17 results on '"Niforou K"'
Search Results
2. Exogenous hormone use and cutaneous melanoma risk in women: The European Prospective Investigation into Cancer and Nutrition
- Author
-
Cervenka, I. Al Rahmoun, M. Mahamat-Saleh, Y. Fournier, A. Boutron-Ruault, M.-C. Severi, G. Caini, S. Palli, D. Ghiasvand, R. Veierod, M.B. Botteri, E. Tjønneland, A. Olsen, A. Fortner, R.T. Kaaks, R. Schulze, M.B. Panico, S. Trichopoulou, A. Dessinioti, C. Niforou, K. Sieri, S. Tumino, R. Sacerdote, C. Bueno-de-Mesquita, B. Sandanger, T.M. Colorado-Yohar, S. Sánchez, M.J. Gil Majuelo, L. Lujan-Barroso, L. Ardanaz, E. Merino, S. Isaksson, K. Butt, S. Ljuslinder, I. Jansson, M. Travis, R.C. Khaw, K.-T. Weiderpass, E. Dossus, L. Rinaldi, S. Kvaskoff, M.
- Abstract
Evidence suggests an influence of sex hormones on cutaneous melanoma risk, but epidemiologic findings are conflicting. We examined the associations between use of oral contraceptives (OCs) and menopausal hormone therapy (MHT) and melanoma risk in women participating in the European Prospective Investigation into Cancer and Nutrition (EPIC). EPIC is a prospective cohort study initiated in 1992 in 10 European countries. Information on exogenous hormone use at baseline was derived from country-specific self-administered questionnaires. We used Cox proportional hazards regression models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). Over 1992–2015, 1,696 melanoma cases were identified among 334,483 women, whereof 770 cases among 134,758 postmenopausal women. There was a positive, borderline-significant association between OC use and melanoma risk (HR = 1.12, 95% CI = 1.00–1.26), with no detected heterogeneity across countries (phomogeneity = 0.42). This risk increased linearly with duration of use (ptrend = 0.01). Among postmenopausal women, ever use of MHT was associated with a nonsignificant increase in melanoma risk overall (HR = 1.14, 95% CI = 0.97–1.43), which was heterogeneous across countries (phomogeneity = 0.05). Our findings do not support a strong and direct association between exogenous hormone use and melanoma risk. In order to better understand these relations, further research should be performed using prospectively collected data including detailed information on types of hormone, and on sun exposure, which may act as an important confounder or effect modifier on these relations. © 2019 UICC
- Published
- 2020
3. Molecular chaperones and proteostasis regulation during redox imbalance
- Author
-
Niforou, K. Cheimonidou, C. Trougakos, I.P.
- Abstract
Free radicals originate from both exogenous environmental sources and as by-products of the respiratory chain and cellular oxygen metabolism. Sustained accumulation of free radicals, beyond a physiological level, induces oxidative stress that is harmful for the cellular homeodynamics as it promotes the oxidative damage and stochastic modification of all cellular biomolecules including proteins. In relation to proteome stability and maintenance, the increased concentration of oxidants disrupts the functionality of cellular protein machines resulting eventually in proteotoxic stress and the deregulation of the proteostasis (homeostasis of the proteome) network (PN). PN curates the proteome in the various cellular compartments and the extracellular milieu by modulating protein synthesis and protein machines assembly, protein recycling and stress responses, as well as refolding or degradation of damaged proteins. Molecular chaperones are key players of the PN since they facilitate folding of nascent polypeptides, as well as holding, folding, and/or degradation of unfolded, misfolded, or non-native proteins. Therefore, the expression and the activity of the molecular chaperones are tightly regulated at both the transcriptional and post-translational level at organismal states of increased oxidative and, consequently, proteotoxic stress, including ageing and various age-related diseases (e.g. degenerative diseases and cancer). In the current review we present a synopsis of the various classes of intra- and extracellular chaperones, the effects of oxidants on cellular homeodynamics and diseases and the redox regulation of chaperones. © 2014 The Authors.
