DNA Lab News

Please take a look in our new article targeting the current status on knowledge on the physical and biological mechanisms of Gold Nanoparticles and the implication in cancer therapy using ionizing and non-ionizing radiations. A collaborative effort between the Physics Department in NTUA, BRFA in Athens and Northumbria University, UK.



"Our latest participation in the International Innovation Summit in Gaziantep,  Turkey 5-7 May 2016 organized by Sanko University. My talk was on the use of bioinformatics towards the better understanding of DNA Damage Response (DDR) pathways. "

Zacharenia Nikitaki, Georgia I. Terzoudi, George Iliakis and Alexandros G. Georgakilas, “Current advances on the detection of complex DNA damage in cellular systems after exposure to ionizing radiation”, COST Action CM1201 : Biomimetic Radical Chemistry & ClicGene meeting, Grenoble-France, 25th  - 27th April 2016 (oral presentation)

Our lab participated in the recent 14th International Workshop on Radiation Damage to DNA


             MARCH 20-24, 2016


Our Phd student Ifigeneia Mavragani received one of the prestigious  ''Young INVESTIGATOR awards''.

Her presentation was entitled:

‘T02 Ifigenia Mavragani, National Technical University of Athens, Greece Identification of the key mechanisms in ionizing radiation-induced non-targeted effects’ 


 Our latest paper in Radiation-induced systemic effects appearing in From themed collection Hot articles in Toxicology Research 2015:



A collaboration between NTUA (Greece) and laboratories in France, Hungary and Germany.

Our new chapter to the upcoming book: "Studies on Experimental Toxicology and Pharmacology"

With a Title: 'Oxidative Stress and DNA Damage Association with Carcinogenesis: A Truth or a Myth?'


Our group’s recent contribution in the eBook entitled  "Radiation-Induced and Oxidative DNA Damages” is now available:







You can also find your and all the others articles on the topic page on the Frontiers web site.



Our recent publication:

The DNA damage response and immune signaling alliance: Is it good or bad? Nature decides when and where!

The characteristic feature of healthy living organisms is the preservation of homeostasis. Compelling evidence highlight that the DNA damage response and repair (DDR/R) and immune response (ImmR) signaling networks work together favoring the harmonized function of (multi)cellular organisms. DNA and RNA viruses activate the DDR/R machinery in the host cells both directly and indirectly. Activation of DDR/R in turn favors the immunogenicity of the incipient cell. Hence, stimulation of DDR/R by exogenous or endogenous insults triggers innate and adaptive ImmR. The immunogenic properties of ionizing radiation, a prototypic DDR/R inducer, serve as suitable examples of how DDR/R stimulation alerts host immunity. Thus, critical cellular danger signals stimulate defense at the systemic level and vice versa. Disruption of DDR/R–ImmR cross talk compromises (multi)cellular integrity, leading to cell-cycle-related and immune defects. The emerging DDR/R–ImmR concept opens up a new avenue of therapeutic options, recalling the Hippocrates quote “everything in excess is opposed by nature!




İnnovation and Bioengineering in Molecular Medicine, Sanko University, Gaziantep-Turkey, 20-21 March 2015 (Invited Talk)

Stress-induced DNA damage biomarkers: applications and limitations



 Με αφορμή μια πρόσφατη αναφορά στον Ελληνικό τύπο για μια δημοσίευση από την ερευνητική κοινοπραξία ‘Getting to know Cancer’

