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Publication

Afatinib and Temozolomide combination inhibits tumorigenesis by targeting EGFRvIII-cMet signaling in glioblastoma cells.

Raghupathy Vengoji | Muzafar A Macha | Rama Krishna Nimmakayala | Satyanarayana Rachagani | Jawed A Siddiqui | Kavita Mallya | Santhi Gorantla | Maneesh Jain | Moorthy P Ponnusamy | Surinder K Batra | Nicole Shonka
Journal of experimental & clinical cancer research : CR | 2019

Glioblastoma (GBM) is an aggressive brain tumor with universal recurrence and poor prognosis. The recurrence is largely driven by chemoradiation resistant cancer stem cells (CSCs). Epidermal growth factor receptor (EGFR) and its mutant EGFRvIII are amplified in ~ 60% and ~ 30% of GBM patients, respectively; however, therapies targeting EGFR have failed to improve disease outcome. EGFRvIII-mediated cross-activation of tyrosine kinase receptor, cMET, regulates GBM CSC maintenance and promote tumor recurrence. Here, we evaluated the efficacy of pan-EGFR inhibitor afatinib and Temozolomide (TMZ) combination on GBM in vitro and in vivo.

Pubmed ID: 31215502

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Associated grants

  • Agency: NCI NIH HHS, United States
    Id: P30 CA036727
  • Agency: NCI NIH HHS, United States
    Id: R01 CA183459
  • Agency: NCI NIH HHS, United States
    Id: R01 CA210637
  • Agency: NCI NIH HHS, United States
    Id: P01 CA217798
  • Agency: NCI NIH HHS, United States
    Id: U01 CA185148

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