Honors & Awards


  • Postdoctoral Fellowship program (30 000$), Stanford Dean’s Postdoctoral Fellowship (01/2019)
  • Best Poster Award, Otolaryngology Head and Neck Surgery, Research Day at Stanford Medical School (10/2018)
  • Very honorable PhD distinction with unanimous congratulations from the jury, The French National Institute of Health and Medical Research (02/2018)
  • Positive comment of “Benkafadar N et al., EMBO Molecular Medicine” in "News & Views”, EMBO Molecular Medicine, 9: 4-6, by Nonnekens J and Hoeijmakers JH (01/2017)
  • Publication of “Cancers & audition: The end of the double penalty”, Languedoc-Roussillon INSERM Newspaper (12/2016)
  • Best Poster Award, Ageing 2016 Meeting (06/2016)
  • Graduate fellowship program (50 000 € / year for 3 years), Foundation of the Future for Medical Research (10/2014)

Professional Education


  • Doctor of Philosophy, Universite De Montpellier (2018)
  • Master of Health and Science, Universite De Montpellier (2014)
  • Doctor of Pharmacy, Universite De Constantine (2012)

Patents


  • Nesrine Benkafadar, Julien Menardo, Jean-Luc Puel and Jing Wang. " Patent WO2017125429A1 The use of a temporary inhibitor of p53 for preventing or reducing cancer relapse", Institut National de la Santé et de la Recherche Médicale (INSERM) - Universite De Montpellier, Jul 27, 2017

All Publications


  • ROS-Induced Activation of DNA Damage Responses Drives Senescence-Like State in Postmitotic Cochlear Cells: Implication for Hearing Preservation. Molecular neurobiology Benkafadar, N., François, F., Affortit, C., Casas, F., Ceccato, J. C., Menardo, J., Venail, F., Malfroy-Camine, B., Puel, J. L., Wang, J. 2019

    Abstract

    In our aging society, age-related hearing loss (ARHL) has become a major socioeconomic issue. Reactive oxygen species (ROS) may be one of the main causal factors of age-related cochlear cell degeneration. We examined whether ROS-induced DNA damage response drives cochlear cell senescence and contributes to ARHL from the cellular up to the system level. Our results revealed that sublethal concentrations of hydrogen peroxide (H2O2) exposure initiated a DNA damage response illustrated by increased γH2AX and 53BP1 expression and foci formation mainly in sensory hair cells, together with increased levels of p-Chk2 and p53. Interestingly, postmitotic cochlear cells exposed to H2O2 displayed key hallmarks of senescent cells, including dramatically increased levels of p21, p38, and p-p38 expression, concomitant with decreased p19 and BubR1 expression and positive senescence-associated β-galactosidase labeling. Importantly, the synthetic superoxide dismutase/catalase mimetic EUK-207 attenuated H2O2-induced DNA damage and senescence phenotypes in cochlear cells in vitro. Furthermore, systemic administration of EUK-207 reduced age-related loss of hearing and hair cell degeneration in senescence-accelerated mouse-prone 8 (SAMP8) mice. Altogether, these findings highlight that ROS-induced DNA damage responses drive cochlear cell senescence and contribute to accelerated ARHL. EUK-207 and likely other antioxidants with similar mechanisms of action could potentially postpone cochlear aging and prevent ARHL in humans.

    View details for DOI 10.1007/s12035-019-1493-6

    View details for PubMedID 30693443

  • New Strategies for Improving the Quality of Life of Cancer Survivors: Reversible p53 Inhibition Journal of Cancer Science & Therapy Benkafadar, N., Coyat, C., Lloyd, R., Puel , J., Wang, J. 2017; 9(6): 490-491
  • Reversible p53 inhibition prevents cisplatin ototoxicity without blocking chemotherapeutic efficacy. EMBO molecular medicine Benkafadar, N., Menardo, J., Bourien, J., Nouvian, R., François, F., Decaudin, D., Maiorano, D., Puel, J., Wang, J. 2017; 9 (1): 7-26

    Abstract

    Cisplatin is a widely used chemotherapy drug, despite its significant ototoxic side effects. To date, the mechanism of cisplatin-induced ototoxicity remains unclear, and hearing preservation during cisplatin-based chemotherapy in patients is lacking. We found activation of the ATM-Chk2-p53 pathway to be a major determinant of cisplatin ototoxicity. However, prevention of cisplatin-induced ototoxicity is hampered by opposite effects of ATM activation upon sensory hair cells: promoting both outer hair cell death and inner hair cell survival. Encouragingly, however, genetic or pharmacological ablation of p53 substantially attenuated cochlear cell apoptosis, thus preserving hearing. Importantly, systemic administration of a p53 inhibitor in mice bearing patient-derived triple-negative breast cancer protected auditory function, without compromising the anti-tumor efficacy of cisplatin. Altogether, these findings highlight a novel and effective strategy for hearing protection in cisplatin-based chemotherapy.

    View details for DOI 10.15252/emmm.201606230

    View details for PubMedID 27794029

    View details for PubMedCentralID PMC5210089

  • Impairment of Visual Function and Retinal ER Stress Activation in Wfs1-Deficient Mice PLOS ONE Bonnet Wersinger, D., Benkafadar, N., Jagodzinska, J., Hamel, C., Tanizawa, Y., Lenaers, G., Delettre, C. 2014; 9 (5)