- Published
- 2014
4. Modulation of the E2F1-driven cancer cell fate by the DNA damage response machinery and potential novel E2F1 targets in osteosarcomas
- Author
-
Liontos, M. Niforou, K. Velimezi, G. Vougas, K. Evangelou, K. Apostolopoulou, K. Vrtel, R. Damalas, A. Kontovazenitis, P. Kotsinas, A. Zoumpourlis, V. Tsangaris, G.Th. Kittas, C. Ginsberg, D. Halazonetis, T.D. Bartek, J. Gorgoulis, V.G.
- Subjects
endocrine system ,biological phenomena, cell phenomena, and immunity - Abstract
Osteosarcoma is the most common primary bone cancer. Mutations of the RB gene represent the most frequent molecular defect in this malignancy. A major consequence of this alteration is that the activity of the key cell cycle regulator E2F1 is unleashed from the inhibitory effects of pRb. Studies in animal models and in human cancers have shown that deregulated E2F1 overexpression possesses either "oncogenic" or " oncosuppressor" properties, depending on the cellular context. To address this issue in osteosarcomas, we examined the status of E2F1 relative to cell proliferation and apoptosis in a clinical setting of human primary osteosarcomas and in E2F1-inducible osteosarcoma cell line models that are wild-type and deficient for p53. Collectively, our data demonstrated that high E2F1 levels exerted a growth-suppressing effect that relied on the integrity of the DNA damage response network. Surprisingly, induction of p73, an established E2F1 target, was also DNA damage response-dependent. Furthermore, a global proteome analysis associated with bioinformatics revealed novel E2F1-regulated genes and potential E2F1-driven signaling networks that could provide useful targets in challenging this aggressive neoplasm by innovative therapies. Copyright © American Society for Investigative Pathology.
- Published
- 2009
5. p57KIP2: 'kip'ing the cell under control
- Author
-
Pateras, I.S. Apostolopoulou, K. Niforou, K. Kotsinas, A. Gorgoulis, V.G.
- Abstract
p57KIP2 is an imprinted gene located at the chromosomal locus 11p15.5. It is a cyclin-dependent kinase inhibitor belonging to the CIP/KIP family, which includes additionally p21CIP1/WAF1 and p27 KIP1. It is the least studied CIP/KIP member and has a unique role in embryogenesis. p57KIP2 regulates the cell cycle, although novel functions have been attributed to this protein including cytoskeletal organization. Molecular analysis of animal models and patients with Beckwith-Wiedemann Syndrome have shown its nodal implication in the pathogenesis of this syndrome. p57KIP2 is frequently down-regulated in many common human malignancies through several mechanisms, denoting its anti-oncogenic function. This review is a thorough analysis of data available on p57KIP2, in relation to p21CIP1/WAF1 and p27 KIP1, on gene and protein structure, its transcriptional and translational regulation, and its role in human physiology and pathology, focusing on cancer development. Copyright © 2009 American Association for Cancer Research.
- Published
- 2009
6. Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints
- Author
-
Bartkova, J., Rezaei, N., Liontos, M., Karakaidos, P., Kletsas, D., Issaeva, N., Vassiliou, L. V. F., Kolettas, E., Niforou, K., Zoumpourlis, Vassilis, Takaoka, M., Nakagawa, H., Tort, F., Fugger, K., Johansson, F., Sehested, M., Andersen, C. L., and Dyrskjot, L
- Subjects
InformationSystems_INFORMATIONSTORAGEANDRETRIEVAL ,ComputingMethodologies_DOCUMENTANDTEXTPROCESSING ,GeneralLiterature_REFERENCE(e.g.,dictionaries,encyclopedias,glossaries) - Abstract
Journal URL: http://www.nature.com/nature/index.html
- Published
- 2008
7. Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints
- Author
-
Bartkova, J. Rezaei, N. Liontos, M. Karakaidos, P. Kletsas, D. Issaeva, N. Vassiliou, L.-V.F. Kolettas, E. Niforou, K. Zoumpourlis, V.C. Takaoka, M. Nakagawa, H. Tort, F. Fugger, K. Johansson, F. Sehested, M. Andersen, C.L. Dyrskjot, L. Ørntoft, T. Lukas, J. Kittas, C. Helleday, T. Halazonetis, T.D. Bartek, J. Gorgoulis, V.G.
