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Showing 1-30 of 3169 results for "05-636" within Papers
Lihua H Wang et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 16(3), 1073-1084 (2010-01-28)
Circulating tumor cells (CTC) in peripheral blood of patients potentially represent a fraction of solid tumor cells available for more frequent pharmacodynamic assessment of drug action than is possible using tumor biopsy. However, currently available CTC assays are limited to
Manuela Terranova-Barberio et al.
Journal of experimental & clinical cancer research : CR, 36(1), 177-177 (2017-12-08)
Recurrence with distant metastases has become the predominant pattern of failure in locally advanced rectal cancer (LARC), thus the integration of new antineoplastic agents into preoperative fluoropyrimidine-based chemo-radiotherapy represents a clinical challenge to implement an intensified therapeutic strategy. The present
Randall J Platt et al.
Cell, 159(2), 440-455 (2014-09-30)
CRISPR-Cas9 is a versatile genome editing technology for studying the functions of genetic elements. To broadly enable the application of Cas9 in vivo, we established a Cre-dependent Cas9 knockin mouse. We demonstrated in vivo as well as ex vivo genome
Amy M Lyndaker et al.
Methods in molecular biology (Clifton, N.J.), 2195, 147-165 (2020-08-28)
Testicular germ cell tumors (TGCTs) are among the most curable solid cancers and are typically highly responsive to conventional DNA-damaging chemotherapies, even in patients with metastatic disease. It has therefore been of great interest to understand the basis for the
Chromosomal rearrangement interferes with meiotic X chromosome inactivation.
Homolka, D; Ivanek, R; Capkova, J; Jansa, P; Forejt, J
Genome Research null
Pot1b deletion and telomerase haploinsufficiency in mice initiate an ATR-dependent DNA damage response and elicit phenotypes resembling dyskeratosis congenita.
He, H; Wang, Y; Guo, X; Ramchandani, S; Ma, J; Shen, MF; Garcia, DA; Deng, Y; Multani et al.
Molecular and cellular biology null
Louise Treanor et al.
International journal of oncology, 37(1), 31-39 (2010-06-02)
We have previously reported that deletion of the retinoblastoma gene Rb leads to rapid but transient p53 stabilisation. We investigated here the pathways involved. We show that upon Rb-deletion dysregulated E2F activates p19ARF expression that localises in the nucleoli. There
Rana Lebdy et al.
EMBO reports, 24(12), e57585-e57585 (2023-11-15)
Faithful DNA replication requires specific proteins that protect replication forks and so prevent the formation of DNA lesions that may damage the genome. Identification of new proteins involved in this process is essential to understand how DNA lesions accumulate in
Prachi N Ghule et al.
Cell cycle (Georgetown, Tex.), 14(15), 2501-2508 (2015-06-02)
Histone Nuclear Factor P (HINFP) is essential for expression of histone H4 genes. Ablation of Hinfp and consequential depletion of histones alter nucleosome spacing and cause stalled replication and DNA damage that ultimately result in genomic instability. Faithful replication and
Putzer J Hung et al.
Cell cycle (Georgetown, Tex.), 16(3), 286-295 (2016-11-11)
Non-homologous end joining (NHEJ) is a major DNA double-strand break (DSB) repair pathway that functions in all phases of the cell cycle. NHEJ repairs genotoxic and physiological DSBs, such as those generated by ionizing radiation and during V(D)J recombination at
Florian J Groelly et al.
EMBO molecular medicine, 14(3), e14501-e14501 (2022-02-03)
The cells with compromised BRCA1 or BRCA2 (BRCA1/2) function accumulate stalled replication forks, which leads to replication-associated DNA damage and genomic instability, a signature of BRCA1/2-mutated tumours. Targeted therapies against BRCA1/2-mutated tumours exploit this vulnerability by introducing additional DNA lesions.
Jie Deng et al.
Zhongguo fei ai za zhi = Chinese journal of lung cancer, 14(11), 841-847 (2011-11-23)
The epidermal growth factor receptor (EGFR) is an important determinant of radioresponse, the elevated expression and activity of which frequently correlates with radioresistance in several cancers, including non-small-cell lung carcinoma (NSCLC). The molecular blockade of EGFR signaling is a promising
Roderick J O'Sullivan et al.
Nature structural & molecular biology, 21(2), 167-174 (2014-01-15)
The mechanism of activation of the alternative lengthening of telomeres (ALT) pathway of mammalian chromosome-end maintenance has been unclear. We have now discovered that co-depletion of the histone chaperones ASF1a and ASF1b in human cells induced all hallmarks of ALT
Virginie Maire et al.
PloS one, 8(5), e63712-e63712 (2013-05-24)
Triple-negative breast cancer (TNBC) represents a subgroup of breast cancers (BC) associated with the most aggressive clinical behavior. No targeted therapy is currently available for the treatment of patients with TNBC. In order to discover potential therapeutic targets, we searched
Evert-Jan Uringa et al.
Molecular biology of the cell, 23(14), 2782-2792 (2012-05-18)
Telomere maintenance and DNA repair are important processes that protect the genome against instability. mRtel1, an essential helicase, is a dominant factor setting telomere length in mice. In addition, mRtel1 is involved in DNA double-strand break repair. The role of
Changhwan Yoon et al.
