Acute Lymphoblastic Leukemia - ALL

Acute lymphoblastic leukemia (ALL) is a malignant disease of the lymphoid cell line occurring predominantly in children. An ALL workup typically includes CBC testing, coagulation studies, and chemistry profiles; definitive diagnosis requires bone marrow biopsy.

Tabs Content

Clinical Overview

Diagnosis

Indications for Testing

Abnormal blood count/peripheral smear
Constitutional symptoms without other etiology

Laboratory Testing

CBC with peripheral smear – leukocytosis and blasts are common
Cytochemical staining – used infrequently due to availability of immunophenotyping
- MPO – usually negative

Immunophenotyping – determine antigen markers for identifying cell lineage and predicting outcome

CD expression – helps establish ALL lineage
B-ALL characterized by B-cell antigens – PAX5, CD19, CD20, CD22, CD24, CD79a
- CD20 – only partially expressed in nonmature forms
- CD10 – frequently expressed

T-ALL characterized by T-cell antigens – CD2, CD3, CD4, CD5, CD7, CD8

Others – CD1a, CD10, CD34, CD55, CD99, HLA-DR, and TdT

Subclassification of T-ALL by stage of normal thymocyte maturation

Subclassification of T-ALL by Stage of Normal Thymocyte Maturation
T-ALL Subtype	CD1a	CD2	cCD3	sCD3	CD4	CD5	CD7	CD8	CD34
Pro-T	-	-	+	-	-	-	+	-	+
Pre-T	-	+	+	-	-	±	-	-	±
Cortical T	+	+	+	-	+	±	+	+	-
Medullary T	-	+	+	+	±^a	±	+	±	-
^aMedullary stage T-ALL shows either CD4 or CD8 expression

May also express myeloid antigens – CD11b, CD13, CD15, CD33

Cytogenetic studies – initial diagnostic workup, prognostic stratification (especially in children), and determination of treatment approach
- Treatment protocols are stratified by age and the presence of t(9;22)
- Majority of B-ALL contains genetic abnormalities, including numerical and structural aberrations [eg, hyperdiploidy, hypodiploidy, translocation, deletion, and duplication/amplification-iAMP(21)]
  - Cytogenetic studies define specific entities with unique phenotypic and prognostic features
- T-ALL/LBL contains TCR gene rearrangements
- iAMP(21) can be identified by FISH or genomic microarray
- See Genetics in Background for specific abnormalities
- Cytogenetic methodologies
  - Chromosome analysis (karyotyping) – use to identify recurrent cytogenetic abnormalities such as hyperdiploidy, hypodiploidy, translocations (including t(9;22) and 11q23/KMT2A rearrangements), deletions, and duplications
    - Cannot detect ETV6-RUNX1 t(12;21), which is chromosomally invisible
    - t(12;21)(p13;q22) can be detected by fluorescence in situ hybridization (FISH)
  - FISH – more sensitive than chromosome analysis in detecting cytogenetic aberrations
    - Probes for adult ALL
      - ALL panel includes BCR-ABL1, TCF3 (E2A), KMT2A (MLL), IGH, and MYC
      - Ph-like ALL panel includes CRLF2, JAK2, EPOR, CSF1R, ABL1, ABL2, PDGFRB
    - Probes for childhood ALL
      - ALL panel includes BCR-ABL1, TEL/AML1 (ETV6-RUNX1), CEP4 and CEP10, and MLL/11q23 rearrangements
      - Ph-like ALL panel includes CRLF2, JAK2, EPOR, CSF1R, ABL1, ABL2, PDGFRB
  - Cytogenomic SNP microarray – detects abnormalities that may not be detected by chromosome analysis or FISH, including microdeletions involving CDKN2A/B, BTG1, IKZF1, and EBF1, as well as microduplications and loss of heterozygosity (LOH)
    - Does not detect BCR-ABL1, TEL/AML (ETV6/RUNX1), or other balanced rearrangements involving KMT2A (MLL), IGH, MYC, and TCF3 loci
    - BCR-ABL1 by next generation sequencing offers advantages over Sanger sequencing

Histology

Bone marrow biopsy – enumerate blasts and collect material for ancillary testing (eg, cytogenetics)
Immunohistochemistry – most useful stains include TdT; CD3; CD10 (CALLA); CD20, L26; CD79A

