Myelodysplastic Syndromes

Myelodysplastic syndromes (MDS) are clonal hematopoietic malignancies, characterized by ineffective hematopoiesis, cytopenia, unilineage or multilineage dysplasia, with increased susceptibility to acute myeloid leukemia (AML).

Cytogenetic studies play a key role in the evaluation of patients with MDS; study results are used to establish a diagnosis, stratify patients into prognostic groups, guide medical management, and monitor disease progression. Clonal abnormalities are observed in ~50% of cases evaluated by metaphase cytogenetic analysis and in up to 80% of cases evaluated by cytogenomic single nucleotide polymorphism (SNP) microarray.

Key Points

Cytogenetic Testing for MDS

Patients who may have clonal genetic abnormalities that can be detected by cytogenomic SNP microarray include normal karyotype, suboptimal (<20) normal metaphases, or failed metaphase chromosome study. Cytogenomic SNP microarray testing can detect copy-number alterations and copy-neutral loss of heterozygosity (LOH), which are often due to mutations and subsequent selection of mutant tumor-suppressor genes and oncogenes. Most MDS-related copy-number alterations identified by cytogenomic SNP microarray may be monitored by fluorescence in situ hybridization (FISH).

  Conventional Cytogenetics (Karyotype) Fluorescence in situ Hybridization Cytogenomic Microarray Testing
Suggested Use Diagnosis, prognosis

May increase diagnostic sensitivity in MDS if metaphase cytogenetic study is suboptimal (<20 normal metaphases) or fails

Use to clarify findings from an abnormal karyotype

  • ​Do not use FISH for MDS-related abnormalities on bone marrow samples obtained for cytopenias when an adequate conventional karyotype is obtained (Choosing Wisely, American Society for Clinical Pathology, 2016)

Use to establish and/or monitor for abnormal clone

Complements conventional cytogenetic methods

Detects copy-number alterations (loss/gain of DNA) and LOH

Only method that can identify MDS-associated LOH (eg, uniparental disomies like UPD7q, UPD11q, and UPD17p)

A more comprehensive analysis of myeloid-associated genomic alterations may be obtained through combined analysis of copy-number, LOH, and somatic mutations using cytogenomic microarray combined with next generation sequencing

Limitations

G-banded metaphase chromosome analysis has limited resolution

May fail to identify subtle abnormalities

Cannot identify cryptic (sequence-level) alterations or LOH

Complex rearrangements or uncertainty of additional genomic material may require further clarification by molecular methods

Success rate dependent on growth of tumor cells in culture

Standard MDS FISH panels are unlikely to increase diagnostic sensitivity when complete (20 cell) metaphase cytogenetic study is normal

Chromosome alterations outside FISH probe region are not detected

Cannot detect LOH

Microarray will detect only copy-number alterations and LOH

Microarray cannot detect balanced genomic rearrangements such as translocations, inversions, or balanced insertions, and may not detect low-level mosaicism (<15-20%)

ARUP Tests

Chromosome Analysis, Bone Marrow with Reflex to Genomic Microarray 2007130

Chromosome Analysis, Bone Marrow 2002292

Myelodysplastic Syndrome (MDS) Panel by FISH 2002709

Acute Myelogenous Leukemia (AML) with Myelodysplastic Syndrome (MDS), or Therapy-Related AML, by FISH 2002653

Cytogenomic SNP Microarray-Oncology 2006325

​Myeloid Malignancies Somatic Mutation and Copy Number Analysis Panel 2012182

Sources: Cazzala, 2011; Shih, 2011; Simons, 2012; Tiu, 2011; Coleman, 2011

Diagnosis

Indications for Testing

Abnormal CBC or peripheral smear in the absence of obvious etiology – cytopenias and dysplastic cells in peripheral smear are most common.