Θα ήθελα να σου επισημάνω μια σειρά δημοσιεύσεων που συμμετέχει το εργαστήριο μας μέσω της ίδιας κοινοπραξίας Getting to know Cancer (http://www.gettingtoknowcancer.org/index.php, με έδρα τον Καναδά), και το μόνο στην Ελλάδα και από τα λίγα στην Ευρώπη στο περιοδικό υψηλού επιστημονικού κύρους Seminars in Cancer Biology. Οι εργασίες αυτές έχουν στόχο την μελέτη διάφορων παραγόντων που σχετίζονται με την καρκινογένεση και τη θεραπεία του καρκίνου όπως η φλεγμονή, το μικροπεριβάλλον ενός όγκου, ο κυτταρικός θάνατος, η ικανότητα διπλασιασμού των καρκινικών κυττάρων κτλ.  
Δες σχετικά στο έγκριτο link στο pubmed:  
Σε μία από τις σημαντικότερες από τις εργασίες αυτές επικεντρωνόμαστε στο ρόλο της φλεγμονής στην καρκινογένεση και στην αντιφλεγμονώδη δράση κάποιων φαρμάκων που στοχεύουν στην αναστολή δράσης διάφορων παραγόντων στο ανθρώπινο σώμα όπως ο παράγοντας αναστολής μετανάστευσης μακροφάγων, της κυκλοοξυγενάσης-2, παράγοντα μεταγραφής πυρηνικού παράγοντα-κΒ αλλά και απλών διατροφικών συστατικών χαμηλού κόστους όπως, η κουρκουμίνη, η ρεσβερατρόλη, επιγαλλοκατεχίνη, γενιστεΐνη, λυκοπένιο και ανθοκυανίνες. Τα τελευταία αυτά συστατικά θεωρούνται χαμηλού κόστους και χαμηλής γενοτοξικότητας μέσα με τα οποία μπορεί να είναι επιτεύξιμοι ταυτόχρονα όλοι οι αντιφλεγμονώδεις και πιθανότατα αντικαρκινικοί στόχοι.
Στο μέλλον, κλινικές μελέτες θα πρέπει να αξιολογήσουν τις συνέργειες που προκύπτουν από ορθολογικά σχεδιασμένα αντιφλεγμονώδη μίγματα (χρησιμοποιώντας συστατικά χαμηλής τοξικότητας), και στη συνέχεια το συνδυασμό όλων αυτών των προσεγγίσεων που στοχεύουν τα σημαντικότερα μονοπάτια σε όλο το φάσμα του καρκίνου (cancer hallmarks).
Η έρευνα αυτή δημοσιεύτηκε στο έγκριτο επιστημονικό περιοδικό διεθνούς κύρους Seminars in Cancer Biology με τίτλο ‘A multi-targeted approach to suppress tumor-promoting inflammation’:



Our new book chapter on Breast Cancer published from InTech entitled : “Breast cancer: It’s all in the DNA


Book Chapter


Our laboratory participates actively in the "Halifax Project" within the "Getting to know cancer" framework, we have here the 1st joint publication in the high impact journal ‘Seminars in Cancer Biology’:


Semin Cancer Biol. 2015 Jan 16. pii: S1044-579X(15)00002-4. doi: 10.1016/j.semcancer.2015.01.001. [Epub ahead of print]

Broad targeting of angiogenesis for cancer prevention and therapy.

Wang Z1, Dabrosin C2, Yin X3, Fuster MM3, Arreola A4, Rathmell WK4, Generali D5, Nagaraju GP6, El-Rayes B6, Ribatti D7, Chen YC8, Honoki K9, Fujii H9, Georgakilas AG10, Nowsheen S11, Amedei A12, Niccolai E12, Amin A13, Ashraf SS14, Helferich B15, Yang X15, Guha G16, Bhakta D16, Ciriolo MR17, Aquilano K17, Chen S18, Halicka D19, Mohammed SI20, Azmi AS21, Bilsland A22, Keith WN22, Jensen LD23.