- Abstract
Recent studies have indicated the existence of tumorigenesis barriers that slow or inhibit the progression of preneoplastic lesions to neoplasia. One such barrier involves DNA replication stress, which leads to activation of the DNA damage checkpoint and thereby to apoptosis or cell cycle arrest, whereas a second barrier is mediated by oncogene-induced senescence. The relationship between these two barriers, if any, has not been elucidated. Here we show that oncogene-induced senescence is associated with signs of DNA replication stress, including prematurely terminated DNA replication forks and DNA double-strand breaks. Inhibiting the DNA double-strand break response kinase ataxia telangiectasia mutated (ATM) suppressed the induction of senescence and in a mouse model led to increased tumour size and invasiveness. Analysis of human precancerous lesions further indicated that DNA damage and senescence markers cosegregate closely. Thus, senescence in human preneoplastic lesions is a manifestation of oncogene-induced DNA replication stress and, together with apoptosis, provides a barrier to malignant progression. ©2006 Nature Publishing Group.
- Published
- 2006
8. Impact of stocking density on broiler growth performance, meat characteristics, behavioural components and indicators of physiological and oxidative stress
- Author
-
Simitzis, P.E., primary, Kalogeraki, E., additional, Goliomytis, M., additional, Charismiadou, M.A., additional, Triantaphyllopoulos, K., additional, Ayoutanti, A., additional, Niforou, K., additional, Hager-Theodorides, A.L., additional, and Deligeorgis, S.G., additional
- Published
- 2012
- Full Text
- View/download PDF
9. The proteome profile of the human osteosarcome Saos2 cell line
- Author
-
Niforou, K. N., Athanasios Anagnostopoulos, Vougas, K., Kittas, C., Gorgoulis, V. G., and Tsangaris, G. T.
10. The proteome profile of the human osteosarcoma U2OS cell line
- Author
-
Niforou, K. N., Athanasios Anagnostopoulos, Vougas, K., Kittas, C., Gorgoulis, V. G., and Tsangaris, G. Th
11. Phytochemical Study and In Vitro Screening Focusing on the Anti-Aging Features of Various Plants of the Greek Flora.
- Author
-
Sklirou AD, Angelopoulou MT, Argyropoulou A, Chaita E, Boka VI, Cheimonidi C, Niforou K, Mavrogonatou E, Pratsinis H, Kalpoutzakis E, Aligiannis N, Kletsas D, Trougakos IP, and Skaltsounis AL
- Abstract
Skin health is heavily affected by ultraviolet irradiation from the sun. In addition, senile skin is characterized by major changes in the collagen, elastin and in the hyaluronan content. Natural products (NPs) have been shown to delay cellular senescence or in vivo aging by regulating age-related signaling pathways. Moreover, NPs are a preferable source of photoprotective agents and have been proven to be useful against the undesirable skin hyperpigmentation. Greek flora harvests great plant diversity with approximately 6000 plant species, as it has a wealth of NPs. Here, we report an extensive screening among hundreds of plant species. More than 440 plant species and subspecies were selected and evaluated. The extracts were screened for their antioxidant and anti-melanogenic properties, while the most promising were further subjected to various in vitro and cell-based assays related to skin aging. In parallel, their chemical profile was analyzed with High-Performance Thin-Layer Chromatography (HPTLC) and/or Ultra-Performance Liquid Chromatography High-Resolution Mass Spectrometry (UPLC-HRMS). A variety of extracts were identified that can be of great value for the cosmetic industry, since they combine antioxidant, photoprotective, anti-melanogenic and anti-aging properties. In particular, the methanolic extracts of Sideritis scardica and Rosa damascena could be worthy of further attention, since they showed interesting chemical profiles and promising properties against specific targets involved in skin aging.
- Published
- 2021
- Full Text
- View/download PDF
12. Exogenous hormone use and cutaneous melanoma risk in women: The European Prospective Investigation into Cancer and Nutrition.