Laboratory Testing

  • Initial testing
    • CBC with differential and morphology
  • Testing to rule out other etiologies in suspected myelodysplastic syndromes (MDS) (see Differential Diagnosis section)
    • Reticulocyte count
    • Vitamin B12
    • Iron studies (including iron, total iron binding capacity, and ferritin)
    • Haptoglobin
    • Direct Coombs
    • C-reactive protein
    • Hepatic function panel (including alanine transaminase, aspartate transaminase, bilirubin, and alkaline phosphatase)
    • Albumin
    • Uric acid
    • Creatinine
    • Serum protein electrophoresis (serum immunoglobulins)
    • Lactate dehydrogenase
    • Beta-2 microglobulin
    • Blood group and antibody screen
    • Serology for hepatitis B, C, and HIV
    • Parvovirus B19, cytomegalovirus (CMV) (European Leukemia Net [ELN], 2013)
    • Paroxysmal nocturnal hemoglobinuria
    • Specific genetic analysis for individuals with suspected inherited condition

Histology

  • Classification based on peripheral smear, bone marrow histology, and cytogenetic testing
    • Bone marrow biopsy – diagnosis almost exclusively made using marrow appearance
      • Criteria – dysplasia in ≥10% of myeloid lineage cells
    • Flow cytometry
      • May be most useful in ruling out other neoplasms associated with cytopenias
      • Absence of  flow cytometric abnormalities does not exclude MDS
    • Cytogenetic testing
      • See Key Points section
    • Molecular genetic testing
      • Recurrent mutations in the following genes have been associated with poor prognosis independent of International Prognostic Scoring System (IPSS)
        • ASXL1, DNMT3A, EZH2, RUNX1, TP53
      • Recurrent mutations in the following genes have uncertain prognostic significance
        • ATRX, BRAF, CBL, CDKN2A, ETV6, GNAS, IDH1/2, JAK2, KRAS, NPM1, NRAS, PRPF40B, PTPN11, PTEN, SETBP1, SF1, SF3A1, SF3B1, SRSF2, STAG2 and other cohesins, TET2, U2AF1, U2AF65, UTX, ZRSR2
    • Immunohistochemistry – CD117 (c-Kit); CD34 (QBEnd/10); myeloperoxidase (MPO) to identify abnormal localization of immature precursors and increased blasts