Prognosis

Adult prognosis by age, white blood cell (WBC) count, and mutation status

Adult Prognosis by Age, WBC, and Mutation Status

Prognosis

Good

Poor

Age

Younger age

Especially <25 yrs when treated with a pediatric protocol

Older age

Individuals >60 yrs have a particularly poor prognosis

High WBC

>30 x 10⁹/L for B-ALL
>100 x 10⁹/L for T-ALL

Genetic abnormalities

BCR-ABL1 t(9;22) positive
- Most frequent chromosomal abnormality
KMT2A (MLL) rearrangements
t(8;14) positive
Complex karyotype (>5 chromosomal abnormalities)
Low hypodiploidy
Near triploidy

Pediatric prognosis by age, WBC, and mutation status

Pediatric Prognosis by Age, WBC, and Mutation Status
Prognosis	Good	Poor
Age	Younger age (1 yr to <10 yrs)	Older age, very young age (<1 yr) High WBC >30 x 10⁹/L for B-ALL >100 x 10⁹/L for T-ALL
Genetic abnormalities	ETV6-RUNX1 t(12;21) positive Hyperdiploidy with gain of chromosomes 4 and 10	BCR-ABL1 t(9;22) positive KMT2A (MLL), CRLF2 rearrangements RUNX1 amplification Low hypodiploidy Near triploidy Early T-cell precursor ALL

Differential Diagnosis

Infection
- Endocarditis
- Myelodysplastic syndrome
Acute myeloid leukemia
Mixed-lineage leukemias
Lymphoma
- Blastic mantle cell
- Burkitt
- Peripheral T-cell
Juvenile rheumatoid arthritis
Ewing sarcoma
Merkel cell carcinoma
Benign proliferative disease
- Benign precursor B-cells (hematogones)
- Normal cortical thymocytes

Monitoring

Repeat polymerase chain reaction (PCR) or FISH testing using leukemia-associated phenotype defined at diagnosis for detection of minimal residual disease (MRD)
- MRD by PCR or FISH defined as >10^-4 cells or >0.01% blasts
- Qualitative/quantitative PCR testing is very sensitive and may detect MRD that is not of clinical concern
  - PCR has lower sensitivity than FISH
- >10% MRD portends higher relapse rate
- B-cell lines MRD can be detected using bone marrow; T-cell lines MRD can be detected using peripheral blood
  - T-ALL – detection of TdT or CD34 confirms MRD
- Relapse mandates new immunophenotyping and molecular testing – karyotype may change and, rarely, second de novo ALL may be discovered

Pharmacogenetics

Thiopurine S-methyltransferase (TPMT)
- Thiopurine prodrugs are metabolized via TPMT enzymatic activity
- Deficiency of TPMT predicts hematopoietic toxicity after thiopurine treatment
- Increased risk of therapy-related acute myeloid leukemia and radiation-induced brain tumors in patients receiving intensive thiopurine therapy
- Testing to determine activity level may be helpful in dosing thiopurine drugs and also help avert bone marrow suppression
  - For deficient activity – dose reduction of 80-90% may be required
  - For intermediate activity – dose reduction of 20-50% may be required
Other pharmacogenetic pathways (no testing currently available)
- During induction therapy for ALL
  - Predominant drug metabolism pathway is via CYP3A
  - CYP3A5 GG genotype (lower CYP3A5 activity) predicts gastrointestinal (GI) toxicity and rates of infection
- During consolidation and continuation phase of therapy
  - Reduced folate carrier AA or AG genotype predicts GI toxicity
- During all phases
  - UGT1A1 promotor repeat polymorphism (UGT1A1 7h) predicts hyperbilirubinemia
- MTHFR polymorphism
  - Probably affects methotrexate toxicity
  - MTHFR C677T variant associated with higher rate of relapse
- Therapy molecular targets
  - Investigational use of imatinib for BCR-ABL1-positive ALL
- Adverse drug effects
  - Polymorphism in eight genes significantly associated with glucocorticoid-induced hypertension (CNTNAP2, LEPR, CRHR1, NTAN1, SLCI2A3, ALPL, BGLAP, and APOB)
  - PAI-1 polymorphism associated with GA/AA genotype – increased risk of glucocorticoid-induced osteonecrosis

