The role of immunoglobulin translocations in the pathogenesis of B-cell malignancies

Willis, Tony G.; Dyer, Martin J.S.

doi:10.1182/blood.v96.3.808

Cited by 241 publications

(84 citation statements)

References 190 publications

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“…These alterations are rare in NSCLC but common in hematologic malignancies, suggesting that GAs found in ctDNA are not always derived from the expected tumor. [17][18][19] The MSAF in these cases was not notably different from the overall population (median 1.66%), and in some cases known driver alterations in NSCLC were also present. Clinical implications of these incidental findings in ctDNA of patients with NSCLC, including the potential for diagnosis of a secondary malignancy or CHIP, 20 warrant further study.…”

Section: Discussionmentioning

confidence: 69%

Hybrid Capture–Based Genomic Profiling of Circulating Tumor DNA from Patients with Advanced Non–Small Cell Lung Cancer

Schrock¹,

Welsh²,

Chung³

et al. 2019

Journal of Thoracic Oncology

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Introduction: Genomic profiling informs selection of matched targeted therapies as part of routine clinical care in NSCLC. Tissue biopsy is the criterion standard; however, genomic profiling of blood-derived circulating tumor DNA (ctDNA) has emerged as a minimally invasive alternative. Methods: Hybrid capture-based genomic profiling of 62 genes was performed on blood-based ctDNA from 1552 patients with NSCLC. Results: Evidence of ctDNA was detected in 80% of samples, and in 86% of these cases, at least one reportable genomic alteration (GA) was detected. Frequently altered genes were tumor protein p53 gene (TP53) (59%), EGFR (25%), and KRAS (17%). Comparative analysis with a tissue genomic database (N ¼ 21,500) showed similar frequencies of GAs per gene, although KRAS mutation and EGFR T790M were more frequent in tissue and ctDNA, respectively (both p < 0.0001), likely reflecting the use of liquid versus tissue biopsy after relapse during targeted therapy. In temporally matched ctDNA and tissue samples from 33 patients with evidence of ctDNA in their blood, 64% of GAs detected in tissue were also detected in ctDNA, including 78% of short variants (58 of 74) and 100% of rearrangements (four of four), but only 16% of amplifications (four of 25).

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Section: Discussionmentioning

confidence: 69%

Hybrid Capture–Based Genomic Profiling of Circulating Tumor DNA from Patients with Advanced Non–Small Cell Lung Cancer

Schrock¹,

Welsh²,

Chung³

et al. 2019

Journal of Thoracic Oncology

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“…The involvement of the immunoglobulin heavy chain locus ( IGH@ ) is well known in mature B‐cell malignancies, in particular the translocation, t(8;14)(q24;q32), involving IGH@ and the MYC gene (Willis & Dyer, 2000). Recently, we have demonstrated a significant role of IGH@ in BCP‐ALL.…”

Section: Hot Topic 3: Translocations Involving the Immunoglobulin Heamentioning

confidence: 99%

Cytogenetics of paediatric and adolescent acute lymphoblastic leukaemia

2008

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Summary Cytogenetics has determined the incidence and prognostic significance of chromosomal abnormalities in acute lymphoblastic leukaemia (ALL). The development of fluorescence in situ hybridization (FISH) and array technologies has led to the discovery of novel aberrations. Five ‘hot topics’ are presented in which cytogenetics and related techniques have been instrumental in understanding the role of genetics in leukaemogenesis: (i) genetic changes are integral to the biology of T‐cell ALL; (ii) intrachromosomal amplification of chromosome 21 is a new recurrent abnormality in precursor‐B ALL (BCP‐ALL); (iii) the immunoglobulin heavy chain gene (IGH@) is significant in BCP‐ALL; (iv) alterations in genes involved in B‐cell development and cell cycle control contribute to the pathogenesis of BCP‐ALL; (v) age‐related cytogenetic profiles define ALL in children and adolescents as distinct biological entities. In this molecular era, cytogenetics continues to be integral to our understanding of the genetics of this disease.

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“…In support of this idea, the use of Ig idiotypic markers indicated an expansion of the IgM + B‐cell precursors in patients with IgA producing plasma cell myelomas (77) and of pre‐B cells belonging to the neoplastic clone in patients with B‐cell leukemias (78) and lymphomas (79). A diverse array of cumulative mutational events from the stem cell onward have now been elucidated in B lineage malignancies, many of which involve immunoglobulin gene translocations (80).…”

Section: Human Immunodeficiencies and Lymphoid Malignanciesmentioning

confidence: 99%

Exploring lymphocyte differentiation pathways

Cooper

2002

Immunological Reviews

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Highlights in a 4-decade exploration of lymphocyte differentiation begin with comparative studies in birds and mammals leading to recognition of the separate T- and B-cell differentiation pathways and their cooperative interaction. The global effects of aborting IgM B-cell development with anti-mu antibodies indicated that B cells can undergo immunoglobulin isotype switching. A search for the mammalian bursa equivalent that began with an extended excursion through the gut-associated lymphoepithelial tissues ultimately led to the hematopoietic tissue origin of mammalian B cells. The identification of the precursors of B cells in hematopoietic tissues provided an expanded view of the life history of B cells. A recurring theme in this essay is the interplay between understanding normal lymphocyte differentiation and the defects that underlie immunodeficiency diseases and lymphoid malignancies.

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The role of immunoglobulin translocations in the pathogenesis of B-cell malignancies

Cited by 241 publications

References 190 publications

Hybrid Capture–Based Genomic Profiling of Circulating Tumor DNA from Patients with Advanced Non–Small Cell Lung Cancer

Hybrid Capture–Based Genomic Profiling of Circulating Tumor DNA from Patients with Advanced Non–Small Cell Lung Cancer

Cytogenetics of paediatric and adolescent acute lymphoblastic leukaemia

Exploring lymphocyte differentiation pathways

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