Hereditary Syndromes/Germline Mutations

  • Germline mutations with predisposition for MDS/acute myeloid leukemia (AML)/myeloproliferative neoplasms (MPN) by established and emerging familial syndromes (National Comprehensive Cancer Network [NCCN], 2017)
    • Familial MDS/AML
      • RUNX1
        • Potentially associated diseases/syndromes – familial platelet disorder with predisposition to AML
        • Clinical phenotype – mild to moderate thrombocytopenia and/or platelet dysfunction, MDS/AML
      • GATA2
        • Potentially associated diseases/syndromes – MonoMAC syndrome, Emberger syndrome, pulmonary alveolar proteinosis, hereditary lymphedema, congenital deafness, cutaneous warts
        • Clinical phenotype – immunodeficiency, transformation to MDS/AML, monosomy 7 and/or somatic ASXL1 mutations
      • ETV6
        • Potentially associated diseases/syndromes – dysmorphic facial features and developmental delay; increased risk for colon and skin cancers, myopathy, and autoimmune disorders
        • Clinical phenotype – chronic thrombocytopenia, myeloid malignancy, or acute lymphoblastic leukemia
      • CEBPA
        • No associated disease/syndromes described
        • Clinical phenotype – AML, typically acquiring a second CEBPA mutation
      • DDX41
        • Potentially associated diseases/syndromes – autoimmune disorders
        • Clinical phenotype – MDS or AML, may acquire second DDX41 mutation
      • ANKRD26
        • Potentially associated diseases/syndromes – thrombocytopenia, leukocytosis
        • Clinical phenotype – moderate thrombocytopenia and/or platelet dysfunction
      • SRP72
        • Potentially associated diseases/syndromes – congenital sensorineural hearing loss
        • Clinical phenotype – bone marrow failure or aplasia
    • Classical inherited bone marrow failure syndromes
      • TERT/TERC
        • Potentially associated diseases/syndromes – nail and skin changes, sensorineural deafness, cirrhosis, hereditary pulmonary fibrosis, emphysema, and signs of early aging (premature graying of hair); increased risk for head and neck cancers, anogenital cancers, and skin cancer
        • Clinical phenotype – myelodysplastic syndromes (MDS)/acute myeloid leukemia (AML)
      • FANC genes DKC
        • Potentially associated diseases/syndromes – Fanconi anemia or dyskeratosis congenita; dysmorphic features, short stature, nail and skin changes, thumb hypoplasia, dysmorphic facial features, pulmonary fibrosis
        • Clinical phenotypes – chronic bone marrow failure and aplastic anemia, clonal neoplasms
      • ELA2, HAX1, GFI1
        • Potentially associated diseases/syndromes – severe congenital neutropenia
        • Clinical phenotypes – variable rates of transformation
    • Other inherited syndromes associated with MDS/AML/MPN
      • TP53
        • Potentially associated diseases/syndromes – Li-Fraumeni syndrome; increased risk of brain tumors, sarcomas, colon, and breast cancers, among others
        • Clinical phenotype – therapy-related neoplasms may emerge after treatment for solid tumors
      • PTPN11, CBL, KRAS, NF1
        • Potentially associated diseases/syndromes – Noonan syndrome, neurofibromatosis
        • Clinical phenotypes – typically presents as juvenile myelomonocytic leukemia
      • BLM
        • Potentially associated diseases/syndromes – Bloom syndrome, short stature, immunodeficiency, microcephaly, high-pitched voice, hypogonadism
      • ATG2B/GSKIP
        • Potentially associated diseases/syndromes – MPNs
        • Clinical phenotypes – myeloproliferative/myelodysplastic overlap features or AML
      • BRCA1/BRCA2
        • Potentially associated diseases/syndromes – increased risk for breast cancer, male breast cancer, ovarian cancer, prostate cancer, and pancreatic cancer, among others
        • Clinical phenotypes – therapy-related neoplasms may emerge after treatment for solid tumors

Prognosis

  • Most accurately defined by cytogenetic testing, fluorescence in situ hybridization (FISH), and cytogenetic single nucleotide polymorphism (SNP) microarray/next generation sequencing (see Key Points section)
  • Revised MDS International Prognostic Scoring System (IPSS-R) variables used in prognostic calculation
    • Cytogenetic risk (refer to IPSS-R table below)
    • Hemoglobin
    • Absolute neutrophil count
    • Platelets
    • Bone marrow blasts (percent)

Differential Diagnosis

  • Cytopenias
    • Pancytopenia
      • Medication/toxin exposure
      • Bone marrow failure – aplastic anemia
      • Hemophagocytic syndrome
      • Acute leukemias – AML, acute lymphoblastic leukemia (ALL)
      • Alcohol abuse
      • Infections
      • Severe nutritional deficiency
      • Bone marrow infiltration by malignancy
  • Isolated anemia
  • Isolated neutropenia
    • Acute leukemias (AML, ALL)
    • Medications (eg, sulfonamides, ganciclovir)
    • HIV
    • Hypersplenism
    • Familial cyclic neutropenia
    • Antineutrophil antibody syndromes
  • Isolated thrombocytopenia
    • Idiopathic thrombocytopenic purpura
    • Hypersplenism
  • Dyserythropoiesis
  • Other

Background

Epidemiology

  • Incidence
    • ~4.9/100,000 in the general population (National Comprehensive Cancer Network [NCCN], 2017)
    • 30-60/100,000 in the elderly population (≥70 years) (NCCN, 2017)
  • Age – median is 65-70
  • Sex – M>F