Background

Epidemiology

Incidence – 1.7/100,000 (National Comprehensive Cancer Network [NCCN], 2015)
- Most common leukemia in childhood – 75-85% of acute leukemias
  - ~3/100,000 (Hunger, 2015)
Age – peak incidence 3-5 years; second peak >50 years
Sex – M<F; ~1:3
Ethnicity
- <3 years – Caucasian predominance
- ≥3 years – African Americans have higher risk

Risk Factors

Ionizing radiation
Genetic diseases – Down syndrome, Fanconi anemia, Bloom syndrome, ataxia telangiectasia, Nijmegen breakage syndrome, Shwachman-Diamond syndrome
Probable factors – hydrocarbon exposure and pesticides
Older age

Genetics

Recurrent genetic abnormalities associated with B-ALL

Recurrent genetic abnormalities associated with B-ALL
Translocation	Gene	Frequency in Adults	Frequency in Children
t(9;22)(q34;q11.2)	BCR-ABL1	25%	2-4%
BCR-ABL1-like	various	10%-30%	15%
t(v;11q23)	MLL	10%	8%
t(1;19)(q23;p13.3)	EZA-PBX1 (TCF3-PBX1)	3%	6%
t(5;14)(q31;q32)	IL3-IGH (ALL with eosinophilia)	<1%	<1%
t(8;14), t(2;8), t(8;22)	MYC	4%	2%
t(12;21)(p13;q22)	TEL-AML (ETV6-RUNX1)	2%	22%
Hyperdiploidy in association with trisomy 4, 10, and 17 (>50 chromosomes)		7%	25%
Hypodiploidy (<44 chromosomes)		2%	1%

Common T-ALL rearrangements

Common T-ALL Rearrangements
Translocation	Gene	Frequency in Adults	Frequency in Children
t(1;14)(p32;q11)	TAL1	12%	7%
t(10;14)(q24;q11.2)	TLX1 (HOX11)	8%	1%
t(5;14)(p35;q32)	HOX11/L2	1%	3%
t(11;14), q11	TCRα and TCRδ	20-25%	10-20%

Clinical Presentation

Nonspecific constitutional symptoms – fever, lethargy, dizziness
Pallor – due to anemia
Failure to thrive
Bruising – due to thrombocytopenia
Infections
Pain in extremities – most prominent in children

ARUP Lab Tests

Tests generally appear in the order most useful for common clinical situations. Click on number for test-specific information in the ARUP Laboratory Test Directory.

Leukemia/Lymphoma Phenotyping by Flow Cytometry 2008003
Method: Flow Cytometry

Recommended Use

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

Antigens included

T cell: CD1, CD2, CD3, CD4, CD5, CD7, CD8, TCR α-β, TCR γ-δ, cytoplasmic CD3

B cell: CD10, CD19, CD20, CD22, CD23, CD103, kappa, lambda, FMC7, cytoplasmic kappa, cytoplasmic lambda

Myelo/Mono: CD11b, CD13, CD14 (Mo2), CD14 (MY4), CD15, CD33, CD64, CD117, myeloperoxidase

Misc: CD11c, CD16, CD25, CD30, CD34, CD38, CD41, CD42b, CD45, CD56, CD57, CD61, HLA-DR, glycophorin, TdT, bcl-2, ALK-1, CD123, CD138, CD200, CD26, CD45

Limitations

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 the 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

Chromosome FISH, Interphase 2002298
Method: Fluorescence in situ Hybridization

Recommended Use

Use to order individual or multiple oncology FISH probes if standard FISH panels are not desired

Specific probes related to ALL must be requested and include BCR-ABL1, KMT2A (MLL), TCF3 (E2A), IGH, and MYC

ARUP Oncology FISH Probes menu

Chromosome Analysis, Bone Marrow with Reflex to Genomic Microarray 2007130
Method: Giemsa Band/Genomic Microarray (Oligo-SNP array)

Recommended Use

Diagnosis, prognosis, and monitoring of hematopoietic neoplasms

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

Chromosome Analysis, Leukemic Blood with Reflex to Genomic Microarray 2007131
Method: Giemsa Band/Genomic Microarray (Oligo-SNP array)

Recommended Use

Diagnosis, prognosis, and monitoring of hematopoietic neoplasms

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

Cytogenomic SNP Microarray - Oncology 2006325
Method: Genomic Microarray (Oligo-SNP Array)

Recommended Use

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

Monitor disease progression and response to therapy

Bone marrow or blood specimens

Limitations

Low-level mosaicism (<15%-20%) may not be detected; test may not be appropriate for individuals with expected lower levels of malignant cells