Author information

  • 1Department of Urology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: zwang0@partners.org.
  • 2Department of Oncology, Linköping University, Linköping, Sweden; Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
  • 3Medicine and Research Services, Veterans Affairs San Diego Healthcare System & University of California, San Diego, San Diego, CA, USA.
  • 4Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA.
  • 5Molecular Therapy and Pharmacogenomics Unit, AO Isituti Ospitalieri di Cremona, Cremona, Italy.
  • 6Department of Hematology and Medical Oncology, Emory University, Atlanta, GA, USA.
  • 7Department of Basic Medical Sciences, Neurosciences and Sensory Organs, University of Bari Medical School, Bari, Italy; National Cancer Institute Giovanni Paolo II, Bari, Italy.
  • 8Department of Biology, Alderson Broaddus University, Philippi, WV, USA.
  • 9Department of Orthopedic Surgery, Arthroplasty and Regenerative Medicine, Nara Medical University, Nara, Japan.
  • 10Physics Department, School of Applied Mathematics and Physical Sciences, National Technical University of Athens, Athens, Greece.
  • 11Mayo Graduate School, Mayo Clinic College of Medicine, Rochester, MN, USA.
  • 12Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy.
  • 13Department of Biology, College of Science, United Arab Emirate University, United Arab Emirates; Faculty of Science, Cairo University, Cairo, Egypt.
  • 14Department of Chemistry, College of Science, United Arab Emirate University, United Arab Emirates.
  • 15University of Illinois at Urbana Champaign, Urbana, IL, USA.
  • 16School of Chemical and Bio Technology, SASTRA University, Thanjavur, India.
  • 17Department of Biology, University of Rome "Tor Vergata", Rome, Italy.
  • 18Ovarian and Prostate Cancer Research Trust Laboratory, Guilford, Surrey, UK.
  • 19New York Medical College, New York City, NY, USA.
  • 20Department of Comparative Pathobiology, Purdue University Center for Cancer Research, West Lafayette, IN, USA.
  • 21School of Medicine, Wayne State University, Detroit, MI, USA.
  • 22Institute of Cancer Sciences, University of Glasgow, Glasgow, UK.
  • 23Department of Medical, and Health Sciences, Linköping University, Linköping, Sweden; Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden. Electronic address: lasse.jensen@liu.se.


        Deregulation of angiogenesis - the growth of new blood vessels from an existing vasculature - is a main driving force in many severe human diseases including cancer. As such, tumor angiogenesis is important for delivering oxygen and nutrients to growing tumors, and therefore considered an essential pathologic feature of cancer, while also playing a key role in enabling other aspects of tumor pathology such as metabolic deregulation and tumor dissemination/metastasis. Recently, inhibition of tumor angiogenesis has become a clinical anti-cancer strategy in line with chemotherapy, radiotherapy and surgery, which underscore the critical importance of the angiogenic switch during early tumor development. Unfortunately the clinically approved anti-angiogenic drugs in use today are only effective in a subset of the patients, and many who initially respond develop resistance over time. Also, some of the anti-angiogenic drugs are toxic and it would be of great importance to identify alternative compounds, which could overcome these drawbacks and limitations of the currently available therapy. Finding "the most important target" may, however, prove a very challenging approach as the tumor environment is highly diverse, consisting of many different cell types, all of which may contribute to tumor angiogenesis. Furthermore, the tumor cells themselves are genetically unstable, leading to a progressive increase in the number of different angiogenic factors produced as the cancer progresses to advanced stages. As an alternative approach to targeted therapy, options to broadly interfere with angiogenic signals by a mixture of non-toxic natural compound with pleiotropic actions were viewed by this team as an opportunity to develop a complementary anti-angiogenesis treatment option. As a part of the "Halifax Project" within the "Getting to know cancer" framework, we have here, based on a thorough review of the literature, identified 10 important aspects of tumor angiogenesis and the pathological tumor vasculature which would be well suited as targets for anti-angiogenic therapy: (1) endothelial cell migration/tip cell formation, (2) structural abnormalities of tumor vessels, (3) hypoxia, (4) lymphangiogenesis, (5) elevated interstitial fluid pressure, (6) poor perfusion, (7) disrupted circadian rhythms, (8) tumor promoting inflammation, (9) tumor promoting fibroblasts and (10) tumor cell metabolism/acidosis. Following this analysis, we scrutinized the available literature on broadly acting anti-angiogenic natural products, with a focus on finding qualitative information on phytochemicals which could inhibit these targets and came up with 10 prototypical phytochemical compounds: (1) oleic acid, (2) tripterine, (3) silibinin, (4) curcumin, (5) epigallocatechin-gallate, (6) kaempferol, (7) melatonin, (8) enterolactone, (9) withaferin A and (10) resveratrol. We suggest that these plant-derived compounds could be combined to constitute a broader acting and more effective inhibitory cocktail at doses that would not be likely to cause excessive toxicity. All the targets and phytochemical approaches were further cross-validated against their effects on other essential tumorigenic pathways (based on the "hallmarks" of cancer) in order to discover possible synergies or potentially harmful interactions, and were found to generally also have positive involvement in/effects on these other aspects of tumor biology. The aim is that this discussion could lead to the selection of combinations of such anti-angiogenic compounds which could be used in potent anti-tumor cocktails, for enhanced therapeutic efficacy, reduced toxicity and circumvention of single-agent anti-angiogenic resistance, as well as for possible use in primary or secondary cancer prevention strategies.