Classification

Classification of MDS, Subtypes
Subtype Blood Bone Marrow

MDS cytopenias with single lineage dysplasia

  • Unicytopenia or bicytopenia
  • Unilineage dysplasia ≥10% of 1 cell line
  • <5% blasts

MDS with ring sideroblasts

  • MDS-RS and single lineage dysplasia
  • MDS-RS and multilineage dysplasia
  • 15% erythroid precursors with ring sideroblasts or ≥5% ring sideroblasts if SF3B1 mutation present
  • <5% blasts

MDS with multilineage dysplasia

  • Cytopenia(s)
  • <1x109/L monocytes
  • Dysplasia in ≥10% of cells in ≥2 hematopoietic lineages
  • ±15% ring sideroblasts
  • <5% blasts

MDS with excess blasts-1 (MDS-EB-1)

  • Cytopenia(s)
  • ≤2-4% blasts
  • <1x109/L monocytes
  • Unilineage or multilineage dysplasia
  • No Auer rods
  • 5-9% blasts
MDS with excess blasts-2 (MDS-EB-2)
  • Cytopenia(s)
  • 5-19% blasts
  • <1x109/L monocytes
  • Unilineage or multilineage dysplasia
  • ± Auer rods
  • 10-19% blasts

MDS, unclassifiable

  • Cytopenia(s)
  • ±1% blasts on at least 2 occasions
  • Unilineage dysplasia or no dysplasia but characteristic MDS cytogenetics
  • <5% blasts

MDS associated with isolated del(5q)

  • Anemia
  • Platelets normal or increased
  • Unilineage erythroid dysplasia
  • Isolated del(5q) cytogenetic abnormality
  • <5% blasts

Refractory cytopenia of childhood

  • Cytopenias
  • <2% blasts
  • Dysplasia in 1-3 lineages
  • <5% blasts
MDS with excess blasts in transformation (MDS-EB-T)
  • Cytopenias
  • 5-19% blasts
  • Multilineage dysplasia
  • 20-29% blasts
  • ± Auer rods
Sources: NCCN, 2017; WHO, 2016
Classification of Myelodysplastic-Myeloproliferative Neoplasms
Subtype Blood Bone Marrow

Chronic myelomonocytic leukemia (CMML) 0

  • >1x109/L monocytes
  • <2% blasts
  • Dysplasia in ≥1 hematopoietic line
  • <5% blasts

CMML 1

  • >1x109/L monocytes
  • 2-4% blasts
  • Dysplasia in ≥1 hematopoietic line
  • 5-9% blasts

CMML 2

  • >1x109/L monocytes
  • 5-19% blasts or Auer rods
  • Dysplasia in ≥1 hematopoietic line
  • 10-19% blasts or Auer rods

Atypical chronic myeloid leukemia (aCML), BCR-ABL1

  • White blood cells (WBC)>13x109/L
  • Neutrophil precursors >10%
  • <20% blasts
  • Dysgranulopoiesis
  • Hypercellular
  • <20% blasts

Chronic neutrophilic leukemia (CNL)a

  • WBC ≥25,000 with PMN/bands ≥80%
  • No dysplasia
  • Mature myeloid hyperplasia
  • <5% blasts
  • No dysplasia

Juvenile myelomonocytic leukemia (JMML)

  • >1x109/L monocytes
  • <20% blasts
  • >1x109/L monocytes
  • <20% blasts

Myelodysplastic or myeloproliferative disease, unclassifiable (overlap syndrome)

  • Dysplasia + myeloproliferative features
  • No prior MDS or myeloproliferative neoplasms (MPN)
  • Dysplasia + myeloproliferative features

MDS/MPN with ring sideroblasts and thrombocytosis

  • Dysplasia + myeloproliferative features
  • Platelets ≥450x109/L
  • ≥15% ring sideroblasts
  • Dysplasia + myeloproliferative features

