: transcription factor for hematopoiesis cells
- RAS: involved in RAS/MAPK pathway
End of V4 Section
Genetic Diagnostic Testing Methods
- Quantification of dysplasia: Microscopy
- Pathology: Immunophenotyping by flow cytometry
- Genetics: Conventional karyotyping. Fluorescence in situ hybridization (FISH) analysis, microarray and sequencing
Familial Forms
No
Additional Information
No
Links
Put your links here (use link icon at top of page)
References
(use the "Cite" icon at the top of the page) (Instructions: Add each reference into the text above by clicking on where you want to insert the reference, selecting the “Cite” icon at the top of the page, and using the “Automatic” tab option to search such as by PMID to select the reference to insert. The reference list in this section will be automatically generated and sorted. If a PMID is not available, such as for a book, please use the “Cite” icon, select “Manual” and then “Basic Form”, and include the entire reference.)
- ↑ Greenberg, P.; et al. (1997-03-15). "International scoring system for evaluating prognosis in myelodysplastic syndromes". Blood. 89 (6): 2079–2088. ISSN 0006-4971. PMID 9058730.
- ↑ Germing, Ulrich; et al. (2006-01). "Refractory anaemia with excess of blasts (RAEB): analysis of reclassification according to the WHO proposals". British Journal of Haematology. 132 (2): 162–167. doi:10.1111/j.1365-2141.2005.05853.x. ISSN 0007-1048. PMID 16398650. Check date values in:
|date=(help) - ↑ 3.0 3.1 Arber DA, et al., (2016). WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues, revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J Editors. IARC Press: Lyon, France, p106-109.
- ↑ Lambertenghi-Deliliers, G.; et al. (1991-06). "Myelodysplastic syndrome with increased marrow fibrosis: a distinct clinico-pathological entity". British Journal of Haematology. 78 (2): 161–166. doi:10.1111/j.1365-2141.1991.tb04411.x. ISSN 0007-1048. PMID 1712222. Check date values in:
|date=(help) - ↑ Bae, E.; et al. (2013-12). "Differential diagnosis of myelofibrosis based on WHO 2008 criteria: acute panmyelosis with myelofibrosis, acute megakaryoblastic leukemia with myelofibrosis, primary myelofibrosis and myelodysplastic syndrome with myelofibrosis". International Journal of Laboratory Hematology. 35 (6): 629–636. doi:10.1111/ijlh.12101. ISSN 1751-553X. PMID 23693053. Check date values in:
|date=(help) - ↑ Orazi, Attilio (2007). "Histopathology in the diagnosis and classification of acute myeloid leukemia, myelodysplastic syndromes, and myelodysplastic/myeloproliferative diseases". Pathobiology: Journal of Immunopathology, Molecular and Cellular Biology. 74 (2): 97–114. doi:10.1159/000101709. ISSN 1015-2008. PMID 17587881.
- ↑ Germing, Ulrich; et al. (2006-12). "Prospective validation of the WHO proposals for the classification of myelodysplastic syndromes". Haematologica. 91 (12): 1596–1604. ISSN 1592-8721. PMID 17145595. Check date values in:
|date=(help) - ↑ Strupp, Corinna; et al. (2003-05). "Refractory anemia with excess of blasts in transformation: analysis of reclassification according to the WHO proposals". Leukemia Research. 27 (5): 397–404. doi:10.1016/s0145-2126(02)00220-5. ISSN 0145-2126. PMID 12620291. Check date values in:
|date=(help) - ↑ Amin, H. M.; et al. (2005-09). "Having a higher blast percentage in circulation than bone marrow: clinical implications in myelodysplastic syndrome and acute lymphoid and myeloid leukemias". Leukemia. 19 (9): 1567–1572. doi:10.1038/sj.leu.2403876. ISSN 0887-6924. PMID 16049515. Check date values in:
|date=(help) - ↑ Grossmann, V.; et al. (2013-09). "Acute erythroid leukemia (AEL) can be separated into distinct prognostic subsets based on cytogenetic and molecular genetic characteristics". Leukemia. 27 (9): 1940–1943. doi:10.1038/leu.2013.144. ISSN 1476-5551. PMID 23648669. Check date values in:
|date=(help) - ↑ Hasserjian, Robert P.; et al. (2010-03-11). "Acute erythroid leukemia: a reassessment using criteria refined in the 2008 WHO classification". Blood. 115 (10): 1985–1992. doi:10.1182/blood-2009-09-243964. ISSN 1528-0020. PMC 2942006. PMID 20040759.
- ↑ Hasle, Henrik (2016-12-02). "Myelodysplastic and myeloproliferative disorders of childhood". Hematology. American Society of Hematology. Education Program. 2016 (1): 598–604. doi:10.1182/asheducation-2016.1.598. ISSN 1520-4383. PMC 6142519. PMID 27913534.
- ↑ Gore, Steven D.; et al. (2013-07). "A multivariate analysis of the relationship between response and survival among patients with higher-risk myelodysplastic syndromes treated within azacitidine or conventional care regimens in the randomized AZA-001 trial". Haematologica. 98 (7): 1067–1072. doi:10.3324/haematol.2012.074831. ISSN 1592-8721. PMC 3696610. PMID 23585522. Check date values in:
|date=(help) - ↑ Germing, Ulrich; et al. (2006-12). "Prospective validation of the WHO proposals for the classification of myelodysplastic syndromes". Haematologica. 91 (12): 1596–1604. ISSN 1592-8721. PMID 17145595. Check date values in:
|date=(help)
Notes
*Primary authors will typically be those that initially create and complete the content of a page. If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome. *Citation of this Page: “Myelodysplastic neoplasm with increased blasts”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated 02/10/2025, https://ccga.io/index.php/HAEM5:Myelodysplastic_neoplasm_with_increased_blasts.