Not recommended for minimal residual disease

Does not detect balanced rearrangements; FISH should be used to evaluate specific balanced rearrangements according to indication

Does not detect base pair mutations and very small deletions/duplications; imbalances of the mitochondrial genome; positional information for chromosome rearrangements; low level clones

Acute Lymphocytic Leukemia (ALL) Panel by FISH, Adult 2002647
Method: Fluorescence in situ Hybridization

Recommended Use

Recommended FISH panel for adults with newly diagnosed B-ALL

FISH probes detect BCR/ABL1 t(9;22), IGH 14q32 rearrangement (partner not determined), MLL 11q23 rearrangement (partner not determined), MYC 8q24 rearrangement (partner not determined), and TCF3 (E2A) t(1;19) translocation

Limitations

Panel detects only the specific aberrations targeted by the probes

Chromosome alterations outside the regions complementary to these FISH probes will not be detected

Acute Lymphocytic Leukemia (ALL) Panel by FISH, Pediatric 2002719
Method: Fluorescence in situ Hybridization

Recommended Use

Recommended FISH panel for children with newly diagnosed ALL

Probes include BCR/ABL1 t(9;22); CEP4, CEP10, RUNX1 (gain of signals); MLL 11q23 rearrangement (partner not determined); TEL/AML (ETV6/RUNX1) t(12;21)

Limitations

Panel detects only the specific aberrations targeted by the probes

Chromosome alterations outside the regions complementary to these FISH probes will not be detected

Ph-Like Acute Lymphocytic Leukemia (ALL) Panel by FISH 3000455
Method: Fluorescence in situ Hybridization

Recommended Use

Recommended FISH panel for individuals suspected of having Ph-like ALL

TdT by Immunohistochemistry 2004142
Method: Immunohistochemistry

Recommended Use

Aid in histologic diagnosis of ALL

Stained and returned to client pathologist; consultation available if needed

CD10 (CALLA) by Immunohistochemistry 2003523
Method: Immunohistochemistry

Recommended Use

Aid in histologic diagnosis of ALL

Stained and returned to client pathologist; consultation available if needed

CD19 by Immunohistochemistry 2005114
Method: Immunohistochemistry

Recommended Use

Aid in histologic diagnosis of B-cell leukemia/lymphoma

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

CD20, L26 by Immunohistochemistry 2003532
Method: Immunohistochemistry

Recommended Use

Aid in histologic diagnosis of ALL

Stained and returned to client pathologist; consultation available if needed

CD79A by Immunohistochemistry 2003800
Method: Immunohistochemistry

Recommended Use

Aid in histologic diagnosis of ALL

Stained and returned to client pathologist; consultation available if needed

CD3 by Immunohistochemistry 2003508
Method: Immunohistochemistry

Recommended Use

Aid in histologic diagnosis of ALL

Stained and returned to client pathologist; consultation available if needed

BCR-ABL1 Mutation Analysis for Tyrosine Kinase Inhibitor Resistance by Next Generation Sequencing (Temporary Referral as of 02/08/18) 2008420
Method: Massively Parallel Sequencing

Recommended Use

Order only for patients with an established diagnosis of a BCR-ABL1 positive leukemia

Use to determine if a mutation is present that would interfere with response to TKI therapy in Philadelphia chromosome positive (Ph+) lymphoblastic leukemia or CML

Detects all common mutations, including T315I

Higher sensitivity than traditional Sanger sequencing techniques

Offers coverage of SH2, SH3, and kinase domain

If 2 mutations are present, this test can potentially determine if they are in cis or in trans

Limitations

A negative result does not exclude mutations below the level of detection or mutations outside the sequenced region of this test

BCR-ABL1, Major (p210), Quantitative 2005017
Method: Quantitative Reverse Transcription Polymerase Chain Reaction

Recommended Use

Aids in diagnosis and monitoring of individuals with Ph+ ALL who have e13a2 or e14a2 transcripts (p210)

Analytical sensitivity – 1:125,000 normal cells

Limitations

Does not detect p190 or p230 form

BCR-ABL1, Minor (p190), Quantitative 2005016
Method: Quantitative Reverse Transcription Polymerase Chain Reaction

Recommended Use

Aids in diagnosis and monitoring of individuals with Ph+ ALL who have e1a2 transcripts (p190)