- Author
-
Cervenka I, Al Rahmoun M, Mahamat-Saleh Y, Fournier A, Boutron-Ruault MC, Severi G, Caini S, Palli D, Ghiasvand R, Veierod MB, Botteri E, Tjønneland A, Olsen A, Fortner RT, Kaaks R, Schulze MB, Panico S, Trichopoulou A, Dessinioti C, Niforou K, Sieri S, Tumino R, Sacerdote C, Bueno-de-Mesquita B, Sandanger TM, Colorado-Yohar S, Sánchez MJ, Gil Majuelo L, Lujan-Barroso L, Ardanaz E, Merino S, Isaksson K, Butt S, Ljuslinder I, Jansson M, Travis RC, Khaw KT, Weiderpass E, Dossus L, Rinaldi S, and Kvaskoff M
- Subjects
- Adult, Aged, Confounding Factors, Epidemiologic, Estrogen Replacement Therapy statistics & numerical data, Europe epidemiology, Female, Humans, Incidence, Melanoma etiology, Middle Aged, Postmenopause, Premenopause, Proportional Hazards Models, Prospective Studies, Risk Factors, Skin Neoplasms etiology, Surveys and Questionnaires statistics & numerical data, Time Factors, Contraceptives, Oral, Hormonal adverse effects, Estrogen Replacement Therapy adverse effects, Melanoma epidemiology, Skin Neoplasms epidemiology
- Abstract
Evidence suggests an influence of sex hormones on cutaneous melanoma risk, but epidemiologic findings are conflicting. We examined the associations between use of oral contraceptives (OCs) and menopausal hormone therapy (MHT) and melanoma risk in women participating in the European Prospective Investigation into Cancer and Nutrition (EPIC). EPIC is a prospective cohort study initiated in 1992 in 10 European countries. Information on exogenous hormone use at baseline was derived from country-specific self-administered questionnaires. We used Cox proportional hazards regression models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). Over 1992-2015, 1,696 melanoma cases were identified among 334,483 women, whereof 770 cases among 134,758 postmenopausal women. There was a positive, borderline-significant association between OC use and melanoma risk (HR = 1.12, 95% CI = 1.00-1.26), with no detected heterogeneity across countries (p
homogeneity = 0.42). This risk increased linearly with duration of use (ptrend = 0.01). Among postmenopausal women, ever use of MHT was associated with a nonsignificant increase in melanoma risk overall (HR = 1.14, 95% CI = 0.97-1.43), which was heterogeneous across countries (phomogeneity = 0.05). Our findings do not support a strong and direct association between exogenous hormone use and melanoma risk. In order to better understand these relations, further research should be performed using prospectively collected data including detailed information on types of hormone, and on sun exposure, which may act as an important confounder or effect modifier on these relations., (© 2019 UICC.)- Published
- 2020
- Full Text
- View/download PDF
13. A Metabolomic Study of Biomarkers of Habitual Coffee Intake in Four European Countries.
- Author
-
Rothwell JA, Keski-Rahkonen P, Robinot N, Assi N, Casagrande C, Jenab M, Ferrari P, Boutron-Ruault MC, Mahamat-Saleh Y, Mancini FR, Boeing H, Katzke V, Kühn T, Niforou K, Trichopoulou A, Valanou E, Krogh V, Mattiello A, Palli D, Sacerdote C, Tumino R, and Scalbert A
- Subjects
- Adult, Aged, Alkaloids blood, Caffeine blood, Europe, Female, Humans, Male, Middle Aged, Prospective Studies, Theophylline blood, Biomarkers blood, Coffee metabolism, Metabolomics
- Abstract
Scope: The goal of this work is to identify circulating biomarkers of habitual coffee intake using a metabolomic approach, and to investigate their associations with coffee intake in four European countries., Methods and Results: Untargeted mass spectrometry-based metabolic profiling is performed on serum samples from 451 participants of the European Prospective Investigation on Cancer and Nutrition (EPIC) originating from France, Germany, Greece, and Italy. Eleven coffee metabolites are found to be associated with self-reported habitual coffee intake, including eight more strongly correlated (r = 0.25-0.51, p < 10E
-07 ). Trigonelline shows the highest correlation, followed by caffeine, two caffeine metabolites (paraxanthine and 5-Acetylamino-6-amino-3-methyluracil), quinic acid, and three compounds derived from coffee roasting (cyclo(prolyl-valyl), cyclo(isoleucyl-prolyl), cyclo(leucyl-prolyl), and pyrocatechol sulfate). Differences in the magnitude of correlations are observed between countries, with trigonelline most highly correlated with coffee intake in France and Germany, quinic acid in Greece, and cyclo(isoleucyl-prolyl) in Italy., Conclusion: Several biomarkers of habitual coffee intake are identified. No unique biomarker is found to be optimal for all tested populations. Instead, optimal biomarkers are shown to depend on the population and on the type of coffee consumed. These biomarkers should help to further explore the role of coffee in disease risk., (© 2019 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)- Published
