Massimo Squatrito Group Leader
T +34 (+34) 917 328 000 (Ext 3850)
msquatrito@cnio.es

A decade of studies has underlined the complexity of the genetic events that characterise the genomic landscapes of common forms of human cancer, including gliomas. While a few cancer genes are mutated at high frequencies (>20%), the greatest number of cancer genes in most patients appear at intermediate frequencies (2–20%) or lower. Strikingly, the functional significance of the vast majority of these alterations still remains elusive. A current high priority in glioma research is to functionally validate candidate genetic alterations in order to distinguish those that are significant for cancer progression and treatment response.

In our laboratory, we use a combination of genomic analyses, mouse models and primary tumour cell cultures, with the main goal of identifying the molecular mechanisms that could provide the basis for novel treatments for glioma patients.

Publications

• Somatic genome editing with the RCAS-TVA-CRISPR-Cas9 system for precision tumor modeling.(2018)
  Oldrini B, Curiel-García Á, Marques C, Matia V, Uluçkan Ö, Graña-Castro O, Torres-Ruiz R, Rodriguez-Perales S, Huse JT, Squatrito M
  Nat Commun 9, 1466-.
• Influenza virus infection causes global RNAPII termination defects.(2018)
  Zhao N, Sebastiano V, Moshkina N, Mena N, Hultquist J, Jimenez-Morales D, Ma Y, Rialdi A, Albrecht R, Fenouil R, Sánchez-Aparicio MT, Ayllon J, Ravisankar S, Haddad B, Ho JSY, Low D, Jin J, Yurchenko V, Prinjha RK, Tarakhovsky A, Squatrito M, Pinto D, Allette K, Byun M, Smith ML, Sebra R, Guccione E, Tumpey T, Krogan N, Greenbaum B, van Bakel H, García-Sastre A, Marazzi I.
  Nat Struct Mol Biol 25, 885-893.
• Inhibition of Trf1 telomere protein impairs tumor initiation and progression in glioblastoma multiform mouse models and patient-derived xenografts.(2017)
  Bejarano L, Schuhmacher AJ, Méndez-Pertuz M, Megías M, Blanco-Aparicio C, Martínez S, Pastor J, Squatrito M, Blasco MA
  Cancer Cell 32, 590-607.
• Tumor Evolution of Glioma-Intrinsic Gene Expression Subtypes Associates with Immunological Changes in the Microenvironment.(2017)
  Wang Q, Hu B, Hu X, Kim H, Squatrito M, Scarpace L, deCarvalho AC, Lyu S, Li P, Li Y, Barthel F, Cho HJ, Lin YH, Satani N, Martinez-Ledesma E, Zheng S, Chang E, Sauvé CG, Olar A, Lan ZD, Finocchiaro G, Phillips JJ, Berger MS, Gabrusiewicz KR, Wang G, Eskilsson E, Hu J, Mikkelsen T, DePinho RA, Muller F, Heimberger AB, Sulman EP, Nam DH, Verhaak RGW.
  Cancer Cell 32, 42-56.
• EGFR feedback-inhibition by Ran-binding protein 6 is disrupted in cancer.(2017)
  Oldrini B, Hsieh WY, Erdjument-Bromage H, Codega P, Carro MS, Curiel-García A, Campos C, Pourmaleki M, Grommes C, Vivanco I, Rohle D, Bielski CM, Taylor BS,Hollmann TJ, Rosenblum M, Tempst P, Blenis J, Squatrito M, Mellinghoff IK
  Nat Commun 8, 2035-.
• GlioVis data portal for visualization and analysis of brain tumor expression datasets.(2017)
  Bowman R, Wang Q, Carro A, Verhaak RGW, Squatrito M
  Neuro-Oncology 19, 139-141.
• Glioblastoma and glioblastoma stem cells are dependent on functional MTH1.(2017)
  Pudelko L, Rouhi P, Sanjiv K, Gad H, Kalderén C, Höglund A, Squatrito M, Schuhmacher AJ, Edwards S, Hägerstrand D, Berglund UW, Helleday T, Bräutigam L
  Oncotarget 8, 84671-84684.
• Targeting MT1-MMP as an ImmunoPET-Based Strategy for Imaging Gliomas.(2016)
  de Lucas AG, Schuhmacher AJ, Oteo M, Romero E, Cámara JA, de Martino A, Arroyo AG, Morcillo MÁ, Squatrito M, Martinez-Torrecuadrada JL, Mulero F
  PLoS ONE 11, e0158634-.
• Take It Down a NOTCH in Forebrain tumors.(2015)
  Oldrini B, Schuhmacher AJ, Squatrito M
  Cancer Cell 28, 681-682.
• Most human non-GCIMP glioblastoma subtypes evolve from a common proneural-like precursor glioma.(2014)
  Ozawa T, Riester M, Cheng YK, Huse JT, Squatrito M, Helmy K, Charles N, Michor F, Holland EC.
  Cancer Cell 26, 288-300.
• A kinase-independent function of AKT promotes cancer cell survival.(2014)
  Vivanco I, Chen ZC, Tanos B, Oldrini B, Hsieh WY, Yannuzzi N, Campos C, Mellinghoff IK
  Elife (in press).
• Histone acetyltransferase PCAF is required for Hedgehog-Gli-dependent transcription and cancer cell proliferation.(2013)
  Malatesta M, Steinhauer C, Mohammad F, Pandey DP, Squatrito M, Helin K
  Cancer Res 73, 6323-6333.