Note: NCCN endorses using both the French-American-British (FAB) and WHO classification criteria for refractory anemia with excess blasts (RAEB) in transformation (RAEB-t) patients

aWHO (2016) includes with MPN classification

Sources: NCCN, 2017; WHO, 2016

Risk Factors

  • Older age
  • Occupational exposures
    • Benzene-containing products
    • Pesticides
    • Organic solvents
    • Heavy metals (lead, arsenic)
  • Drug exposures
    • Alkylating agents, purine analogues, topoisomerase inhibitors
    • Azathioprine
    • Mycophenolate
  • Radiation
  • Genetic
    • Down syndrome
    • Fanconi anemia
    • Familial myelodysplasia
    • Diamond-Blackfan syndrome
    • Neurofibromatosis

Pathophysiology

  • Clonal expansion of the multipotential hematopoietic cell
  • Primary mechanism is defective maturation of marrow cells coupled with premature cell death

Clinical Presentation

  • May be asymptomatic
    • Disease is generally indolent, with blood counts remaining relatively stable over months or longer
  • Most common symptoms
    • Pallor, weakness, exertional dyspnea – secondary to anemia
    • Recurrent infections – secondary to neutropenia
    • Bleeding/bruising – secondary to thrombocytopenia
  • May have concomitant immune disorders (eg, relapsing polychondritis, vasculitis)
  • Complications
    • 25-30% progress to AML; incidence depends on MDS subtype
      • Lower response rate to standard therapy for patients >65 years with de novo AML
    • Death from complications of cytopenia (neutropenia in particular)

Pediatrics

Epidemiology

  • Incidence – rare; 1/million (National Comprehensive Cancer Network [NCCN], 2017)
  • Age – 6.8 years median

Risk Factors

  • Strongly associated with congenital disorders – evident in at least 50% of cases
    • Congenital disorders include
      • Down syndrome
      • Fanconi syndrome
      • Trisomy 8
      • Diamond-Blackfan anemia
      • Neurofibromatosis type 1
      • Bloom syndrome
      • Noonan syndrome
      • Congenital neutropenia (Kostmann syndrome)
      • Shwachman-Diamond syndrome
      • Dubowitz syndrome
  • Prior exposure to radiation or chemotherapy

Classification

  • Patients with 2-19% blasts in peripheral blood and/or 5-19% blasts in bone marrow may be classified using the adult schema provisional – excludes patients with Down syndrome
  • Additional pediatric entity of refractory cytopenia of childhood is recognized
    • <2% blasts in peripheral blood and <5% blasts in bone marrow
    • Bilineage dysplasia

Clinical Presentation

  • May be asymptomatic
  • Most common symptoms
    • Pallor, weakness, exertional dyspnea – secondary to anemia
    • Hepatomegaly/splenomegaly
    • Arthralgias

Laboratory Testing

See Diagnosis and Key Points

Differential Diagnosis

ARUP Lab Tests

Diagnosis, prognosis, and monitoring of hematopoietic neoplasms

Reflex pattern: if chromosome analysis is normal or no growth, then genomic microarray testing will be added

Use for ordering individual or multiple oncology FISH probes if standard FISH panels are not desired

ARUP Oncology FISH Probes menu

Use in conjunction with conventional cytogenetics for diagnosis, prognosis, and monitoring of MDS

Probes include del(5q), -7/del(7q), + 8, del(20q); each probe can be run as a part of the panel or individually

Panel detects only the specific aberrations targeted by the probes

Preferred test at time of diagnosis for detecting prognostically important genomic abnormalities in leukemias/lymphomas and solid tumors involving loss/gain of DNA and loss of heterozygosity (LOH)

Monitor disease progression and response to therapy

Bone marrow or blood specimens

Low-level mosaicism (<15-20%) may not be detected

May not be appropriate for individuals with expected lower levels of malignant cells

