Research Interests

The main research interest of the Molecular Carcinogenesis Group (MCG) is focused on deciphering how cells react to oncogenic stimuli to preserve homeostasis. Within this context it investigates how cell cycle deregulation, genomic instability and senescence fuels cancer progression. Based on the extensive molecular pathology experience that the group possesses, notable clinico-pathological observations are functionally recapitulated in vitro and in vivo, aiming to decode the underlying mechanisms driving aberrant cellular behavior. The major achievements of the group are the following:

1Establishing the “Oncogene-induced DNA damage model for cancer development”

… establishing Genomic Instability and Senescence, as hallmarks of cancer​

2Clarifying the functional interplay of the two major antitumor barriers: DDR and ARF

2 Clarifying the functional interplay of the two major antitumor barriers: DDR and AR
Functional interplay between the DNA-damage-response kinase ATM and ARF tumour suppressor
The DNA damage checkpoint precedes activation of ARF in response to escalating oncogenic stress during tumorigenesis

3Revealing the oncogenic role of the replication licensing machinery in cancer

3 Revealing the oncogenic role of the replication licensing machinery in cancer

4Demonstrating that Genomic Instability  drives Escape from Senescence fueling Cancer Progression

4 Demonstrating that Genomic Instability drives Escape from Senescence fueling Cancer Progression
Prolonged expression of p21 WAF1/Cip1 in p53-null cells as a driving force for escape from senescence and cancer progression
Escape from oncogene-induced senescence
chapter4.4

… “One model to rule them all”​

Setting the order of the hallmarks of cancer

5 Developing pioneer senescence biomarkers (SenTraGorTM GLF16)

5 Developing pioneer senescence biomarkers (SenTraGorTM GLF16)
Development of SenTraGor, an innovative tool for senescence detection
Hallmarks of senescence and guidelines for detection
 
SeneQuest: Free web-resource application for identification of factors and conditions involved in senescence
Development of GLF16, an improved analog of SenTraGor
Algorithmic assessment of senescence in experimental and clinical samples

6Understanding how cellular senescence is involved in age-related pathologies

6 Understanding how cellular senescence is involved in age-related pathologies
Bacterial genotoxins induce T cell senescence
Physiological hypoxia restrains SASP
Pulmonary infection by SARS-CoV-2 induces senescence accompanied by an inflammatory phenotype in severe COVID-19: possible implications for viral mutagenesis
Cellular senescence and cardiovascular diseases
Implication of senescence in giant cell arteritis

7Exploiting molecular patterns for precision medicine based cancer therapy

7 Exploiting molecular patterns for precision medicine based cancer therapy
Is exclusive Skp2 targeting always beneficial in cancer therapy?
RASSF1A-mediated mechanism controlling tumor dedifferentiation and aggressive oncogenic behavior
A GATA2‑CDC6 axis modulates androgen receptor blockade‑induced senescence in prostate cancer
Loss of the tumour suppressor LKB1/STK11 uncovers a leptin-mediated sensitivity mechanism to mitochondrial uncouplers for targeted cancer therapy

8Contributing to our understanding of the role that inflammation plays in cancer

8 Contributing to our understanding of the role that inflammation plays in cancer
Non cell-autonomous role of mutant p53 gain-of-function: reprogramming the microenvironment
Notably, it appears that replication stress plays a role in inflammatory processes

9Development of machine learning algorithms to predict biological responses

9 Development of machine learning algorithms to predict biological responses
Machine learning algorithms to predict drug responses in cancer
Rshiny: Free web-resource application connecting molecular defects with drug response
Machine learning algorithms to predict drug responses in cancer

10 Providing anthropological evidence of humans evolution

10 Providing anthropological evidence of humans evolution