Molecular Diagnostics of Lymphoid Neoplasms

  • Deniz Peker
  • Jianguo Tao
  • Ling ZhangEmail author
Part of the Cancer Growth and Progression book series (CAGP, volume 16)


According to 2008 World Health Organization (WHO) Classification of Tumors of Hematopoietic and Lymphoid Tissue, lymphoid neoplasms are divided into two, mature and immature (precursors), forms including mature B and T/NK cell leukemia/lymphomas and B and T-lymphoblastic leukemia/lymphomas (B-ALL/LBL, T-ALL/LBL). Nowadays a variety of molecular methods are introduced for the modern classification of lymphoid neoplasm system. Although morphological characteristics remain the cornerstone of the evaluation of lymphoid neoplasm, ancillary studies e.g. immunophenotyping and PCR study for T- and B-cell gene rearrangements are routinely implicated in daily service. Different from myeloid neoplasms, the application of molecular/genetic diagnosis and subclassification of lymphoid neoplasm are mainly limited in B-ALL. There are few known protooncogenes or cytogenetic abnormalities in the certain T/NK or B lymphoid malignancies. The chapter focuses on common molecular diagnostic approaches and molecules that implicated in therapeutic strategies, predicting prognosis and monitoring minimal residual disease.


Lymphoid malignancy Cytogenetics Molecular Gene rearrangement Diagnostic and prognostic implications Novel molecular techniques 



Activated B cell-like type


Anaplastic large cell kinase


Acute lymphoblastic leukemias


Anaplastic large T cell lymphoma


Ataxia telangiectasia mutated gene


B-lymphoblastic leukemia/lymphoma


Burkitt lymphoma


B-cell prolymphocytic leukemia


Cyclin dependent kinase 6 gene


Chronic lymphocytic leukemia/small lymphocytic lymphoma


Central nervous system


Common region of amplification


Death-associated protein kinase 1


Diffuse large B-cell lymphoma


Formalin-fixed and paraffin-embedded


Fluorescence in situ hybridization


Fine needle aspirate


Germinal center B-cell like


Intrachromosomal amplification of chromosome 21


Lymphoplasmacytic lymphoma


Major breakpoint cluster region


“minor” breakpoint cluster region


Mycosis fungoides


Multiplex ligation-dependent probe amplification


Minimal residual disease


Natural killer


Non-germinal center B-cell like


Nucleophosmin gene


Polymerase Chain Reaction


Peripheral T cell lymphoma, not otherwise specified


Reverse Polymerase Chain Reaction


Somatic hypermutation


Splenic marginal zone lymphoma


Single Nucleotide Polymorphism Array


T-lymphoblastic leukemia/lymphoma


T cell gene rearrangement


Tyrosine kinase inhibitor


Uniparental disomy


World Health Organization


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Copyright information

© Springer Science+Business Media Dordrecht 2014

Authors and Affiliations

  1. 1.Department of Pathology and Cell BiologyUniversity of South Florida College of MedicineTampaUSA
  2. 2.Department of Hematopathology and Laboratory MedicineMoffitt Cancer Center & Research InstituteTampaUSA

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