The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Recent advances in the use of PI3K inhibitors for glioblastoma multiforme: current preclinical and clinical development
Open accessAbstract
Glioblastoma multiforme (GBM) is the most common and aggressive malignant primary tumor in the central nervous system. One of the most widely used chemotherapeutic drugs for GBM is temozolomide, which is a DNA-alkylating agent and its efficacy is dependent on MGMT methylation status. Little progress in improving the prognosis of GBM patients has been made in the past ten years, urging the development of more effective molecular targeted therapies. Hyper-activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway is frequently found in a variety of cancers including GBM, and it plays a central role in the regulation of tumor cell survival, growth, motility, angiogenesis and metabolism. Numerous PI3K inhibitors including pan-PI3K, isoform-selective and dual PI3K/mammalian target of rapamycin (mTOR) inhibitors have exhibited favorable preclinical results and entered clinical trials in a range of hematologic malignancies and solid tumors. Furthermore, combination of inhibitors targeting PI3K and other related pathways may exert synergism on suppressing tumor growth and improving patients' prognosis. Currently, only a handful of PI3K inhibitors are in phase I/II clinical trials for GBM treatment. In this review, we focus on the importance of PI3K/Akt pathway in GBM, and summarize the current development of PI3K inhibitors alone or in combination with other inhibitors for GBM treatment from preclinical to clinical studies.
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Cites
Radiotherapy Plus Concomitant and Adjuvant Temozolomide for Glioblastoma
Stupp, R., Mason, W. P., van den Bent, M. J., Weller, M., Fisher, B., Taphoorn, M. J. B., Belanger, K., Brandes, A. A., Marosi, C., Bogdahn, U., et al. (2005) · New England Journal of Medicine · doi:10.1056/nejmoa043330 · Cited by 21,807
The phosphoinositide 3-kinase pathway
Cantley, L. C. (2002) · Science · doi:10.1126/science.296.5573.1655 · Cited by 5,621
The Somatic Genomic Landscape of Glioblastoma
Brennan, C. W., Verhaak, R. G. W., McKenna, A., Campos, B., Noushmehr, H., Salama, S. R., Zheng, S., Chakravarty, D., Sanborn, J. Z., Berman, S. H., et al. (2013) · Cell · doi:10.1016/j.cell.2013.09.034 · Cited by 5,016
Self-citationThe functions and regulation of the PTEN tumour suppressor
Song, M. S., Salmena, L., & Pandolfi, P. P. (2012) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3330 · Cited by 1,926
Overcoming the blood–brain tumor barrier for effective glioblastoma treatment
van Tellingen, O., Yetkin-Arik, B., de Gooijer, M. C., Wesseling, P., Wurdinger, T., & de Vries, H. E. (2015) · Drug Resistance Updates · doi:10.1016/j.drup.2015.02.002 · Cited by 1,035
RAS Interaction with PI3K: More Than Just Another Effector Pathway
Castellano, E., & Downward, J. (2011) · Genes & Cancer · doi:10.1177/1947601911408079 · Cited by 762
Shimizu, T., Tolcher, A. W., Papadopoulos, K. P., Beeram, M., Rasco, D. W., Smith, L. S., Gunn, S., Smetzer, L., Mays, T. A., Kaiser, B., et al. (2012) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-11-2381 · Cited by 431
Bedard, P. L., Tabernero, J., Janku, F., Wainberg, Z. A., Paz-Ares, L., Vansteenkiste, J., Van Cutsem, E., Pérez-García, J., Stathis, A., Britten, C. D., et al. (2015) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-14-1814 · Cited by 324
Sunayama, J., Matsuda, K.-I., Sato, A., Tachibana, K., Suzuki, K., Narita, Y., Shibui, S., Sakurada, K., Kayama, T., Tomiyama, A., et al. (2010) · Stem Cells · doi:10.1002/stem.521 · Cited by 218
Foster, P., Yamaguchi, K., Hsu, P. P., Qian, F., Du, X., Wu, J., Won, K.-A., Yu, P., Jaeger, C. T., Zhang, W., et al. (2015) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-14-0833 · Cited by 58
Cited by
The pathogenic role of PI3K/AKT pathway in cancer onset and drug resistance: an updated review
Rascio, F., Spadaccino, F., Rocchetti, M. T., Castellano, G., Stallone, G., Netti, G. S., & Ranieri, E. (2021) · Cancers · doi:10.3390/cancers13163949 · Cited by 497
The interplay of ROS and the PI3K/Akt pathway in autophagy regulation
Kma, L., & Baruah, T. J. (2022) · Biotechnology and Applied Biochemistry · doi:10.1002/bab.2104 · Cited by 394
Glioblastoma Multiforme: An Overview of Emerging Therapeutic Targets
Taylor, O. G., Brzozowski, J. S., & Skelding, K. A. (2019) · Frontiers in Oncology · doi:10.3389/fonc.2019.00963 · Cited by 322
Temozolomide and Other Alkylating Agents in Glioblastoma Therapy
Strobel, H., Baisch, T., Fitzel, R., Schilberg, K., Siegelin, M. D., Karpel-Massler, G., Debatin, K.-M., & Westhoff, M.-A. (2019) · Biomedicines · doi:10.3390/biomedicines7030069 · Cited by 279
Glioblastoma Therapy: Past, Present and Future
Obrador, E., Moreno-Murciano, P., Oriol-Caballo, M., López-Blanch, R., Pineda, B., Gutiérrez-Arroyo, J., Loras, A., Gonzalez-Bonet, L., Martinez-Cadenas, C., Estrela, J., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25052529 · Cited by 271
Metadata
- Authors
- Zhao, H.-F., Wang, J., Shao, W., Wu, C.-P., Chen, Z.-P., To, S.-S. T., & Li, W.-P.
- Venue
- Molecular Cancer
- Published
- 2017-06-07
- Volume
- 16
- Issue
- 1
- Pages
- 100-100
- ISSN
- 1476-4598 (ISSN-L)
- OpenAlex
- W2621838563
- Cited by
- 251
- References
- 10
- FWCI
- 11.78
- Type
- journal article
- Language
- en
- Open access
- gold
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- Zhao, H.-F., Wang, J., Shao, W., Wu, C.-P., Chen, Z.-P., To, S.-S. T., & Li, W.-P. (2017). Recent advances in the use of PI3K inhibitors for glioblastoma multiforme: current preclinical and clinical development. Molecular Cancer. https://doi.org/10.1186/s12943-017-0670-3
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