Telomeric association in women with breast and uterine cervix cancer

Paz‐y‐Miño, César; Sánchez, María Eugenia; Pozo, Mercedes Del; Baldéon, Ma.Augusta; Córdova, Augusta; Gutiérrez, Sara; Peñaherrera, Ma.Serena; Neira, Marco; Ocampo, Ligia; Leone, Paola

doi:10.1016/s0165-4608(96)00420-7

Cited by 10 publications

(8 citation statements)

References 29 publications

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“…Ulcerative colitis is characterized by an increased risk for colorectal cancer, which may be linked to global genomic instability. Chromosome aberrations and telomere fusions in PBLs have often been used as markers for genetic cancer risk and have been found at higher frequencies in UC 14–22 . This is the first study to investigate whether chromosome instability in UC PBLs could be caused by accelerated telomere shortening induced by chronic inflammation.…”

Section: Discussionmentioning

confidence: 95%

“…Higher frequencies of chromosomal rearrangements and telomere fusions have also been observed in peripheral blood lymphocytes (PBLs) in UC 14 . This may indicate a global predisposition towards genomic instability in IBD, which could represent a biomarker for increased cancer risk, as has been observed in several other malignant and premalignant diseases, 15–20 including colon cancer 21 and celiac disease 22 . Alternatively, this chromosome instability could be caused by environmental factors including those related to inflammation.…”

Section: Introductionmentioning

confidence: 90%

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Lymphocyte telomere dynamics and telomerase activity in inflammatory bowel disease: effect of drugs and smoking

Getliffe

Dulaimi

Martin‐Ruiz³

et al. 2005

Aliment Pharmacol Ther

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SUMMARYBackground: The chromosome instability observed in peripheral blood lymphocytes in ulcerative colitis could be a biomarker of cancer susceptibility. Aim: To determine whether accelerated telomere shortening could explain chromosome instability and assess the effect of drugs and smoking on telomere dynamics in these cells. Methods: Peripheral blood lymphocytes were isolated from ulcerative colitis, Crohn's disease and noninflammatory bowel disease control patients. Telomere lengths were measured by quantitative real-time polymerase chain reaction. After activation and cell separation, telomerase activity and human telomerase reverse transcriptase messenger ribonucleic acid were measured by telomerase repeat amplification protocol enzyme-linked immunosorbent serological assay and

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Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 90%

Lymphocyte telomere dynamics and telomerase activity in inflammatory bowel disease: effect of drugs and smoking

Getliffe

Dulaimi

Martin‐Ruiz³

et al. 2005

Aliment Pharmacol Ther

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“…[9][10][11]23 It is also noteworthy that the phenomenon of telomeric associations is not specific and can be found in a variety of neoplasms. [24][25][26][27][28] Therefore, the identification of telomeric associations in just one case of soft tissue giant cell tumor can hardly be regarded as solid evidence that both tumors belong to one unified entity.…”

Section: Discussionmentioning

confidence: 99%

Giant cell tumor of soft tissue is genetically distinct from its bone counterpart

2017

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Giant cell tumors of bone are locally aggressive bone neoplasms with a predilection for young adults. Histologically, they are composed of histiocytoid to spindled mononuclear cells, admixed with numerous large osteoclastic giant cells. Giant cell tumors of soft tissue are rare tumors that bear striking histological resemblance to giant cell tumors of bone and might be regarded as a soft tissue analog thereof. Point mutations of the H3F3A gene (coding for a histone H3.3 protein) at the Gly34 codon, mostly G34W resulting from a GGG>TGG nucleotide change, have recently been identified in a vast majority of giant cell tumors of bone. To delineate the possible pathogenic linkage between both tumor types, we analyzed the H3F3A genotypes in a series of 15 giant cell tumors of soft tissue by Sanger sequencing and found no mutation in any case. We then sequenced cognate histone H3 genes with an identical nucleotide sequence ('GGG') at the codon Gly34, including the H3F3B, H3F3C, HIST2H3A, HIST2H3C, and HIST2H3D genes, and no somatic mutation was detected. These results reveal that giant cell tumors of soft tissue are probably genetically distinct from their bone counterparts and suggest that they might be pathogenically unrelated. Given the prominence of non-neoplastic cells in these tumors and the limitations of the current study, however, analyses using more sensitive techniques might be required to solve the issue.

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“…In support of this, telomere shortening and instability was recently shown in a human tumor cell line expressing an NBS1 allele with mutated ATM-phosphorylation sites (16). Telomere associations are cytogenetic anomalies in which telomeres are observed in unusually close proximity to one another; these events have been reported not only in ataxia telangiectasia (21,22), but also in tumor cells, for example, from breast cancer (23). The cause of telomere association and their downstream effects are not well understood.…”

Section: Introductionmentioning

confidence: 99%

NBS1 Knockdown by Small Interfering RNA Increases Ionizing Radiation Mutagenesis and Telomere Association in Human Cells

et al. 2005

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Hypomorphic mutations which lead to decreased function of the NBS1 gene are responsible for Nijmegen breakage syndrome, a rare autosomal recessive hereditary disorder that imparts an increased predisposition to development of malignancy. The NBS1 protein is a component of the MRE11/ RAD50/NBS1 complex that plays a critical role in cellular responses to DNA damage and the maintenance of chromosomal integrity. Using small interfering RNA transfection, we have knocked down NBS1 protein levels and analyzed relevant phenotypes in two closely related human lymphoblastoid cell lines with different p53 status, namely wild-type TK6 and mutated WTK1. Both TK6 and WTK1 cells showed an increased level of ionizing radiation-induced mutation at the TK and HPRT loci, impaired phosphorylation of H2AX (;-H2AX), and impaired activation of the cell cycle checkpoint regulating kinase, Chk2. In TK6 cells, ionizing radiationinduced accumulation of p53/p21 and apoptosis were reduced. There was a differential response to ionizing radiation-induced cell killing between TK6 and WTK1 cells after NBS1 knockdown; TK6 cells were more resistant to killing, whereas WTK1 cells were more sensitive. NBS1 deficiency also resulted in a significant increase in telomere association that was independent of radiation exposure and p53 status. Our results provide the first experimental evidence that NBS1 deficiency in human cells leads to hypermutability and telomere associations, phenotypes that may contribute to the cancer predisposition seen among patients with this disease. (Cancer Res 2005; 65(13): 5544-53)

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Telomeric association in women with breast and uterine cervix cancer

Cited by 10 publications

References 29 publications

Lymphocyte telomere dynamics and telomerase activity in inflammatory bowel disease: effect of drugs and smoking

Lymphocyte telomere dynamics and telomerase activity in inflammatory bowel disease: effect of drugs and smoking

Giant cell tumor of soft tissue is genetically distinct from its bone counterpart

NBS1 Knockdown by Small Interfering RNA Increases Ionizing Radiation Mutagenesis and Telomere Association in Human Cells

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