Modern views on the recurrence of meningiomas
DOI:
https://doi.org/10.25305/unj.243332Keywords:
meningioma, skull base, recurrence, NF2, ФI3K, HH, TRAF7, AKT3, PIK3CA, PI-K3R1, PRKAR1AAbstract
Meningiomas are common tumors of the central nervous system. Grade I meningiomas are generally considered to be "benign". However, a certain percentage of these tumors have a more aggressive course, similar to malignant tumors. Numerous observations have shown that even in the case of radical removal of the tumor, the latter recur within the next 10 years. Recent molecular studies have shed new light on meningioma subtypes, their behavior, the prospect of new treatment, and prognostic features for patients. The study of V.E. Clark et al. found a number of mutations in NF2 meningiomas, namely TRAF7 (tumor necrosis factor receptor 7 factor), KLF4 (Kruppel-like factor 4c), AKT1 and SMO. The pattern between the type of mutation and the tumor location was established: posterior cranial fossa, parasagittal area, falx, torculae and intraventricular sections - loss of NF2 or chromosome 22, olfactory groove and middle cranial fossa - KLF4 / TRAF7, olfactory groove, - PIK3CA, middle parts of the anterior cranial fossa and middle cranial fossa - AKT1 / POLR2, olfactory groove - SMO. The selection criteria in the study, which analyzed data from 469 meningiomas of a known molecular subgroup, were the degree of resection, postoperative irradiation, postoperative neuroimaging and time to recurrence (if present). Molecular subgroups of meningiomas had different clinical manifestations during the two years of follow-up, with several aggressive subgroups (NF2, PI3K, HH, TRAF7) recurring at an average rate 22 times faster than less aggressive tumors (KLF4, POLR2A, SMARCB1). PI3K-activated meningiomas recurred earlier than tumors in other groups. The potentially more aggressive group of meningiomas with HH, NF2, and TRAF7 mutations demonstrated a high recurrence rate after 60 months of follow-up (35.3, 43.7, and 36.4%, respectively), whereas most tumor recurrences with PI3K mutations were reported within the first 24 months (75,0%).
Classification of meningiomas by genomic mutations is a promising tool. Its introduction into clinical practice will make it possible to predict the aggressiveness of meningiomas and the risk of their recurrence, which will help to give a more accurate prognosis for patients and develop effective therapeutic methods for these tumors.
References
Ostrom QT, Gittleman H, Fulop J, Liu M, Blanda R, Kromer C, Wolinsky Y, Kruchko C, Barnholtz-Sloan JS. CBTRUS Statistical Report: Primary Brain and Central Nervous System Tumors Diagnosed in the United States in 2008-2012. Neuro Oncol. 2015 Oct;17 Suppl 4(Suppl 4):iv1-iv62. doi: 10.1093/neuonc/nov189.
Youngblood MW, Miyagishima DF, Jin L, Gupte T, Li C, Duran D, Montejo JD, Zhao A, Sheth A, Tyrtova E, Özduman K, Iacoangeli F, Peyre M, Boetto J, Pease M, Avşar T, Huttner A, Bilguvar K, Kilic T, Pamir MN, Amankulor N, Kalamarides M, Erson-Omay EZ, Günel M, Moliterno J. Associations of meningioma molecular subgroup and tumor recurrence. Neuro Oncol. 2021 May 5;23(5):783-794. doi: 10.1093/neuonc/noaa226.
Adegbite AB, Khan MI, Paine KW, Tan LK. The recurrence of intracranial meningiomas after surgical treatment. J Neurosurg. 1983 Jan;58(1):51-6. doi: 10.3171/jns.1983.58.1.0051.
Mansouri A, Klironomos G, Taslimi S, Kilian A, Gentili F, Khan OH, Aldape K, Zadeh G. Surgically resected skull base meningiomas demonstrate a divergent postoperative recurrence pattern compared with non-skull base meningiomas. J Neurosurg. 2016 Aug;125(2):431-40. doi: 10.3171/2015.7.JNS15546.
Louis DN, Perry A, Reifenberger G, von Deimling A, Figarella-Branger D, Cavenee WK, Ohgaki H, Wiestler OD, Kleihues P, Ellison DW. The 2016 World Health Organization Classification of Tumors of the Central Nervous System: a summary. Acta Neuropathol. 2016 Jun;131(6):803-20. doi: 10.1007/s00401-016-1545-1.
Karsy M, Guan J, Cohen A, Colman H, Jensen RL. Medical Management of Meningiomas: Current Status, Failed Treatments, and Promising Horizons. Neurosurg Clin N Am. 2016 Apr;27(2):249-60. doi: 10.1016/j.nec.2015.11.002.
Preusser M, Brastianos PK, Mawrin C. Advances in meningioma genetics: novel therapeutic opportunities. Nat Rev Neurol. 2018 Feb;14(2):106-115. doi: 10.1038/nrneurol.2017.168.