Oncogenesis, 10(1), 12-12 (2021-01-21)
The self-renewal transcription factor Nanog and the phosphoinositide 3-kinase (PI3K)-Akt pathway are known to be essential for maintenance of mesenchymal stem cells. We evaluated their contribution to the maintenance of CD133(+) cancer stem-like cells (CSCs) and spheroid-forming cells in patient-derived
Ribonucleotide reductase and thymidylate synthase or exogenous deoxyribonucleosides reduce DNA damage and senescence caused by C-MYC depletion.
Mannava, S; Moparthy, KC; Wheeler, LJ; Leonova, KI; Wawrzyniak, JA; Bianchi-Smiraglia et al.
Aging null
Yang Zhou et al.
PLoS genetics, 14(8), e1007463-e1007463 (2018-08-14)
Meiosis is a germ cell-specific division that is indispensable for the generation of haploid gametes. However, the regulatory mechanisms of meiotic initiation remain elusive. Here, we report that the Wdr62 (WD40-repeat protein 62) is involved in meiotic initiation as a
Stefanie Liedtke et al.
Stem cells translational medicine, 4(6), 576-589 (2015-04-23)
Comprehensive analyses comparing individual DNA damage response (DDR) of induced pluripotent stem cells (iPSCs) with neonatal stromal cells with respect to their developmental age are limited. The imperative necessity of providing developmental age-matched cell sources for meaningful toxicological drug safety
Xiaojun Liu et al.
Cancer research, 65(15), 6874-6881 (2005-08-03)
2'-C-cyano-2'-deoxy-1-beta-D-arabino-pentofuranosylcytosine (CNDAC) is a nucleoside analogue with a novel mechanism of action that is currently being evaluated in clinical trials. Incorporation of CNDAC triphosphate into DNA and extension during replication leads to single-strand breaks directly caused by beta-elimination. These breaks
Andrea Schäfer et al.
Genes & development, 32(11-12), 742-762 (2018-06-10)
Changes in DNA methylation are among the best-documented epigenetic alterations accompanying organismal aging. However, whether and how altered DNA methylation is causally involved in aging have remained elusive. GADD45α (growth arrest and DNA damage protein 45A) and ING1 (inhibitor of
Kyota Fujita et al.
Nature communications, 8(1), 1864-1864 (2017-12-02)
YAP and its neuronal isoform YAPdeltaC are implicated in various cellular functions. We found that expression of YAPdeltaC during development, but not adulthood, rescued neurodegeneration phenotypes of mutant ataxin-1 knock-in (Atxn1-KI) mice. YAP/YAPdeltaC interacted with RORα via the second WW
Michal Zimmermann et al.
Cell reports, 40(2), 111081-111081 (2022-07-14)
Combinations of ataxia telangiectasia- and Rad3-related kinase inhibitors (ATRis) and poly(ADP-ribose) polymerase inhibitors (PARPis) synergistically kill tumor cells through modulation of complementary DNA repair pathways, but their tolerability is limited by hematological toxicities. To address this, we performed a genome-wide
Kameron Azarm et al.
Nature communications, 11(1), 3321-3321 (2020-07-06)
Human telomeres are bound by the telomere repeat binding proteins TRF1 and TRF2. Telomere shortening in human cells leads to a DNA damage response that signals replicative senescence. While insufficient loading of TRF2 at shortened telomeres contributes to the DNA
Sara Giovannini et al.
Nucleic acids research, 47(17), 9132-9143 (2019-07-23)
Poly(ADP-ribose) polymerases (PARPs) facilitate the repair of DNA single-strand breaks (SSBs). When PARPs are inhibited, unrepaired SSBs colliding with replication forks give rise to cytotoxic double-strand breaks. These are normally rescued by homologous recombination (HR), but, in cells with suboptimal
Valentina Turinetto et al.
Stem cells (Dayton, Ohio), 30(7), 1414-1423 (2012-05-26)
Phosphorylation of histone H2AX (γH2AX) is known to be the earliest indicator of DNA double-strand breaks. Recently, it has been shown that mouse embryonic stem cells (mESCs) have very high basal levels of γH2AX, even when they have not been
Hongyu Chen et al.
Cell proliferation, 53(3), e12780-e12780 (2020-02-08)
RING finger protein 8 (RNF8) is an E3 ligase that plays an essential role in DSB repair. p53 is a well-established tumour suppressor and cellular gatekeeper of genome stability. This study aimed at investigating the functional correlations between RNF8 and
Laia Castells-Roca et al.
NPJ breast cancer, 7(1), 117-117 (2021-09-11)
The tumor suppressor FANCD1/BRCA2 is crucial for DNA homologous recombination repair (HRR). BRCA2 biallelic pathogenic variants result in a severe form of Fanconi anemia (FA) syndrome, whereas monoallelic pathogenic variants cause mainly hereditary breast and ovarian cancer predisposition. For decades
Stefano J Mandriota et al.
The Journal of biological chemistry, 285(17), 13092-13106 (2010-02-24)
Carriers of mutations in the cell cycle checkpoint protein kinase ataxia telangiectasia mutated (ATM), which represent 1-2% of the general population, have an increased risk of breast cancer. However, experimental evidence that ATM deficiency contributes to human breast carcinogenesis is
Jing Li et al.
Clinical and translational medicine, 11(12), e627-e627 (2021-12-20)
Acidic nucleoplasmic DNA-binding protein 1 (And-1), an important factor for deoxyribonucleic acid (DNA) replication and repair, is overexpressed in many types of cancer but not in normal tissues. Although multiple independent studies have elucidated And-1 as a promising target gene
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