Modified allelic replication in lymphocytes of patients with neurofibromatosis type 1

Reish, Orit; Orlovski, Ana; Mashevitz, Maya; Sher, Carron; Libman, Vitalia; Rosenblat, Malka; Avivi, Lydia

doi:10.1016/s0165-4608(02)00858-0

Cited by 13 publications

(13 citation statements)

References 29 publications

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“…Among these are tumor suppressor genes like tumor protein P53 ( p53 ), retinoblastoma 1 ( RB1) ; DNA repair related genes like ATM ; and classical oncogenes like c-myc , HER-2/neu [11,159,160]. These replication timing changes can be specific to one allele resulting in asynchronous replication of the two alleles [11,159,160,162], or biallelic, causing a uniform change of the replication timing of the gene [11]. The B-cell lymphoma 2 (Bcl2) gene, which is frequently translocated in human follicular lymphoma is associated with a change from middle to early replication in the translocated gene in correlation with its overexpression [163].…”

Section: Replication Timingmentioning

confidence: 99%

Perturbations in the Replication Program Contribute to Genomic Instability in Cancer

Blumenfeld

Ben-Zimra

Simon

2017

IJMS

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Cancer and genomic instability are highly impacted by the deoxyribonucleic acid (DNA) replication program. Inaccuracies in DNA replication lead to the increased acquisition of mutations and structural variations. These inaccuracies mainly stem from loss of DNA fidelity due to replication stress or due to aberrations in the temporal organization of the replication process. Here we review the mechanisms and impact of these major sources of error to the replication program.

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Section: Replication Timingmentioning

confidence: 99%

Perturbations in the Replication Program Contribute to Genomic Instability in Cancer

Blumenfeld

Ben-Zimra

Simon

2017

IJMS

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“…Surprisingly, the asynchronous replication pattern observed in cancer patients is not restricted to tumor tissue but also occurs in noncancerous cells as well [66,67,68,69,70]. This is best exemplified by the presence of aberrant asynchronous replication between alleles in the peripheral lymphocytes of individuals with solid tumors [66,67].…”

Section: Dna Replication Timing and The Evolution Of The Cancer Gementioning

confidence: 99%

“…This is best exemplified by the presence of aberrant asynchronous replication between alleles in the peripheral lymphocytes of individuals with solid tumors [66,67]. This replication asynchrony has been documented at multiple loci for many cancer-related genes and many other genomic locations indicating that this is not just the deregulation of a single locus or a single chromosome, but a widespread phenomenon [66,68,71].…”

Section: Dna Replication Timing and The Evolution Of The Cancer Gementioning

confidence: 99%

“…This replication asynchrony has been documented at multiple loci for many cancer-related genes and many other genomic locations indicating that this is not just the deregulation of a single locus or a single chromosome, but a widespread phenomenon [66,68,71]. Interestingly, this altered replication-timing pattern is present in pre-malignant cells, in individuals pre-disposed to cancer, and in individuals living in polluted areas with a high likelihood of getting cancer, suggesting that this may be an early event during carcinogenesis [63,65,67,72]. The replication asynchrony observed in cancerous tissue and normal cells in individuals with cancer is generally a result of the earlier replication of one of the alleles [67,70,72], however, in some cases the delayed replication of one allele has been detected [71].…”

Section: Dna Replication Timing and The Evolution Of The Cancer Gementioning

confidence: 99%

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DNA replication timing, genome stability and cancer

Donley

Thayer

2013

Seminars in Cancer Biology

109

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Normal cellular division requires that the genome be faithfully replicated to ensure that unaltered genomic information is passed from one generation to the next. DNA replication initiates from thousands of origins scattered throughout the genome every cell cycle; however, not all origins initiate replication at the same time. A vast amount of work over the years indicates that different origins along each eukaryotic chromosome are activated in early, middle or late S phase. This temporal control of DNA replication is referred to as the replication-timing program. The replication-timing program represents a very stable epigenetic feature of chromosomes. Recent evidence has indicated that the replication-timing program can influence the spatial distribution of mutagenic events such that certain regions of the genome experience increased spontaneous mutagenesis compared to surrounding regions. This influence has helped shape the genomes of humans and other multicellular organisms and can affect the distribution of mutations in somatic cells. It is also becoming clear that the replication-timing program is deregulated in many disease states, including cancer. Aberrant DNA replication timing is associated with changes in gene expression, changes in epigenetic modifications and an increased frequency of structural rearrangements. Furthermore, certain replication timing changes can directly lead to overt genomic instability and may explain unique mutational signatures that are present in cells that have undergone the recently described processes of “chromothripsis” and “kataegis”. In this review, we will discuss how the normal replication timing program, as well as how alterations to this program, can contribute to the evolution of the genomic landscape in normal and cancerous cells.

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“…Of fundamental importance is whether replication timing can be reorganized during cancer progression. Some studies have found that replication timing is asynchronous in multiple types of cancer [Amiel et al, 1997, 1998; Korenstein‐Ilan et al, 2002; Reish et al, 2003; Dotan et al, 2004]. Other studies have found late replication in diseases characterized by chromosome instability [Otto et al, 1981; Kuhn et al, 1987] and translocations [Breger et al, 2005].…”

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confidence: 99%

Rational approach to implementation of prostate cancer antigen 3 into clinical care

Wang

Chinnaiyan

Dunn

et al. 2009

Cancer

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Background Prostate cancer gene 3 (PCA3) encodes a prostate-specific messenger RNA (mRNA) that serves as the target for a novel urinary molecular assay for prostate cancer detection. Our objective is to evaluate the ability of PCA3 in addition to serum prostate-specific antigen (PSA) to predict cancer detection by extended template biopsy. Methods From September 2006 to December 2007, whole urine samples were collected after attentive digital rectal exam from 187 men prior to ultrasound-guided 12-core prostate biopsy in a urology outpatient clinic. Urine PCA3/PSA mRNA ratio scores were measured within one month and serum PSA within six months of biopsy. These were related to cancer positivity on biopsy. Results Overall, 87/187 (46.5%) biopsies were positive for cancer. Sensitivity and specificity of PCA3 score ≥35 for positive biopsy were 52.9% and 80.0%; positive and negative predictive values were 69.7% and 66.1%. Using receiver operating characteristic curve (ROC) analysis, PSA alone resulted in an area under the curve (AUC) of 0.63 for prostate cancer detection; PSA + PCA3 score resulted in an AUC of 0.71. The likelihood of prostate cancer detection rose with increasing PCA3 score ranges (p>0.0001), providing possible PCA3 score parameters for stratification into low, moderate, high, and very high risk groups for biopsy positivity. Conclusion Adding PCA3 to serum PSA improves prostate cancer prediction. Use of PCA3 in a clinical setting may help risk-stratify patients for biopsy and cancer detection, although a large-scale validation study is needed to address assay standardization, optimal cut-off values and appropriate patient populations.

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Modified allelic replication in lymphocytes of patients with neurofibromatosis type 1

Cited by 13 publications

References 29 publications

Perturbations in the Replication Program Contribute to Genomic Instability in Cancer

Perturbations in the Replication Program Contribute to Genomic Instability in Cancer

DNA replication timing, genome stability and cancer

Rational approach to implementation of prostate cancer antigen 3 into clinical care

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