Comparative genomic hybridization reveals previously undescribed amplifications and deletions in the chronic myeloid leukemia-derived K-562 cell line

Rodley, Philip; McDonald, Margaret; Price, Brent; Fright, Richard; Morris, Christine M.

doi:10.1002/(sici)1098-2264(199705)19:1<36::aid-gcc6>3.0.co;2-1

Cited by 26 publications

(11 citation statements)

References 27 publications

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“…41 Several amplification mechanisms have been proposed, that is, looping out of extra chromosomal sequences 42 without evidence of chromosomal rearrangements, breakage-fusion-bridge cycles that can be triggered by fragile site induction 43 and a translocationdeletion-amplification model. 44,45 Most of these mechanisms rely on unequal segregation of chromosome sequences during mitosis.…”

Section: Discussionmentioning

confidence: 99%

Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRβ-HOXA rearrangement: a study of the Groupe Francophone de Cytogénétique Hématologique

Cauwelier

Cavé

Gervais³

et al. 2006

Leukemia

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Recently, we and others described a new chromosomal rearrangement, that is, inv(7)(p15q34) and t(7;7)(p15;q34) involving the T-cell receptor beta (TCRb) (7q34) and the HOXA gene locus (7p15) in 5% of T-cell acute lymphoblastic leukemia (T-ALL) patients leading to transcriptional activation of especially HOXA10. To further address the clinical, immunophenotypical and molecular genetic findings of this chromosomal aberration, we studied 330 additional T-ALLs. This revealed TCRb-HOXA rearrangements in five additional patients, which brings the total to 14 cases in 424 patients (3.3%). Real-time quantitative PCR analysis for HOXA10 gene expression was performed in 170 T-ALL patients and detected HOXA10 overexpression in 25.2% of cases including all the cases with a TCRb-HOXA rearrangement (8.2%). In contrast, expression of the short HOXA10 transcript, HOXA10b, was almost exclusively found in the TCRb-HOXA rearranged cases, suggesting a specific role for the HOXA10b short transcript in TCRb-HOXA-mediated oncogenesis. Other molecular and/or cytogenetic aberrations frequently found in subtypes of T-ALL (SIL-TAL1, CALM-AF10, HOX11, HOX11L2) were not detected in the TCRb-HOXA rearranged cases except for deletion 9p21 and NOTCH1 activating mutations, which were present in 64 and 67%, respectively. In conclusion, this study defines TCRb-HOXA rearranged T-ALLs as a distinct cytogenetic subgroup by clinical, immunophenotypical and molecular genetic characteristics.

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Section: Discussionmentioning

confidence: 99%

Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRβ-HOXA rearrangement: a study of the Groupe Francophone de Cytogénétique Hématologique

Cauwelier

Cavé

Gervais³

et al. 2006

Leukemia

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“…However, amplification of 9q34 is not correlated with currently used histopathological parameters for defining benign and malignant features, neither could it be used as a prognostic parameter. Candidate amplified genes mapped to this locus might be the cellular oncogene c-abl (16,17), the tumor suppressor gene described as tuberous sclerosis gene TSC1 (18,19), which is characterized by the widespread development of distinctive tumors termed hamartomas (20). Furthermore, it has been reported that 9q34 encompasses the locus or the loci for ovarian cancer and the familial nevoid basal cell carcinoma syndrome (Gorlin syndrome) (21), transitional cell carcinoma of the bladder (22,23) and other genes, such as steroidogenic factor 1 (24).…”

Section: Amplification Of 9q34mentioning

confidence: 99%

Amplification of 9q34 in childhood adrenocortical tumors: a specific feature unrelated to ethnic origin or living conditions

