Abstract
The main reason for the low efficiency of glioblastoma therapy is its resistance to therapeutic procedures. The development of multidrug resistance occurs as a result of the selection of tumor clones during therapy. The resistant cell clones to radiotherapy and chemotherapy can proliferate, leading to tumor growth, in which its own vascular network is formed (angiogenesis), which promotes cell migration, invasion and the appearance of metastases and recurrent glioblastoma. The review examines the relationship at the molecular level of multidrug resistance with proliferation, angiogenesis, migration, metastasis, and the formation of glioblastoma relapses, with an emphasis on identifying new targets among proteins, microRNAs, signal transduction kinases, transcription factors, tumor-supressor genes and oncogenes.
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