Assessing current therapeutic approaches to decode potential resistance mechanisms in glioblastomas

Chun-I Sze, Wan Pei Su, Ming Fu Chiang, Chen Yu Lu, Yu An Chen, Nan-Shan Chang

Research output: Contribution to journalShort survey

12 Citations (Scopus)

Abstract

Unique astrocytic cell infiltrating growth and glial tumor growth in the confined skull make human glioblastoma (GBM) one of the most difficult cancers to treat in modern medicine. Prognosis for patients is very poor, as they die more or less within 12 months. Patients either die of the cancer itself, or secondary complications such as cerebral edema, herniations, or hemorrhages. GBMs rarely metastasize to other organs. However, GBM recurrence associated with resistance to therapeutic drugs is common. Patients die shortly after relapse. GBM is indeed an outstanding cancer model to search for potential mechanisms for drug resistance. Here, we reviewed the current cancer biology of gliomas and their pathophysiological events that contribute to the development of therapeutic resistance. We have addressed the potential roles of cancer stem cells, epigenetic modifications, and epithelial mesenchymal transition (EMT) in the development of resistance to inhibitor drugs in GBMs. The potential role of TIAF1 (TGF-β-induced antiapoptotic factor) overexpression and generation of intratumor amyloid fibrils for conferring drug resistance in GBMs is discussed.

Original languageEnglish
Article numberArticle 00059
JournalFrontiers in Oncology
Volume3 MAR
DOIs
Publication statusPublished - 2013 Dec 24

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Glioblastoma
Neoplasms
Drug Resistance
Therapeutics
Recurrence
Modern 1601-history
Epithelial-Mesenchymal Transition
Neoplastic Stem Cells
Brain Edema
Cerebral Hemorrhage
Growth
Amyloid
Epigenomics
Skull
Glioma
Neuroglia
Pharmaceutical Preparations

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

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abstract = "Unique astrocytic cell infiltrating growth and glial tumor growth in the confined skull make human glioblastoma (GBM) one of the most difficult cancers to treat in modern medicine. Prognosis for patients is very poor, as they die more or less within 12 months. Patients either die of the cancer itself, or secondary complications such as cerebral edema, herniations, or hemorrhages. GBMs rarely metastasize to other organs. However, GBM recurrence associated with resistance to therapeutic drugs is common. Patients die shortly after relapse. GBM is indeed an outstanding cancer model to search for potential mechanisms for drug resistance. Here, we reviewed the current cancer biology of gliomas and their pathophysiological events that contribute to the development of therapeutic resistance. We have addressed the potential roles of cancer stem cells, epigenetic modifications, and epithelial mesenchymal transition (EMT) in the development of resistance to inhibitor drugs in GBMs. The potential role of TIAF1 (TGF-β-induced antiapoptotic factor) overexpression and generation of intratumor amyloid fibrils for conferring drug resistance in GBMs is discussed.",
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Assessing current therapeutic approaches to decode potential resistance mechanisms in glioblastomas. / Sze, Chun-I; Su, Wan Pei; Chiang, Ming Fu; Lu, Chen Yu; Chen, Yu An; Chang, Nan-Shan.

In: Frontiers in Oncology, Vol. 3 MAR, Article 00059, 24.12.2013.

Research output: Contribution to journalShort survey

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AU - Sze, Chun-I

AU - Su, Wan Pei

AU - Chiang, Ming Fu

AU - Lu, Chen Yu

AU - Chen, Yu An

AU - Chang, Nan-Shan

PY - 2013/12/24

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AB - Unique astrocytic cell infiltrating growth and glial tumor growth in the confined skull make human glioblastoma (GBM) one of the most difficult cancers to treat in modern medicine. Prognosis for patients is very poor, as they die more or less within 12 months. Patients either die of the cancer itself, or secondary complications such as cerebral edema, herniations, or hemorrhages. GBMs rarely metastasize to other organs. However, GBM recurrence associated with resistance to therapeutic drugs is common. Patients die shortly after relapse. GBM is indeed an outstanding cancer model to search for potential mechanisms for drug resistance. Here, we reviewed the current cancer biology of gliomas and their pathophysiological events that contribute to the development of therapeutic resistance. We have addressed the potential roles of cancer stem cells, epigenetic modifications, and epithelial mesenchymal transition (EMT) in the development of resistance to inhibitor drugs in GBMs. The potential role of TIAF1 (TGF-β-induced antiapoptotic factor) overexpression and generation of intratumor amyloid fibrils for conferring drug resistance in GBMs is discussed.

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