Figueiredo

Ribeiro

Zambetti

et al. 2000

Braz J Med Biol Res

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Adrenocortical tumors (ACT) in children under 15 years of age exhibit some clinical and biological features distinct from ACT in adults. Cell proliferation, hypertrophy and cell death in adrenal cortex during the last months of gestation and the immediate postnatal period seem to be critical for the origin of ACT in children. Studies with large numbers of patients with childhood ACT have indicated a median age at diagnosis of about 4 years. In our institution, the median age was 3 years and 5 months, while the median age for first signs and symptoms was 2 years and 5 months (N = 72). Using the comparative genomic hybridization technique, we have reported a high frequency of 9q34 amplification in adenomas and carcinomas. This finding has been confirmed more recently by investigators in England. The lower socioeconomic status, the distinctive ethnic groups and all the regional differences in Southern Brazil in relation to patients in England indicate that these differences are not important to determine 9q34 amplification. Candidate amplified genes mapped to this locus are currently being investigated and Southern blot results obtained so far have discarded amplification of the abl oncogene. Amplification of 9q34 has not been found to be related to tumor size, staging, or malignant histopathological features, nor does it seem to be responsible for the higher incidence of ACT observed in Southern Brazil, but could be related to an ACT from embryonic origin.

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“…Only one cell line, K-562, has been reported with this alteration hitherto. [34][35][36] K-562 was established in 1970 37 and has been widely distributed since; whereas SPI-802 was first reported more than 10 years later. 38 Conventional karyotyping revealing the presence of a der(2;11)(q10;q10) marker chromosome as originally described additionally confirms the real identity of SPI-802.…”

Section: Cross-contamination Of Hematopoietic Cell Linesmentioning

confidence: 99%

False human hematopoietic cell lines: cross-contaminations and misinterpretations

1999

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nized in the scientific community. Even if the contaminating cells have only a slight growth advantage, the intruding cells will overgrow and completely replace the original cell line, sooner or later. The most notorious culprit of such cross-contamination is, of course, the infamous solid tumor cell line HeLa. 3 The history of cell cross-contamination in cell cultures is long and painful; the first report on cell line cross-contamination appeared in 1957. [4][5][6][7][8][9] The advent of forensic DNA profiling and its application to cell line identity testing now permits the detection and identification of cell line crosscontamination with levels of sensitivity and accuracy greatly surpassing those achievable in classical surveys. The salient aspects of this common cell culture problem have been highlighted in a recent review. 9 It has been estimated that more than one-third (!) of cell cultures in use are cross-contaminated either with cells from other species (interspecies contamination) or with unrelated cells from the same species (intraspecies contamination). 9 Such cell cultures may be grown, maintained, and used for years, and results may be published without documented authenticity of the cells. The potential problems and even dangers in using cross-contaminated cell cultures for the quality of research and production in virtually any scientific or biomedical area cannot be overemphasized (invalid research results, financial loss, bodily harm, etc).Our cell line bank experience shows that in a recent series from 1990 to 1998 a large percentage of allegedly new human cell lines (cell lines derived from solid tumors and hematopoietic malignancies) which were received from the original investigators (in contrast to cell cultures obtained from secondary sources) were cross-contaminated with other cell lines: 10• 45/252 (18%) human cell lines were false; • 27/93 (29%) original donors supplied false cell lines. High incidence of cross-contaminated cell linesOur data on cross-contaminated cell lines quoted above are, presumably, only the tip of the iceberg: as pointed out, these findings refer to cell lines which were received from the original investigators. Commonly, cell lines are passed from laboratory to laboratory and here the percentages of false cell lines are definitely higher. While undoubtedly the majority of cases go unnoticed or are occasionally detected and then silently corrected, the frequency of intra-and interspecies contamination events can be surmised from several publications that offer résumés of experiences with cultures submitted specifically for monitoring and excluding crosscontamination.Nelson-Rees et al [5][6][7]11 found that 41/253 (16%) cell cultures from 45 laboratories were not as they were purported to be;

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Comparative genomic hybridization reveals previously undescribed amplifications and deletions in the chronic myeloid leukemia-derived K-562 cell line

Cited by 26 publications

References 27 publications

Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRβ-HOXA rearrangement: a study of the Groupe Francophone de Cytogénétique Hématologique

Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRβ-HOXA rearrangement: a study of the Groupe Francophone de Cytogénétique Hématologique

Amplification of 9q34 in childhood adrenocortical tumors: a specific feature unrelated to ethnic origin or living conditions

False human hematopoietic cell lines: cross-contaminations and misinterpretations

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