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Molecular Mechanisms and Therapies of Brain Tumors

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 February 2025 | Viewed by 1526

Special Issue Editor


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Guest Editor
Department of Neurology, University of Medicine and Pharmacy, 200349 Craiova, Romania
Interests: brain tumors; signal transduction; cell proliferation; apoptosis; targeted therapies

Special Issue Information

Dear Colleagues,

Brain tumors are abnormal mass tissues inside the brain. Their cells have an uncontrollable growth and multiplication. Primary brain tumors originate from tissues of the brain or the brain’s surroundings. They can be glial or non-glial, benignant or malignant. In recent years, many advances have been made regarding the molecular biology of brain tumors. Molecular events like signal transduction, cell proliferation, development and apoptosis have helped us to better understand these tumor formations. This has also led to the discovery of some new molecular markers and, in recent years, of brain tumor stem cells. Nowadays, a better diagnosis and staging of this disease and new therapeutic approaches are available. Standard treatment for brain tumors is represented by surgery, radiotherapy and chemotherapy. In particular, malignant brain tumor treatment remains a great challenge. Targeted therapies, gene therapies, genome editing therapies and cell-based therapies are currently being validated in preclinical and ongoing clinical trials and represent a hope for patients with brain tumors.

We invite you to submit novel research about molecular mechanisms and therapies in brain tumors. Original articles, review articles and short communications within the described research field are welcome.

Dr. Oana Alexandru
Guest Editor

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Keywords

  • brain tumors
  • molecular mechanisms
  • signal transduction
  • cell proliferation
  • apoptosis
  • targeted therapies
  • chemotherapy
  • radiotherapy

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Published Papers (1 paper)

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Research

13 pages, 2642 KiB  
Article
CEP-1347 Boosts Chk2-Mediated p53 Activation by Ionizing Radiation to Inhibit the Growth of Malignant Brain Tumor Cells
by Yuta Mitobe, Shuhei Suzuki, Kazuki Nakamura, Yurika Nakagawa-Saito, Senri Takenouchi, Keita Togashi, Asuka Sugai, Yukihiko Sonoda, Chifumi Kitanaka and Masashi Okada
Int. J. Mol. Sci. 2024, 25(17), 9473; https://doi.org/10.3390/ijms25179473 - 30 Aug 2024
Viewed by 1065
Abstract
Radiation therapy continues to be the cornerstone treatment for malignant brain tumors, the majority of which express wild-type p53. Therefore, the identification of drugs that promote the ionizing radiation (IR)-induced activation of p53 is expected to increase the efficacy of radiation therapy for [...] Read more.
Radiation therapy continues to be the cornerstone treatment for malignant brain tumors, the majority of which express wild-type p53. Therefore, the identification of drugs that promote the ionizing radiation (IR)-induced activation of p53 is expected to increase the efficacy of radiation therapy for these tumors. The growth inhibitory effects of CEP-1347, a known inhibitor of MDM4 expression, on malignant brain tumor cell lines expressing wild-type p53 were examined, alone or in combination with IR, by dye exclusion and/or colony formation assays. The effects of CEP-1347 on the p53 pathway, alone or in combination with IR, were examined by RT-PCR and Western blot analyses. The combination of CEP-1347 and IR activated p53 in malignant brain tumor cells and inhibited their growth more effectively than either alone. Mechanistically, CEP-1347 and IR each reduced MDM4 expression, while their combination did not result in further decreases. CEP-1347 promoted IR-induced Chk2 phosphorylation and increased p53 expression in concert with IR in a Chk2-dependent manner. The present results show, for the first time, that CEP-1347 is capable of promoting Chk2-mediated p53 activation by IR in addition to inhibiting the expression of MDM4 and, thus, CEP-1347 has potential as a radiosensitizer for malignant brain tumors expressing wild-type p53. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapies of Brain Tumors)
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