Gain of the short arm of chromosome 2 (2p) is a frequent recurring chromosome aberration in untreated chronic lymphocytic leukemia (CLL) at advanced stages

Chapiro, Élise; Leporrier, Nathalie; Radford‐Weiss, Isabelle; Bastard, Christian; Mossafa, Hossein; Leroux, Dominique; Tigaud, Isabelle; Braekeleer, Marc De; Terré, Christine; Brizard, Françoise; Callet‐Bauchu, Evelyne; Struski, Stéphanie; Véronèse, Lauren; Fert‐Ferrer, Sandra; Taviaux, Sylvie; Lesty, Claude; Davi, Frédéric; Merle-Béral, Hélène; Bernard, Olivier A.; Sutton, Laurent; Raynaud, Sophie; Nguyen‐Khac, Florence

doi:10.1016/j.leukres.2009.03.042

Cited by 54 publications

(55 citation statements)

References 18 publications

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“…Interestingly, 2p gain was detected as the sole cytogenetic lesion in six cases: this is unlike most reports [14,15,19,20,39] where 2p gain was always detected together with the most frequent cytogenetic lesions. In the remaining 11 cases, 2p gain was significantly associated with the presence of 11q deletion (P 5 0.016).…”

Section: Discussioncontrasting

confidence: 91%

“…Although previous studies suggested various genes (REL, BCL11A, MYCN, ALK, and more recently ACP1) [14][15][16][17][18][19][20][21][22]24] as potential targets of the 2p gain, no firm data supporting this notion are available. We used a microarray technology approach in order to characterize the putative critical region of 2p gain as well as the deregulated genes in the context of the chromosomal alteration.…”

Section: Discussionmentioning

confidence: 99%

“…Previous retrospective studies based on FISH, comparative genomic hybridization (aCGH) and SNP array identified 2p gain as a recurrent alteration in CLL associated with advanced Binet stage, UM status of IGHV gene and 17p13 deletion [12,[14][15][16][17][18][19][20][21][22]24,[39][40][41][42].…”

Section: Discussionmentioning

confidence: 99%

“…Whole genome analyses have provided additional information on novel recurrent alterations in CLL, such as gain of the short arm of chromosome 2 (2p). In particular, these studies focused on putative oncogenes such as BCL11A, REL, and MYCN, located at 2p, as possible deregulated targets [14][15][16][17][18][19][20][21][22][23][24]. However, with the exception of a very recent report [25], most of the available and representative studies investigating 2p gain have been performed in quite heterogeneous and retrospective series of patients encompassing various stages of the disease, making it difficult to ascertain the involvement and role of 2p gain in the disease.…”

Section: Introductionmentioning

confidence: 99%

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Chromosome 2p gain in monoclonal B‐cell lymphocytosis and in early stage chronic lymphocytic leukemia

et al. 2012

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Recent studies have described chromosome 2p gain as a recurrent lesion in chronic lymphocytic leukemia (CLL). We investigated the 2p gain and its relationship with common prognostic biomarkers in a prospective series of 69 clinical monoclonal B-cell lymphocytosis (cMBL) and 218 early stage (Binet A) CLL patients. The 2p gain was detected by FISH in 17 patients (6%, 16 CLL, and 1 cMBL) and further characterized by single nucleotide polymorphism-array. Overall, unfavorable cytogenetic deletions, i.e., del(11)(q23) and del(17)(p13) (P 5 0.002), were significantly more frequent in 2p gain cases, as well as unmutated status of IGHV (P < 1 3 10 24 ) and CD38 (P < 1 3 10 24 ) and ZAP-70 positive expression (P 5 0.003). Furthermore, 2p gain patients had significantly higher utilization of stereotyped B-cell receptors compared with 2p negative patients (P 5 0.009), and the incidence of stereotyped subset #1 in 2p gain patients was significantly higher than that found in the remaining CLLs (P 5 0.031). Transcriptional profiling analysis identified several genes significantly upregulated in 2p gain CLLs, most of which mapped to 2p. Among these, NCOA1 and ROCK2 are known for their involvement in tumor progression in several human cancers, whereas among those located in different chromosomes, CAV1 at 7q31.1 has been recently identified to play a critical role in CLL progression. Thus, 2p gain can be present since the early stages of the disease, particularly in those cases characterized by other poor prognosis markers. The finding of genes upregulated in the cells with 2p gain provides new insights to define the pathogenic role of this lesion. Am. J. Hematol. 88:24-31, 2013. V

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Section: Discussioncontrasting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Chromosome 2p gain in monoclonal B‐cell lymphocytosis and in early stage chronic lymphocytic leukemia

et al. 2012

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“…These findings were confirmed by FISH with the LSI ALK, LSI NMYC, CEP 2 and REL-specific BAC probes. Our research team published finding 2p gains in another cohort of CLL cases 24 , and its prognostic significance was re- cently confirmed by Chapiro et al 34 . In 3 patients, the 2p gain was accompanied by other cytogenetic abnormalities (nos.…”

Section: Discussionsupporting

confidence: 60%

Array-based karyotyping in chronic lymphocytic leukemia (CLL) detects new unbalanced abnormalities that escape conventional cytogenetics and CLL FISH panel

Urbánková¹,

Papajík²,

Plachy³

et al. 2014

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Aims. Chronic lymphocytic leukemia (CLL) is the most common adult leukemia with a very heterogeneous course. Progress in molecular genetic characterization of CLL has confirmed the prognostic role of unbalanced chromosomal abnormalities currently defined by molecular cytogenetic methods: conventional karyotyping and FISH. However, a significant percentage of genomic abnormalities escapes routine investigation due to the limitations of these methods. It is presently clear that some of these aberrations have impact on prognosis and disease progression. Methods. We examined copy number changes in the tumor genomes of 50 CLL patients using bacterial artificial chromosome (BAC) and/or oligonucleotide array platforms. We compared the results of arrayCGH with those obtained by FISH and conventional cytogenetics and evaluated their clinical importance. Results. A total of 111 copy number changes were detected in 43 patients (86%) with clonal abnormalities present in at least 23% of the cells. Moreover, 14 patients (28%) were found to have 39 genomic changes that had not been detected by standard cytogenetic and/or FISH analyses. These included possibly prognostically important recurrent 2p and 8q24 gains. The most frequent unbalanced changes involved chromosomes 18, 7, 3, 9 and 17. We also determined the minimal deleted region on chromosome 6q in 7 cases by chromosome 6/7 specific array. Conclusions. The results showed that a subset of potentially significant genomic aberrations in CLL is being missed by the current routine techniques. Further, we clearly demonstrated the robustness, high sensitivity and specificity of the arrayCGH analysis as well as its potential for use in routine screening of CLL.

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The genetics of mature B‐cell malignancies

Strefford¹,

Fitzgibbon²,

Rose-Zerilli³

et al. 2016

The Genetic Basis of Haematological Cancers

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Gain of the short arm of chromosome 2 (2p) is a frequent recurring chromosome aberration in untreated chronic lymphocytic leukemia (CLL) at advanced stages

Cited by 54 publications

References 18 publications

Chromosome 2p gain in monoclonal B‐cell lymphocytosis and in early stage chronic lymphocytic leukemia

Chromosome 2p gain in monoclonal B‐cell lymphocytosis and in early stage chronic lymphocytic leukemia

Array-based karyotyping in chronic lymphocytic leukemia (CLL) detects new unbalanced abnormalities that escape conventional cytogenetics and CLL FISH panel

The genetics of mature B‐cell malignancies

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