- 2019
- Full Text
- View/download PDF
14. Molecular chaperones and proteostasis regulation during redox imbalance.
- Author
-
Niforou K, Cheimonidou C, and Trougakos IP
- Subjects
- Animals, Electron Transport, Endoplasmic Reticulum metabolism, Endoplasmic Reticulum Chaperone BiP, Free Radicals metabolism, Heat-Shock Proteins physiology, Homeostasis, Humans, Models, Biological, Oxidants metabolism, Oxidation-Reduction, Proteasome Endopeptidase Complex metabolism, Protein Folding, Protein Processing, Post-Translational, Protein Stability, Proteome, Reactive Nitrogen Species metabolism, Reactive Oxygen Species metabolism, Molecular Chaperones physiology, Oxidative Stress physiology, Proteins metabolism
- Abstract
Free radicals originate from both exogenous environmental sources and as by-products of the respiratory chain and cellular oxygen metabolism. Sustained accumulation of free radicals, beyond a physiological level, induces oxidative stress that is harmful for the cellular homeodynamics as it promotes the oxidative damage and stochastic modification of all cellular biomolecules including proteins. In relation to proteome stability and maintenance, the increased concentration of oxidants disrupts the functionality of cellular protein machines resulting eventually in proteotoxic stress and the deregulation of the proteostasis (homeostasis of the proteome) network (PN). PN curates the proteome in the various cellular compartments and the extracellular milieu by modulating protein synthesis and protein machines assembly, protein recycling and stress responses, as well as refolding or degradation of damaged proteins. Molecular chaperones are key players of the PN since they facilitate folding of nascent polypeptides, as well as holding, folding, and/or degradation of unfolded, misfolded, or non-native proteins. Therefore, the expression and the activity of the molecular chaperones are tightly regulated at both the transcriptional and post-translational level at organismal states of increased oxidative and, consequently, proteotoxic stress, including ageing and various age-related diseases (e.g. degenerative diseases and cancer). In the current review we present a synopsis of the various classes of intra- and extracellular chaperones, the effects of oxidants on cellular homeodynamics and diseases and the redox regulation of chaperones.
- Published
- 2014
- Full Text
- View/download PDF
15. p57KIP2: "Kip"ing the cell under control.
- Author
-
Pateras IS, Apostolopoulou K, Niforou K, Kotsinas A, and Gorgoulis VG
- Subjects
- Animals, Cyclin-Dependent Kinase Inhibitor p57 chemistry, Cyclin-Dependent Kinase Inhibitor p57 genetics, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Humans, Neoplasms genetics, Neoplasms pathology, RNA, Messenger genetics, RNA, Messenger metabolism, Cell Cycle, Cyclin-Dependent Kinase Inhibitor p57 metabolism
- Abstract
p57(KIP2) is an imprinted gene located at the chromosomal locus 11p15.5. It is a cyclin-dependent kinase inhibitor belonging to the CIP/KIP family, which includes additionally p21(CIP1/WAF1) and p27(KIP1). It is the least studied CIP/KIP member and has a unique role in embryogenesis. p57(KIP2) regulates the cell cycle, although novel functions have been attributed to this protein including cytoskeletal organization. Molecular analysis of animal models and patients with Beckwith-Wiedemann Syndrome have shown its nodal implication in the pathogenesis of this syndrome. p57(KIP2) is frequently down-regulated in many common human malignancies through several mechanisms, denoting its anti-oncogenic function. This review is a thorough analysis of data available on p57(KIP2), in relation to p21(CIP1/WAF1) and p27(KIP1), on gene and protein structure, its transcriptional and translational regulation, and its role in human physiology and pathology, focusing on cancer development.
- Published
- 2009
- Full Text
- View/download PDF
16. Modulation of the E2F1-driven cancer cell fate by the DNA damage response machinery and potential novel E2F1 targets in osteosarcomas.
