DNA Methylation Changes in the <i>IL‐I</i> (2F) Chromosomal Region of Some Radiation‐Induced Acute Myeloid Leukaemias Carrying Chromosome 2 Rearrangements

Silver, Andrew; George, Andrew M.; Masson, W.K.; Breckon, G.; Adam, Julie; Cox, Roger

doi:10.1002/gcc.2870030508

Cited by 11 publications

(15 citation statements)

References 11 publications

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“…These were diagnosed on the basis of established histopathological criteria and studied either at the primary stage or at the in vivo passages given elsewhere (7). DNA Preparation, Digestion, and Analysis.…”

Section: Methodsmentioning

confidence: 99%

“…DNA fragments were transferred to Hybond N+ membranes (Amersham) using 0.4 M NaOH and hybridized overnight at 480C with a (TTAGGG)4 synthetic oligonucleotide prepared and labeled as described elsewhere (11). Conditions for membrane hybridization and washing were the same as those described (7). Membranes were subsequently autoradiographed overnight using intensifying screens (Kodak The publication costs of this article were defrayed in part by page charge payment.…”

Section: Methodsmentioning

confidence: 99%

“…Preliminary evidence on the irregular inheritance patterns for these variant sequences is discussed together with the proposal that one form of these telomere sequence arrays either represents or is closely linked to a locus that influences chromosome 2 breakage patterns in hemopoietic cells following irradiation and, through this, susceptibility to induced myeloid leukemia. tion events in a number ofAMLs (7). This RSS-expressing 2F region shows genetic homologies with the human 2q12-21 region (8) that encodes FRA2B and a telomere repeat sequence (9).…”

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confidence: 94%

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Telomere-like DNA polymorphisms associated with genetic predisposition to acute myeloid leukemia in irradiated CBA mice.

Silver¹,

Cox²

1993

Proc. Natl. Acad. Sci. U.S.A.

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There is evidence that interstitial telomere (TTAGGG)n-like sequences at chromosome 2 fragile sites play an important role in the somatic events that characterize the earliest phases of radiation-induced acute myeloid leukemia in the CBA/H mouse. Here we show that the highly inbred CBA/H colony unexpectedly contains four genotypic variants for telomere-like sequence arrays and that almost all induced myeloid leukemias derive from one of the variant subpopulations that constitutes approximately 20% of the colony. Preliminary evidence on the irregular inheritance patterns for these variant sequences is discussed together with the proposal that one form of these telomere sequence arrays either represents or is closely linked to a locus that influences chromosome 2 breakage patterns in hemopoietic cells following irradiation and, through this, susceptibility to induced myeloid leukemia.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 94%

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Telomere-like DNA polymorphisms associated with genetic predisposition to acute myeloid leukemia in irradiated CBA mice.

Silver¹,

Cox²

1993

Proc. Natl. Acad. Sci. U.S.A.

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“…Nuclei were counted and approximately 1×10 6 were embedded in 1% low gelling temperature agarose (Flowgen). Agarose plugs were then processed according to Anand (1986) and the DNA in plugs digested with 80 U Hinf1 for 4 h at 37°C, as described previously (Silver et al, 1991). DNA was fractionated though a 1% agarose gel in 0.5 × Trisborate-EDTA buffer by pulsed field gel electrophoresis (PFGE) using a CHEF mapper system (Biorad).…”

Section: Telomere Length Analysismentioning

confidence: 99%

Telomerase activity in melanoma and non-melanoma skin cancer

Parris

Jezzard

Silver³

et al. 1998

Br J Cancer

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Summary Telomeres are specialized structures consisting of repeat arrays of TTAGGG n located at the ends of chromosomes. They are essential for chromosome stability and, in the majority of normal somatic cells, telomeres shorten with each cell division. Most immortalized cell lines and tumours reactivate telomerase to stabilize the shortening chromosomes. Telomerase activation is regarded as a central step in carcinogenesis and, here, we demonstrate telomerase activation in premalignant skin lesions and also in all forms of skin cancer. Telomerase activation in normal skin was a rare event, and among 16 samples of normal skin (one with a history of chronic sun exposure) 12.5% (2 out of 16) exhibited telomerase activity. One out of 16 (6.25%) benign proliferative lesions, including viral and seborrhoeic wart samples, had telomerase activity. In premalignant actinic keratoses and Bowen's disease, 42% (11 out of 26) of samples exhibited telomerase activity. In the basal cell carcinoma and cutaneous malignant melanoma (CMM) lesions, telomerase was activated in 77% (10 out of 13) and 69% (22 out of 32) respectively. However, only 25% (3 out of 12) of squamous cell carcinomas (SCC) had telomerase activity. With the exception of one SCC sample, telomerase activity in a positive control cell line derived from a fibrosarcoma (HT1080) was not inhibited when mixed with the telomerase-negative SCC or CMM extracts, indicating that, overall, Taq polymerase and telomerase inhibitors were not responsible for the negative results. Mean telomere hybridizing restriction fragment (TRF) analysis was performed in a number of telomerase-positive andnegative samples and, although a broad range of TRF sizes ranging from 3.6 to 17 kb was observed, a relationship between telomerase status and TRF size was not found.

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“…These data provide strong evidence indicating that imprinting may play an important role in the acquired chromosomal rearrangement and add a new dimension to the whole field of human hemopoietically derived cancers; in most of them, somatic chromosomal rearrangements are involved. It has been reported that a similar mechanism operates in certain murine leukemias (Silva et al, 1991), and it has been proposed that translocation of a n imprinted gene to a new location may activate these genes Reik, 1992). We suggest that imprinted genes play a special role in carcinogenesis through two independent mechanisms: 1) a n imprinted gene may act as a tumor suppressor gene and imprinting inactivates one of the gene's allele; 2) they act through a "gain of function" mechanism as oncogenes; if during translocation the imprinted gene loses the "imprinting sequence" that inhibited its expression, the genes become activated.…”

mentioning

confidence: 88%