• Our article features as the one of the most cited articles in Mutation Research high impact journal:


Most Cited Mutation Research - Reviews Articles



Role of oxidatively induced DNA lesions in human pathogenesis

Volume 704, Issues 1-3, April 2010, Pages 152-159
Olga A. Sedelnikova | Christophe E. Redon | Jennifer S. Dickey | Asako Nakamura | Alexandros G. Georgakilas | William M. Bonner

Genome stability is essential for maintaining cellular and organismal homeostasis, but it is subject to many threats. One ubiquitous threat is from a class of compounds known as reactive oxygen species (ROS), which can indiscriminately react with many cellular biomolecules including proteins, lipids, and DNA to produce a variety of oxidative lesions. These DNA oxidation products are a direct risk to genome stability, and of particular importance are oxidative clustered DNA lesions (OCDLs), defined as two or more oxidative lesions present within 10 bp of each other. ROS can be produced by exposure of cells to exogenous environmental agents including ionizing radiation, light, chemicals, and metals. In addition, they are produced by cellular metabolism including mitochondrial ATP generation. However, ROS also serve a variety of critical cellular functions and optimal ROS levels are maintained by multiple cellular antioxidant defenses. Oxidative DNA lesions can be efficiently repaired by base excision repair or nucleotide excision repair. If ROS levels increase beyond the capacity of its antioxidant defenses, the cell's DNA repair capacity can become overwhelmed, leading to the accumulation of oxidative DNA damage products including OCDLs, which are more difficult to repair than individual isolated DNA damage products. Here we focus on the induction and repair of OCDLs and other oxidatively induced DNA lesions. If unrepaired, these lesions can lead to the formation of mutations, DNA DSBs, and chromosome abnormalities. We discuss the roles of these lesions in human pathologies including aging and cancer, and in bystander effects.



41st Annual Meeting of the European Radiation Research Society:

Please see the photo from my talk and link http://www.err2014.gr/

Local Organizing Committee

Gabriel Pantelias, NCSR "Demokritos", Greece  Georgia Terzoudi, NCSR
"Demokritos", Greece  George Iliakis, University of Essen, Germany
Alexandros Georgakilas, NTUA, Greece  Vasiliki Hatzi, NCSR "Demokritos",    
Greece  Administrative Secretary: Klio Makrigiannaki, NCSR "Demokritos",
Greece  Software Platform for Registrations and Abstracts: Nikos Tsamis,
Eventora, Greece




New Joint Publication with Professor Gorgoulis group (UOA, School of Medicine):

Cell Mol Life Sci. 2014 Sep 20. [Epub ahead of print]


Are common fragile sites merely structural domains or highly organized "functional" units susceptible to oncogenic stress?

Georgakilas AG1, Tsantoulis P, Kotsinas A, Michalopoulos I, Townsend P, Gorgoulis VG.

Author information

  • 1Physics Department, School of Applied Mathematical and Physical Sciences, National Technical University of Athens (NTUA), Zografou, 15780, Athens, Greece.


Common fragile sites (CFSs) are regions of the genome with a predisposition to DNA double-strand breaks in response to intrinsic (oncogenic) or extrinsic replication stress. CFS breakage is a common feature in carcinogenesis from its earliest stages. Given that a number of oncogenes and tumor suppressors are located within CFSs, a question that emerges is whether fragility in these regions is only a structural "passive" incident or an event with a profound biological effect. Furthermore, there is sparse evidence that other elements, like non-coding RNAs, are positioned with them. By analyzing data from various libraries, like miRbase and ENCODE, we show a prevalence of various cancer-related genes, miRNAs, and regulatory binding sites, such as CTCF within CFSs. We propose that CFSs are not only susceptible structural domains, but highly organized "functional" entities that when targeted, severe repercussion for cell homeostasis occurs.