Major Achievements

Our group played a major role in:

i) Establishing the “Oncogene-induced DNA damage model for cancer development” (Science 2008; Nat Rev Mol Cell Biol 2010; J Pathol 2018) (Figures 1-6, 8). Based on: Cancer Res 2001; J Pathol 2002; J Pathol 2004; Nature 2005; Nature 2006; J Pathol 2006; Cancer Res 2007 (1); Oncogene 2008; Blood 2008; Am J Pathol 2009; Nat Genet 2011; Nat Cell Biol 2011; Cancer Res 2012; Cell Death Differ 2014; Cell Mol Life Sci 2014; Cell Rep 2015; Nat Cell Biol 2016; Genomics 2018; Genome Biol 2018 and currently the broader role of DNA Damage response pathway in disease development (Cell 2016).

ii) Demonstrating that oncogene-induced senescence is a DNA damage stress response acting as a barrier to cancer (Nature 2006; Cancer Res 2007; Am J Pathol 2009; Curr Opin Cell Biol 2010; Nat Cell Biol 2011; Cell Death Differ 2015; Nat Cell Biol 2016; BMC Genomics 2018; Genome Biol 2018) (Figures 2,5,6).

iii) Clarifying the functional interplay and the timeline of events underlying the two major antitumor checkpoint responses, i.e. DDR and ARF (Nat Cell Biol 2013; Cell Death Diff 2013; Cell Cycle 2014) (Figure 2).

iv) Revealing the oncogenic role of replication licensing factors Cdc6 and Cdt1 by inducing DNA replication stress and deregulating transcription (Am J Pathol 2004; Nature 2006; Cancer Res 2007, J Cell Biol 2011; Transcription 2012; Semin Cancer Biol 2016; Nat Commun 2016; Nat Cell Biol 2016; PNAS 2016; BMC Genomics 2018; Genome Biol 2018) (Figures 2-6).

v) Understanding how cellular senescence is involved in age-related pathologies, including cancer (EMBO J 2003; Lab Invest 2005; Nature 2006; Am J Pathol 2009; Aging 2013; Aging Cell  2013; Stem Cells 2013; Cell Death Differ 2015; Mech Ageing Dev 2016; Aging Cell  2017; J Pathol 2018; Int J Mol Sci 2018; Pharmacol Ther 2019 (1); Nat Commun 2020 (1); Nat Commun 2020 (2)) (Figures 2,5,6,8,10). Our research has led to the development of a pioneer senescence biomarker (commercially available under the trademark SenTraGorTM) able to detect senescence in any biological material including archival (Aging 2013; Aging Cell 2017; Int J Mol Sci 2018; Meth Mol Biol 2019; Pharmacol Ther 2019 (1); Cell 2019; Nat Protoc in press).

vi) Contributing to our understanding of the role that inflammation plays in cancer development (Cancer Res 2007 (2); Cancer Cell 2013; Cancer Cell 2014; Pharmacol Ther 2015; Cell Death Differ 2015; Cell Rep 2016; Nat Commun 2018; Nat Commun 2020 (2)) (Figures 7,8).

vii) Providing evolutionary evidence that modern humans dispersed into Europe and Asia (150 thousand years) earlier than initially thought (Nature 2019) (Figure 9).

viii) Development of machine learning algorithms to predict drug response and survival of cancer patients (Pharmacol Ther 2019 (2); Cell Reports 2019; Cancer Res 2020) (Figure 11).

1. Genomic instability — an evolving hallmark of cancer

Nat Rev Mol Cell Biol 2010

2. An Oncogene-Induced DNA Damage Model for Cancer Development


Science 2008
Nature 2005
Nature 2006
Nature Cell Biol 2013
CDD 2013

3. The role of Cdc6 in cancer progression


Am J Pathol 2004
Cancer Res 2007
J Cell Biol 2011
Transcription 2012

4. Oncogenic Cdc6 as a molecular switch during cancer development

J Cell Biol 2011
Transcription 2012

5. Prolonged expression of p21WAF1/Cip1 in p53-null cells as a driving force for cancer progression

.Model 6 Home page


Re-replicating cell (video)
Escaped and dividing cells (video)

 Nat Cell Biol 2016

RAD52 recruitment OFF cells (video)
RAD52 recruitment ON cells (video)

Genome Biology 2018

6. SenTraGor: a novel reagent to detect senescent cells

Aging 2013
Meth Mod Biol 2017
Aging Cell 2017
Meth Mol Biol 2018
Cell 2019

7. The non cell-autonomous role of mutant p53 gain-of-function: reprogramming the microenvironment

Nat Commun 2018 Model 

i)Cancer Cell & Microenvironment 2014
iia)Nat Commun 2018
iib)Nat Commun 2018

8. Integrating the DNA damage and protein stress responses during cancer development and treatment


J Pathol 2018

9. Apidima Cave fossils provide earliest evidence of Homo sapiens in Eurasia


(a) Analysis of two human fossil skulls (Apidima 1 and Apidima2) found during excavations at Apidima cave in Mani, Peloponnese, showed that fossil find Apidima 1 was dated about 210.000 years old. It represented a modern human with archaic characteristics, indicating an early Homo sapiens. Apidima 2 was dated 170.000 years old, with Neanderthal features. These findings imply that early modern humans spread into Eurasia 150 thousand years earlier than thought.

Nature 2019


(b) In a bone fragment (LAO1/S1) found adjacent to the human skull Apidima 1, we identified, using an innovative reagent (SenTraGor) that we developed, the presence of lipofuscin a potent biomarker of senescence.

Nature 2019
Pharmacology –Therapeutics 2018
Cell 2019

10. Cellular Senescence: Defining a Path Forward

The Hallmarks of the Senescence Phenotype

Cell 2019

11. Machine learning algorithms to predict drug responses in cancer


Pharmacology – Therapeutics 2019


Cell Reports 2019

VG New

Prof. Vassilis G. Gorgoulis

Laboratory of Histology-Embryology
Molecular Carcinogenesis Group
Medical School
National and Kapodistrian University of Athens


Biomedical Research Foundation of the Academy of Athens


Faculty Institute for Cancer Sciences, University of Manchester,
Manchester Academic Health Science Centre, Manchester, UK

Manchester Centre for Cellular Metabolism,
University of Manchester, Manchester Academic Health Science Centre, Manchester


EMBO member






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