- Author
-
Liontos M, Niforou K, Velimezi G, Vougas K, Evangelou K, Apostolopoulou K, Vrtel R, Damalas A, Kontovazenitis P, Kotsinas A, Zoumpourlis V, Tsangaris GT, Kittas C, Ginsberg D, Halazonetis TD, Bartek J, and Gorgoulis VG
- Subjects
- Adolescent, Adult, Aged, Aged, 80 and over, Apoptosis physiology, Blotting, Western, Bone Neoplasms genetics, Cell Line, Tumor, Cell Proliferation, Child, DNA Damage, DNA Repair, DNA-Binding Proteins metabolism, E2F1 Transcription Factor genetics, Electrophoresis, Gel, Two-Dimensional, Female, Flow Cytometry, Fluorescent Antibody Technique, Humans, Immunohistochemistry, In Situ Nick-End Labeling, Male, Middle Aged, Nuclear Proteins metabolism, Osteosarcoma genetics, Tumor Protein p73, Tumor Suppressor Protein p53 deficiency, Tumor Suppressor Proteins metabolism, Young Adult, Bone Neoplasms metabolism, E2F1 Transcription Factor metabolism, Gene Expression Regulation, Neoplastic, Osteosarcoma metabolism
- Abstract
Osteosarcoma is the most common primary bone cancer. Mutations of the RB gene represent the most frequent molecular defect in this malignancy. A major consequence of this alteration is that the activity of the key cell cycle regulator E2F1 is unleashed from the inhibitory effects of pRb. Studies in animal models and in human cancers have shown that deregulated E2F1 overexpression possesses either "oncogenic" or "oncosuppressor" properties, depending on the cellular context. To address this issue in osteosarcomas, we examined the status of E2F1 relative to cell proliferation and apoptosis in a clinical setting of human primary osteosarcomas and in E2F1-inducible osteosarcoma cell line models that are wild-type and deficient for p53. Collectively, our data demonstrated that high E2F1 levels exerted a growth-suppressing effect that relied on the integrity of the DNA damage response network. Surprisingly, induction of p73, an established E2F1 target, was also DNA damage response-dependent. Furthermore, a global proteome analysis associated with bioinformatics revealed novel E2F1-regulated genes and potential E2F1-driven signaling networks that could provide useful targets in challenging this aggressive neoplasm by innovative therapies.
- Published
- 2009
- Full Text
- View/download PDF
17. Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints.
- Author
-
Bartkova J, Rezaei N, Liontos M, Karakaidos P, Kletsas D, Issaeva N, Vassiliou LV, Kolettas E, Niforou K, Zoumpourlis VC, Takaoka M, Nakagawa H, Tort F, Fugger K, Johansson F, Sehested M, Andersen CL, Dyrskjot L, Ørntoft T, Lukas J, Kittas C, Helleday T, Halazonetis TD, Bartek J, and Gorgoulis VG
- Subjects
- Animals, Cell Cycle Proteins genetics, Cell Line, Cyclin E genetics, Cyclin-Dependent Kinase Inhibitor p16 physiology, DNA, DNA Replication, Genes, mos, Humans, Mice, Neoplasm Invasiveness genetics, Nuclear Proteins genetics, Precancerous Conditions genetics, Precancerous Conditions pathology, Cell Transformation, Neoplastic genetics, Cellular Senescence genetics, DNA Damage, Oncogenes
- Abstract
Recent studies have indicated the existence of tumorigenesis barriers that slow or inhibit the progression of preneoplastic lesions to neoplasia. One such barrier involves DNA replication stress, which leads to activation of the DNA damage checkpoint and thereby to apoptosis or cell cycle arrest, whereas a second barrier is mediated by oncogene-induced senescence. The relationship between these two barriers, if any, has not been elucidated. Here we show that oncogene-induced senescence is associated with signs of DNA replication stress, including prematurely terminated DNA replication forks and DNA double-strand breaks. Inhibiting the DNA double-strand break response kinase ataxia telangiectasia mutated (ATM) suppressed the induction of senescence and in a mouse model led to increased tumour size and invasiveness. Analysis of human precancerous lesions further indicated that DNA damage and senescence markers cosegregate closely. Thus, senescence in human preneoplastic lesions is a manifestation of oncogene-induced DNA replication stress and, together with apoptosis, provides a barrier to malignant progression.
- Published
- 2006
- Full Text
- View/download PDF
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