Analytical sensitivity – 1:125,000 normal cells

Limitations

Does not detect p210 or p230 form

BCR-ABL1, Qualitative with Reflex to BCR-ABL1 Quantitative 2005010
Method: Reverse Transcription Polymerase Chain Reaction

Recommended Use

Recommended when submitting initial diagnostic sample for Ph+ ALL (no previous BCR-ABL1 testing)

Reflex pattern – if the qualitative test is positive, the appropriate corresponding quantitative test is performed

Medical Reviewers

Kelley, Todd, MD, MS, Medical Director, Molecular Hematopathology and Hematopathology; Co-Scientific Director, NGS and Biocomputing, at ARUP Laboratories; Associate Professor of Clinical Pathology, University of Utah

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

Perkins, Sherrie L., MD, PhD, Chief Executive Officer at ARUP Laboratories ; Professor of Pathology, University of Utah

Salama, Mohamed E., MD, Laboratory Section Chief, Hematopathology, at ARUP Laboratories; Professor of Clinical Pathology, Chief of Hematopathology, and Director of the Hematopathology Fellowship Program, University of Utah

References

Guidelines

Brüggemann M, Schrauder A, Raff T, Pfeifer H, Dworzak M, Ottmann OG, Asnafi V, Baruchel A, Bassan R, Benoit Y, Biondi A, Cavé H, Dombret H, Fielding AK, Foà R, Gökbuget N, Goldstone AH, Goulden N, Henze G, Hoelzer D, Janka-Schaub GE, Macintyre EA, Pieters R, Rambaldi A, Ribera J, Schmiegelow K, Spinelli O, Stary J, von Stackelberg A, Kneba M, Schrappe M, van Dongen JJ, European Working Group for Adult Acute Lymphoblastic Leukemia (EWALL), International Berlin-Frankfurt-Münster Study Group (I-BFM-SG). Standardized MRD quantification in European ALL trials: proceedings of the Second International Symposium on MRD assessment in Kiel, Germany, 18-20 September 2008. Leukemia. 2010; 24(3): 521-35. PubMed
Protocol for the Examination of Specimens From Patients With Hematopoietic Neoplasms Involving the Bone Marrow. Based on AJCC/UICC TNM, 7th ed. Protocol web posting date: Jun 2012. College of American Pathologists (CAP). Northfield, IL [Revised: Jun 2012; Accessed: Apr 2018]
NCCN Clinical Practice Guidelines in Oncology, Acute Lymphoblastic Leukemia.. National Comprehensive Cancer Network. Fort Washington, PA [Accessed: Apr 2018]
Hampel H, Bennett RL, Buchanan A, Pearlman R, Wiesner GL, Guideline Development Group, American College of Medical Genetics and Genomics Professional Practice and Guidelines Committee and National Society of Genetic Counselors Practice Guidelines Committee. A practice guideline from the American College of Medical Genetics and Genomics and the National Society of Genetic Counselors: referral indications for cancer predisposition assessment. Genet Med. 2015; 17(1): 70-87. PubMed

General References

Brüggemann M, Gökbuget N, Kneba M. Acute lymphoblastic leukemia: monitoring minimal residual disease as a therapeutic principle. Semin Oncol. 2012; 39(1): 47-57. PubMed

Cornell RF, Palmer J. Adult acute leukemia. Dis Mon. 2012; 58(4): 219-38. PubMed

Digiuseppe JA. Acute lymphoblastic leukemia: diagnosis and detection of minimal residual disease following therapy. Clin Lab Med. 2007; 27(3): 533-49, vi. PubMed

Harrison CJ. Acute lymphoblastic leukemia. Clin Lab Med. 2011; 31(4): 631-47, ix. PubMed

Hunger SP, Mullighan CG. Acute Lymphoblastic Leukemia in Children. N Engl J Med. 2015; 373(16): 1541-52. PubMed

Iacobucci I, Papayannidis C, Lonetti A, Ferrari A, Baccarani M, Martinelli G. Cytogenetic and molecular predictors of outcome in acute lymphocytic leukemia: recent developments. Curr Hematol Malig Rep. 2012; 7(2): 133-43. PubMed

Inaba H, Greaves M, Mullighan CG. Acute lymphoblastic leukaemia. Lancet. 2013; 381(9881): 1943-55. PubMed