Formalin-fixed, paraffin-embedded (FFPE) specimens must contain a region with ≥50% tumor

Not recommended for minimal residual disease (MRD)

Does not detect:

  • Balanced rearrangements; FISH should be used to evaluate specific balanced rearrangements according to indication
  • Base pair mutations and very small deletions/duplications
  • Imbalances of the mitochondrial genome
  • Low-level clones

Does not provide positional information for chromosome rearrangements

Use in conjunction with conventional cytogenetics for diagnosis, prognosis, and monitoring in therapy-related MDS or AML associated with MDS

Probes include -5/del(5q), -7/del(7q), 11q23 rearrangements 

MLL gene at 11q23 has multiple translocation partners which are not identified by this test

Panel detects only the specific aberrations targeted by the probes

Assess for single gene mutations, including substitutions and insertions and deletions that may have diagnostic, prognostic, and/or therapeutic significance in MDS and MDS/myeloproliferative neoplasms (MPN) overlap disorders

Combines cytogenomic microarray with an NGS sequencing panel

Refer to Additional Technical Information document for further content

Variants may be present below the limit of detection (LOD) of 5% allele frequency

Lower limit of detection for large variants (>30bp) has not been validated

Not intended to detect minimal residual disease

Panel includes ASXL1, ASXL2, BCOR, BCORL1, BRAF, CALR, CBL, CEBPA, CSF3R, DNMT1, DNMT3A, EED, ELANE, ETNK1, ETV6, EZH2, FAM5C, FLT3, GATA1, GATA2, HNRNPK, IDH1, IDH2, JAK2, JAK3, KDM6A, KIT, KRAS, LUC7L2, MAP2K1, MLL, MPL, NOTCH1, NPM1, NRAS, NSD1, PHF6, PRPF40B, PRPF8, PTPN11, RAD21, RUNX1, SETBP1, SF1, SF3A1, SF3B1, SMC1A, SMC3, SRSF2, STAG2, SUZ12, TET2, TP53, U2AF1, U2AF2, WT1, ZRSR2

Assess for single gene mutations, including substitutions and insertions and deletions that may have diagnostic, prognostic, and/or therapeutic significance in MDS and MDS/MPN overlap disorders

Refer to Additional Technical Information document for further content

Variants may be present below the limit of detection (LOD) of 5% allele frequency

Lower limit of detection for large variants (>30bp) has not been validated

Not intended to detect minimal residual disease

Panel includes ASXL1, ASXL2, BCOR, BCORL1, BRAF, CALR, CBL, CEBPA, CSF3R, DNMT1, DNMT3A, EED, ELANE, ETNK1, ETV6, EZH2, FAM5C, FLT3, GATA1, GATA2, HNRNPK, IDH1, IDH2, JAK2, JAK3, KDM6A, KIT, KRAS, LUC7L2, MAP2K1, MLL, MPL, NOTCH1, NPM1, NRAS, NSD1, PHF6, PRPF40B, PRPF8, PTPN11, RAD21, RUNX1, SETBP1, SF1, SF3A1, SF3B1, SMC1A, SMC3, SRSF2, STAG2, SUZ12, TET2, TP53, U2AF1, U2AF2, WT1, ZRSR2

Humanitarian device; authorized by Federal law for use in the qualitative detection of PDGFRB gene rearrangement in patients with myelodysplastic syndrome/myeloproliferative disease (MDS/MPD)

The effectiveness of this device for this use has not been demonstrated; caution: federal law restricts this device to sale by or on the order of a licensed practitioner

PDGFRB FISH for Gleevec Eligibility in MDS/MPD is an in vitro diagnostic test intended for the qualitative detection of PDGFRB gene rearrangement from fresh bone marrow samples of patients with MDS/MPD with a high index of suspicion based on karyotyping showing a 5q31-33 anomaly

