Anaplastic Oligodendroglioma

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Retrieved

2021-01-18

Source

Wikipedia

Trials

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Genes

IDH2, IDH1, DTX1, POT1, HES1, TP73-AS1, HEY1, GDNF, CIC, CDKN2A, TP53, MGMT, EGFR, PTEN, PDGFRA, CCNO, KIT, SST, FUBP1, MKI67, VEGFA, OLIG2, POLA1, MSH6, APTX, BCL2, MIB1, GFAP, CDK4, OLIG1

IDH2, IDH1, DTX1, POT1, HES1, TP73-AS1, HEY1, GDNF, CIC, CDKN2A, TP53, MGMT, EGFR, PTEN, PDGFRA, CCNO, KIT, SST, FUBP1, MKI67, VEGFA, OLIG2, POLA1, MSH6, APTX, BCL2, MIB1, GFAP, CDK4, OLIG1, SLC2A1, SOX2, ZAR1, TCF12, PLA2G4C, DHDDS, SOX17, PIEZO1, CHPT1, GLIPR1, ANGPT2, NOS1, PLA2G4A, PIK3CA, CASP3, CDK2, CDKN2B, CDKN2C, CHI3L1, COX8A, DPYD, FASN, HTC2, IGFBP2, STMN1, LGALS3, LIG4, MCM6, MDM2, MDM4, MSH2, CCND1, NOS2, PDGFB, ABCB1, LOC110806263

Drugs

(S)-perillyl alcohol temozolomide, 1,2:5,6-Dianhydrogalactitol, 18-(p-[124I]-iodophenyl)octadecyl phosphocholine

(S)-perillyl alcohol temozolomide, 1,2:5,6-Dianhydrogalactitol, 18-(p-[124I]-iodophenyl)octadecyl phosphocholine, 2-hydroxyoleic acid, 4,6,8-trihydroxy-10-(3,7,11-trimethyldodeca-2,6,10-trienyl)-5,10-dihydrodibenzo[b,e][1,4] diazepin-11-one, 4-[123I] iodo-L-phenylalanine, 4-[131I] iodo-L-phenylalanine, 5-aminolevulinic acid hydrochloride ( GLEOLAN, GLIOLAN ), 7-beta-hydroxycholesteryl-3-beta-oleate, Adenoviral vector serotype 5 encoding the human interleukin-12 p70 transgene, Adenovirus serotype 5 containing partial E1A deletion and an integrin-binding domain, Adenovirus-associated vector containing human Fas-c gene, Adenovirus-mediated Herpes Simplex Virus-thymidine kinase (HKSV-tk) gene ( CEREPRO ), Allogeneic and autologous haptenised and irradiated cells and cell lysates derived from glioma, Asunercept, Autologous Tumor-Derived gp96 Heat Shock Protein-Peptide Complex ( ONCOPHAGE ), Autologous dendritic cells pulsed with RNA from glioma stem cells, Autologous dendritic cells pulsed with autologous cell lysate, Autologous dendritic cells pulsed with tumour antigen-derived synthetic peptides (MAGE-1, HER-2, AIM-2, TRP-2, gp-100, and interleukin-13 receptor alpha), Autologous ex-vivo-expanded leucocytes treated with 5-aza-2'-deoxycytidine, Autologous glioma tumour cells treated with antisense molecule directed against the insulin-like growth factor type 1 receptor, Bevacizumab ( Equidacent, AVASTIN, Aybintio, MVASI ), Biotinylated anti-tenascin monoclonal antibody for use with 90-Yttrium, Boswellia serrata resin dry extract, Cannabidiol ( EPIDIOLEX, EPIDYOLEX ), Carmustine ( GLIADEL, BICNU, CARMUSTINE OBVIUS ), Carmustine (solution for intratumoral injection), Cilengitide, Combination of carboplatin and sodium valproate, Delta-9-tetrahydrocannabinol and cannabidiol from extracts of the Cannabis sativa L. plant, Doxorubicin (administered after synthetic double-stranded siRNA oligonucleotide directed against claudin-5 complexed with polyethyleneimine), Doxorubicin hydrochloride (drug eluting beads), Dronabinol and cannabidiol, Eflornithine, Enzastaurin hydrochloride, Erlotinib hydrochloride ( TARCEVA ), Florilglutamic acid (18F), Fluciclovine (18F), Flucytosine ( ANCOTIL ), Gadodiamide (liposomal), Galunisertib, Gimatecan, Glutathione-pegylated liposomal doxorubicin hydrochloride, H-Arg-Pro-Lys-Pro-Gln-Gln-Phe-2Thi-Gly-Leu-Met(O2)-NH2-DOTA-213-bismuth, H-Arg-Pro-Lys-Pro-Gln-Gln-Phe-2Thi-Gly-Leu-Met(O2)-NH2-DOTA-225-Actinium, Herpes simplex virus lacking infected cell protein 34.5, Human transferrin conjugated to mutant diphtheria toxin, Humanised monoclonal antibody against epidermal growth factor receptor, Humanised recombinant monoclonal antibody against epidermal growth factor receptor conjugated to maleimidocaproyl monomethylauristatin F, IL-12-secreting dendritic cells, loaded with autologous tumour lysate, Iodine (131I) anti-nucleohistone H1 chimeric biotinylated monoclonal antibody, Iodine (131I) anti-tenascin monoclonal antibody 81C6, Iodine (131I) chlorotoxin, Irinotecan hydrochloride (drug eluting beads), L-cysteine, L-leucyl-L-alpha-glutamyl-L-alpha-glutamyl-L-lysyl-L-lysylglycyl-L-asparaginyl-L-tyrosyl-L-valyl-L-valyl-L-threonyl-L-alpha-aspartyl-L-histidyl-S-[1-[(4-carboxycyclohexyl)methyl]-2,5-dioxo-3-pyrrolidinyl]-complex with keyhole limpet haemocyanin, Larotrectinib ( VITRAKVI ), Marizomib, N-(4-Methoxyphenyl)-N,2,6-trimethylfuro[2,3-d]pyrimidin-4-amine, Nimotuzumab ( THERALOC ), Oligonucleotide phosphorothioate (TAAACGTTATAACGTTATGACGTCAT), Onfekafusp alfa, Paclitaxel-succinate-Arg-Arg-Leu-Ser-Tyr-Ser-Arg-Arg-Arg-Phe, Picropodophyllin, Pritumumab, Pseudomonas exotoxin (domains II/III)-Interleukin 13 chimeric protein, Recombinant fusion protein of circulary-permuted IL-4 and pseudomonas exotoxin A, [IL-4(38-37)-PE38KDEL], Recombinant human bone morphogenetic protein 4, Regorafenib ( STIVARGA ), Salmonella typhi Ty21a strain transfected with a plasmid vector encoding the human vascular endothelial growth factor receptor 2, Synthetic double-stranded siRNA oligonucleotide directed against claudin-5 complexed with polyethyleneimine (prior to administration of doxorubicin), Talampanel, Technetium (99mTc) tetrofosmin, Temozolomide ( TEMODAL, TEMODAR ), Topotecan hydrochloride (liposomal), Trabedersen, Tranilast, Veledimex, Vocimagene amiretrorepvec, Zoledronic acid, Zotiraciclib

