Benutzerspezifische Werkzeuge

Translational Oncology

Platzhalter Bild

Dr. Mohamed Elgendy

Group Leader


Research focus

Cancer cells require dramatically high levels of energy and biomass to fuel their rapid growth. How tumors alter their metabolism to meet these high demands has always fascinated scientists. Cytosolic glycolysis and mitochondrial oxidative phosphorylation “OXPHOS” are the main energy-producing pathways. For decades, metabolic reprogramming of tumors was perceived as only increased glycolysis as postulated by Otto Warburg almost a century ago. This simplistic view has recently been challenged and revised as we started to realize that tumor metabolism is more heterogeneous than initially assumed. The concept of metabolic plasticity has recently emerged as we started to realize that some tumors are able to switch between alternative metabolic programs to meet challenges exerted by drugs targeted against a certain metabolic pathway or during the course of tumorigenesis. We aim to:

Specific expertise

  • Tumor metabolism
  • Anti-cancer drug resistance
  • Cancer cell death
  • Oncogenic switches

 Funding

Lab Members

Brandt, KerstinTechnician
Dr. Elgendy, MohammedGroup leader
Ferucci, FilippoPhD-student

Selected Publications

  •  Elgendy, M, Ciro, M, Hosseini, A, Weiszmann, J, Mazzarella, L, Ferrari, E, Cazzoli, R, Curigliano, G, DeCensi, A, Bonanni, B, Budillon, A, Pelicci, P G, Janssens, V, Ogris, M, Baccarini, M, Lanfrancone, L, Weckwerth, W, Foiani, M and Minucci, S. Combination of Hypoglycemia and Metformin Impairs Tumor Metabolic Plasticity and Growth by Modulating the PP2A-GSK3beta-MCL-1 Axis. Cancer Cell35: 798-815 e5 (2019)
  • Elgendy, M, Fusco, J P, Segura, V, Lozano, M D, Minucci, S, Echeveste, J I, Gurpide, A, Andueza, M, Melero, I, Sanmamed, M F, Ruiz, M R, Calvo, A, Pascual, J I, Velis, J M, Minana, B, Valle, R D, Pio, R, Agorreta, J, Abengozar, M, Colecchia, M, Brich, S, Renne, S L, Guruceaga, E, Patino-Garcia, A and Perez-Gracia, J L. Identification of mutations associated with acquired resistance to sunitinib in renal cell cancer. Int J Cancer145: 1991-2001 (2019)
  • Abdel-Aziz, A K, Abdel-Naim, A B, Shouman, S, Minucci, S and Elgendy, M. From Resistance to Sensitivity: Insights and Implications of Biphasic Modulation of Autophagy by Sunitinib. Front Pharmacol8: 718 (2017)
  • Elgendy, M, Abdel-Aziz, A K, Renne, S L, Bornaghi, V, Procopio, G, Colecchia, M, Kanesvaran, R, Toh, C K, Bossi, D, Pallavicini, I, Perez-Gracia, J L, Lozano, M D, Giandomenico, V, Mercurio, C, Lanfrancone, L, Fazio, N, Nole, F, Teh, B T, Renne, G and Minucci, S. Dual modulation of MCL-1 and mTOR determines the response to sunitinib. J Clin Invest127: 153-168 (2017)
  • Ferrari, E, Bruhn, C, Peretti, M, Cassani, C, Carotenuto, W V, Elgendy, M, Shubassi, G, Lucca, C, Bermejo, R, Varasi, M, Minucci, S, Longhese, M P and Foiani, M. PP2A Controls Genome Integrity by Integrating Nutrient-Sensing and Metabolic Pathways with the DNA Damage Response. Mol Cell67: 266-281 e4 (2017)
  • Elgendy, M, Ciro, M, Abdel-Aziz, A K, Belmonte, G, Dal Zuffo, R, Mercurio, C, Miracco, C, Lanfrancone, L, Foiani, M and Minucci, S. Beclin 1 restrains tumorigenesis through Mcl-1 destabilization in an autophagy-independent reciprocal manner. Nat Commun5: 5637 (2014)
  • Elgendy, M, Sheridan, C, Brumatti, G and Martin, S J. Oncogenic Ras-induced expression of Noxa and Beclin-1 promotes autophagic cell death and limits clonogenic survival. Mol Cell42: 23-35 (2011)
  • Sheridan, C, Brumatti, G, Elgendy, M, Brunet, M and Martin, S J. An ERK-dependent pathway to Noxa expression regulates apoptosis by platinum-based chemotherapeutic drugs. Oncogene29: 6428-41 (2010)
  • Logue, S E, Elgendy, M and Martin, S J. Expression, purification and use of recombinant annexin V for the detection of apoptotic cells. Nat Protoc4: 1383-95 (2009)