The PDGFRB FISH assay is indicated as an aid in the selection of MDS/MPD patients for whom Gleevec (imatinib mesylate) treatment is being considered; this assay is for professional use only and is to be performed at a single laboratory site

Aid in histologic diagnosis of MDS

Stained and returned to client pathologist for interpretation; consultation available if needed

Refer to ARUP Immunohistochemistry Stain Offerings brochure at www.aruplab.com/ap/resources

Aid in histologic diagnosis of MDS; identify abnormal localization of immature precursors and increased blasts

Stained and returned to client pathologist; consultation available if needed

Refer to ARUP Immunohistochemistry Stain Offerings brochure at www.aruplab.com/ap/resources

Related Tests

Diagnosis, prognosis, and monitoring of hematopoietic neoplasms

This test is intended for oncology studies; for chromosome analysis to evaluate for a constitutional finding, order Chromosome Analysis, Peripheral Blood

Diagnosis, prognosis, and monitoring of hematopoietic neoplasms

Reflex pattern: microarray performed when karyotype results are normal or no growth

Preferred test for formalin-fixed, paraffin-embedded (FFPE) tissue specimens at time of diagnosis for detecting prognostically important genomic abnormalities in leukemias/lymphomas and solid tumors involving loss/gain of DNA, loss of heterozygosity (LOH)

Monitor disease progression and response to therapy

Low-level mosaicism (<15-20%) may not be detected

May not be appropriate for individuals with expected lower levels of malignant cells

FFPE specimens must contain a region with ≥50% tumor

Not recommended for minimal residual disease (MRD)

Does not detect:

  • Balanced rearrangements; fluorescence in situ hybridization (FISH) should be used to evaluate specific balanced rearrangements according to indication
  • Base pair mutations and very small deletions/duplications
  • Imbalances of the mitochondrial genome
  • Low-level clones

Does not provide positional information for chromosome rearrangements

Aid in evaluation of hematopoietic neoplasms (ie, leukemia, lymphoma)

Specimens include bone marrow, whole blood, tissue, or fluid

Monitor therapy in patients with established diagnosis of hematopoietic neoplasms

Markers selected based on provided clinical history and/or previous test results

Some hematopoietic neoplasms do not show phenotypic abnormalities and therefore may not be detected by flow cytometry

Poor cell viability may adversely affect antigens and impede ability to properly identify neoplastic cells

Flow results cannot be used alone to diagnose malignancy; should be interpreted in conjunction with morphology, clinical information, and other necessary ancillary tests for a definitive diagnosis

Antigens included:

T cell: CD1a, CD2, CD3, CD4, CD5, CD7, CD8, TCR γ-δ, cytoplasmic CD3

B cell: CD10, CD19, CD20, CD22, CD23, CD103, CD200, kappa, lambda, cytoplasmic kappa, cytoplasmic lambda

Myeloid/monocyte: CD11b, CD13, CD14 (Mo2), CD14 (MY4), CD15, CD33, CD64, CD117, myeloperoxidase

Miscellaneous: CD11c, CD16, CD25, CD30, CD34, CD38, CD41, CD42b, CD45, CD56, CD57, CD61, HLA-DR, glycophorin, TdT, bcl-2, ALK-1, CD123, CD138, CD26, CD45, CRLF-2

Medical Experts

Contributor

Lamb

Allen N. Lamb, PhD, FACMG
Allen N. Lamb, PhD, FACMG
Retired Former Professor of Clinical Pathology, University of Utah
Retired Former Laboratory Section Chief, Cytogenetics and Genomic Microarray, ARUP Laboratories
Contributor

Toydemir

Reha Toydemir, MD, PhD, FACMG

Assistant Professor of Clinical Pathology, and Adjunct Assistant Professor of Pediatrics, University of Utah

Medical Director, Cytogenetics and Genomics, at ARUP Laboratories

References

Additional Resources
Resources from the ARUP Institute for Clinical and Experimental Pathology®