Hamaratoglu F, Willecke M, Kango-Singh M, Nolo R, Hyun E, Tao C, Jafar-Nejad H, Halder G. The tumour-suppressor genes NF2/Merlin and Expanded act through Hippo signalling to regulate cell proliferation and apoptosis. Nat Cell Biol. 2006 Jan;8(1):27-36. doi: 10.1038/ncb1339.
James MF, Han S, Polizzano C, Plotkin SR, Manning BD, Stemmer-Rachamimov AO, Gusella JF, Ramesh V. NF2/merlin is a novel negative regulator of mTOR complex 1, and activation of mTORC1 is associated with meningioma and schwannoma growth. Mol Cell Biol. 2009 Aug;29(15):4250-61. doi: 10.1128/MCB.01581-08.
James MF, Stivison E, Beauchamp R, Han S, Li H, Wallace MR, Gusella JF, Stemmer-Rachamimov AO, Ramesh V. Regulation of mTOR complex 2 signaling in neurofibromatosis 2-deficient target cell types. Mol Cancer Res. 2012 May;10(5):649-59. doi: 10.1158/1541-7786.MCR-11-0425-T.
Mei Y, Du Z, Hu C, Greenwald NF, Abedalthagafi M, Agar NYR, Dunn GP, Bi WL, Santagata S, Dunn IF. Osteoglycin promotes meningioma development through downregulation of NF2 and activation of mTOR signaling. Cell Commun Signal. 2017 Sep 18;15(1):34. doi: 10.1186/s12964-017-0189-7.
Morrison H, Sperka T, Manent J, Giovannini M, Ponta H, Herrlich P. Merlin/neurofibromatosis type 2 suppresses growth by inhibiting the activation of Ras and Rac. Cancer Res. 2007 Jan 15;67(2):520-7. doi: 10.1158/0008-5472.CAN-06-1608.
Rong R, Tang X, Gutmann DH, Ye K. Neurofibromatosis 2 (NF2) tumor suppressor merlin inhibits phosphatidylinositol 3-kinase through binding to PIKE-L. Proc Natl Acad Sci U S A. 2004 Dec 28;101(52):18200-5. doi: 10.1073/pnas.0405971102.
Karsy M, Guan J, Cohen A, Colman H, Jensen RL. Medical Management of Meningiomas: Current Status, Failed Treatments, and Promising Horizons. Neurosurg Clin N Am. 2016 Apr;27(2):249-60. doi: 10.1016/j.nec.2015.11.002.
Clark VE, Erson-Omay EZ, Serin A, Yin J, Cotney J, Ozduman K, Avşar T, Li J, Murray PB, Henegariu O, Yilmaz S, Günel JM, Carrión-Grant G, Yilmaz B, Grady C, Tanrikulu B, Bakircioğlu M, Kaymakçalan H, Caglayan AO, Sencar L, Ceyhun E, Atik AF, Bayri Y, Bai H, Kolb LE, Hebert RM, Omay SB, Mishra-Gorur K, Choi M, Overton JD, Holland EC, Mane S, State MW, Bilgüvar K, Baehring JM, Gutin PH, Piepmeier JM, Vortmeyer A, Brennan CW, Pamir MN, Kiliç T, Lifton RP, Noonan JP, Yasuno K, Günel M. Genomic analysis of non-NF2 meningiomas reveals mutations in TRAF7, KLF4, AKT1, and SMO. Science. 2013 Mar 1;339(6123):1077-80. doi: 10.1126/science.1233009.
Brastianos PK, Horowitz PM, Santagata S, Jones RT, McKenna A, Getz G, Ligon KL, Palescandolo E, Van Hummelen P, Ducar MD, Raza A, Sunkavalli A, Macconaill LE, Stemmer-Rachamimov AO, Louis DN, Hahn WC, Dunn IF, Beroukhim R. Genomic sequencing of meningiomas identifies oncogenic SMO and AKT1 mutations. Nat Genet. 2013 Mar;45(3):285-9. doi: 10.1038/ng.2526.
Clark VE, Harmancı AS, Bai H, Youngblood MW, Lee TI, Baranoski JF, Ercan-Sencicek AG, Abraham BJ, Weintraub AS, Hnisz D, Simon M, Krischek B, Erson-Omay EZ, Henegariu O, Carrión-Grant G, Mishra-Gorur K, Durán D, Goldmann JE, Schramm J, Goldbrunner R, Piepmeier JM, Vortmeyer AO, Günel JM, Bilgüvar K, Yasuno K, Young RA, Günel M. Recurrent somatic mutations in POLR2A define a distinct subset of meningiomas. Nat Genet. 2016 Oct;48(10):1253-9. doi: 10.1038/ng.3651.
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Copyright (c) 2022 Mykola O. Guk, Mykhailo B. Bandrivskyi, Olena O. Danevych, Artur O. Mumlev , Dmitry M. Tsyurupa, Andrey A. Chukov, Vasyl V. Kondratyuk
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