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Anaplastic oligodendroglioma is a neuroepithelial tumor which is believed to originate from oligodendrocytes, a cell type of the glia. In the World Health Organization (WHO) classification of brain tumors, anaplastic oligodendrogliomas are classified as grade III. In the course of the disease, they can degenerate into WHO grade IV glioblastoma. The vast majority of oligodendrogliomas occur sporadically, without a confirmed cause and without inheritance within a family.

Pathogenesis

The (malignant) anaplastic oligodendroglioma belongs to the group of diffuse glioma and arises in the central nervous system (brain and spinal cord) from precursor stem cells of the oligodendrocytes. This tumor occurs primarily in middle adulthood with a frequency peak in the 4th and 5th decade of life.

Diagnosis

The most important diagnostic procedure is magnetic resonance imaging (MRI). Occasionally, outside of routine diagnostics, the metabolism in the tissue is shown using positron emission tomography (PET). The diagnosis is confirmed by a fine tissue examination following an operation. Anaplastic oligodendrogliomas often show a loss of genetic material. About 50 to 70% of WHO grade III anaplastic oligodendrogliomas have combined allele losses on the short arm of chromosome 1 (1p) and the long arm of chromosome 19 (19q). This change is mostly referred to as "1p / 19q Co Deletion". It can be seen as favorable for the patient and makes a response to radiation or chemotherapy more likely. The designation of grade III oligodendroglioma (high grade) generally subsumes the previous diagnoses of anaplastic or malignant oligodendroglioma.

Histopathological image of anaplastic oligodendroglioma in cerebrum. Hematoxylin & eosin stain.
Zooming, note the irregular cell- and nucleus-shapes

Treatment

Surgery can help reduce symptoms caused by the tumor. As complete as possible removal of the tumor visible on the MRI is preferred, provided the location of the tumor allows this. Since the cells of an anaplastic oligodendroglioma have already migrated into the surrounding healthy brain tissue at the time of diagnosis, a complete surgical removal of all tumor cells is not possible. The "1p / 19q Codeletion" marker plays an increasingly important role in the selection of therapy and therapy combinations. Because of the indolent nature of this tumor and the potential morbidity associated with neurosurgery, chemotherapy and radiation therapy, most neurooncologists will initially pursue a course of watchful waiting and treat patients symptomatically. Symptomatic treatment often includes the use of anticonvulsants for seizures and steroids for brain swelling. For further treatment, radiation or chemotherapy with temozolomide or a chemotherapy with Procarbazine, CCNU and Vincristine (PCV) has been shown to be effective and was the most commonly used chemotherapy regimen used for treating anaplastic oligodendrogliomas.

Prognosis

5–Year relative survival rate: Age 20–44, 76%. Age 45–54, 67%. Age 55–64, 45%. Procarbazine, lomustine and vincristine have been used since May 1975. For 46 years, new therapeutic options have been regularly tested as part of therapy studies to improve the treatment of anaplastic oligodendroglioma.

Research

As of 2021^[update], a definitive cure is not possible with anaplastic oligodendrogliomas of WHO grade III. A retrospective study on 1054 patients with anaplastic oligodendroglioma, presented during the 2009 ASCO Annual Meeting, suggests that PCV therapy may be effective. Median time to progression for patients with 1p19q co-deletion was longer following PCV alone (7.6 years) than with temozolomide alone (3.3 years); median overall survival was also longer with PCV treatment versus temozolomide treatment (not reached, vs. 7.1 years). A recent long-term study does affirm that radiation combined with adjuvant chemotherapy is significantly more efficacious for anaplastic oligodendroglioma patients with 1p 19q co-deleted tumors and has become the new standard of care. It is possible that radiotherapy may prolong the overall time to progression for non-deleted tumors. If the tumor mass compresses adjacent brain structures, a neurosurgeon will typically remove as much of the tumor as he or she can without damaging other critical, healthy brain structures. Recent studies suggest that radiation does not improve overall survival (even when age, clinical data, histological grading, and type of surgery are considered).