Margolin JF. Molecular diagnosis and risk-adjusted therapy in pediatric hematologic malignancies: a primer for pediatricians. Eur J Pediatr. 2011; 170(4): 419-25. PubMed

Morrissette JJ, Bagg A. Acute myeloid leukemia: conventional cytogenetics, FISH, and moleculocentric methodologies. Clin Lab Med. 2011; 31(4): 659-86, x. PubMed

Mrózek K, Harper DP, Aplan PD. Cytogenetics and molecular genetics of acute lymphoblastic leukemia. Hematol Oncol Clin North Am. 2009; 23(5): 991-1010, v. PubMed

Peters JM, Ansari Q. Multiparameter flow cytometry in the diagnosis and management of acute leukemia. Arch Pathol Lab Med. 2011; 135(1): 44-54. PubMed

Swerdlow S, Campo E, Harris N, Jaffe E, Pileri S, Harald S, Thiele J, Vardiman J. WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues, 4th ed. Lyon, France: International Agency for Research on Cancer, 2008.

Zweidler-McKay PA, Hilden JM. The ABCs of infant leukemia. Curr Probl Pediatr Adolesc Health Care. 2008; 38(3): 78-94. PubMed

References from the ARUP Institute for Clinical and Experimental Pathology^®

Baughn LB, Biegel JA, South ST, Smolarek TA, Volkert S, Carroll AJ, Heerema NA, Rabin KR, Zweidler-McKay PA, Loh M, Hirsch B. Integration of cytogenomic data for furthering the characterization of pediatric B-cell acute lymphoblastic leukemia: a multi-institution, multi-platform microarray study. Cancer Genet. 2015; 208(1-2): 1-18. PubMed

Gu G, Sederberg MC, Drachenberg MR, South ST. IGF2BP1: a novel IGH translocation partner in B acute lymphoblastic leukemia. Cancer Genet. 2014; 207(7-8): 332-4. PubMed

Meyer JA, Zhou D, Mason CC, Downie JM, Rodic V, Abromowitch M, Wistinghausen B, Termuhlen AM, Angiolillo AL, Perkins SL, Lones MA, Barnette P, Schiffman JD, Miles RR. Genomic characterization of pediatric B-lymphoblastic lymphoma and B-lymphoblastic leukemia using formalin-fixed tissues. Pediatr Blood Cancer. 2016; PubMed

Patel S, Mason CC, Glenn MJ, Paxton CN, South ST, Cessna MH, Asch J, Cobain EF, Bixby DL, Smith LB, Reshmi S, Gastier-Foster JM, Schiffman JD, Miles RR. Genomic analysis of adult B-ALL identifies potential markers of shorter survival. Leuk Res. 2017; 56: 44-51. PubMed

Ridges S, Heaton WL, Joshi D, Choi H, Eiring A, Batchelor L, Choudhry P, Manos EJ, Sofla H, Sanati A, Welborn S, Agarwal A, Spangrude GJ, Miles RR, Cox JE, Frazer K, Deininger M, Balan K, Sigman M, Müschen M, Perova T, Johnson R, Montpellier B, Guidos CJ, Jones DA, Trede NS. Zebrafish screen identifies novel compound with selective toxicity against leukemia. Blood. 2012; 119(24): 5621-31. PubMed

Staddon JH, Smock KJ, Schiffman JD, Fluchel MN, Engel ME, Weyrich AS, Campbell RA. Pegasparaginase treatment alters thrombin generation by modulating the protein C and S system in acute lymphoblastic leukaemia/lymphoma. Blood Coagul Fibrinolysis. 2015; 26(7): 840-3. PubMed

Educational Videos

Last Update: July 2018


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	Acute Lymphoblastic Leukemia - ALL. ARUP Consult^©. Retrieved July 19, 2018, from: https://arupconsult.com/content/acute-lymphoblastic-leukemia

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Acute Lymphoblastic Leukemia - ALL

Diagnosis

Indications for Testing

Laboratory Testing

Histology

Prognosis

Differential Diagnosis

Monitoring

Pharmacogenetics

Background

Epidemiology

Risk Factors

Genetics

Clinical Presentation

ARUP Lab Tests

Medical Reviewers

References

Guidelines

General References

References from the ARUP Institute for Clinical and Experimental Pathology®

References from the ARUP Institute for Clinical and Experimental Pathology^®