MRI-based radiomics signature and clinical factor for predicting H3K27M mutation in pediatric high-grade gliomas located in the midline of the brain

Author(s):  
Chenqing Wu ◽  
Hui Zheng ◽  
Jinning Li ◽  
Yuzhen Zhang ◽  
Shaofeng Duan ◽  
...  
2019 ◽  
Vol 131 ◽  
pp. 174-176 ◽  
Author(s):  
Giuseppe La Rocca ◽  
Giovanni Sabatino ◽  
Roberto Altieri ◽  
Francesco Signorelli ◽  
Luca Ricciardi ◽  
...  

2002 ◽  
Vol 57 (12) ◽  
pp. 1098-1108 ◽  
Author(s):  
A Oatridge ◽  
J.V Hajnal ◽  
N Saeed ◽  
E.S Newlands ◽  
W.L Curati ◽  
...  

Author(s):  
G.E. Laramore ◽  
M. Diener-West ◽  
T.W. Griffin ◽  
M.L. Griem ◽  
F.J. Thonas ◽  
...  

2010 ◽  
Vol 34 (4) ◽  
pp. 601-611 ◽  
Author(s):  
Ashok J. Kumar ◽  
Norman E. Leeds ◽  
Vinodh A. Kumar ◽  
Gregory N. Fuller ◽  
Frederick F. Lang ◽  
...  

2018 ◽  
Vol 29 (21) ◽  
pp. 2509-2515 ◽  
Author(s):  
Devin B. Mair ◽  
Heather M. Ames ◽  
Rong Li

High-grade gliomas are especially difficult tumors to treat due to their invasive behavior. This has led to extensive research focusing on arresting glioma cell migration. Cell migration involves the sensing of a migratory cue, followed by polarization in the direction of the cue, and reorganization of the actin cytoskeleton to allow for a protrusive leading edge and a contractile trailing edge. Transmission of these forces to produce motility also requires adhesive interactions of the cell with the extracellular microenvironment. In glioma cells, transmembrane receptors such as CD44 and integrins bind the cell to the surrounding extracellular matrix that provides a substrate on which the cell can exert the requisite forces for cell motility. These various essential parts of the migratory machinery are potential targets to halt glioma cell invasion. In this review, we discuss the mechanisms of glioma cell migration and how they may be targeted in anti-invasion therapies.


Cancers ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 979 ◽  
Author(s):  
Quentin Fuchs ◽  
Marina Pierrevelcin ◽  
Melissa Messe ◽  
Benoit Lhermitte ◽  
Anne-Florence Blandin ◽  
...  

The brain tumor microenvironment has recently become a major challenge in all pediatric cancers, but especially in brain tumors like high-grade gliomas. Hypoxia is one of the extrinsic tumor features that interacts with tumor cells, but also with the blood–brain barrier and all normal brain cells. It is the result of a dramatic proliferation and expansion of tumor cells that deprive the tissues of oxygen inflow. However, cancer cells, especially tumor stem cells, can endure extreme hypoxic conditions by rescheduling various genes’ expression involved in cell proliferation, metabolism and angiogenesis and thus, promote tumor expansion, therapeutic resistance and metabolic adaptation. This cellular adaptation implies Hypoxia-Inducible Factors (HIF), namely HIF-1α and HIF-2α. In pediatric high-grade gliomas (pHGGs), several questions remained open on hypoxia-specific role in normal brain during gliomagenesis and pHGG progression, as well how to model it in preclinical studies and how it might be counteracted with targeted therapies. Therefore, this review aims to gather various data about this key extrinsic tumor factor in pHGGs.


2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi42-vi43
Author(s):  
Rituraj Upadhyay ◽  
Swapnil Khose ◽  
Halyna Pokhylevych ◽  
Arnold dela Cruz Paulino ◽  
Mary Frances McAleer ◽  
...  

Abstract BACKGROUND Primary spinal high-grade gliomas(S-HGG) are rare, aggressive tumors and radiation therapy(RT) plays a dominant role in the management given their infiltrative nature. We conducted a single-institution retrospective review to study the clinicopathological features and management of S-HGGs. METHODS Patients with biopsy-proven S-HGG who received RT from 2001-2020 were analyzed for patient, tumor, and treatment characteristics. Kaplan-Meier estimate and Cox proportional hazard regression method were used for survival analyses. RESULTS Twenty-nine patients were identified with a median age of 25.9 years (range 1-74y). Four patients had gross total resection(GTR) while 25 underwent subtotal resection or biopsy. Nineteen patients had WHO grade 4 tumor. IDH1 mutation and MGMT promoter methylation were analyzed in 14 and four patients respectively; all were IDH wildtype and MGMT-promoter unmethylated. H3K27M mutation was present in five out of 10 patients tested. Twenty-two patients received photon-based radiation and 7 received proton therapy. Median RT dose was 50.4 Gy (range 39.6-54Gy) with 79% receiving >45Gy. 65% patients received concurrent chemotherapy, most commonly temozolomide. Twenty-three (79%) patients had documented recurrence. Overall, 16 patients relapsed locally, 10 relapsed in the brain and 8 developed leptomeningeal disease; only 8(35%) had isolated local relapse. Median OS from diagnosis was 21.3 months and median PFS after RT was 9.7 months. On univariate analysis, age, sex, GTR, grade, RT modality, RT dose and concurrent chemotherapy did not predict for survival. Patients with H3K27M mutation had a poorer median PFS after RT compared to those without the mutation but the difference did not reach statistical significance (p = 0.26). CONCLUSIONS Although 86% of patients had gross disease at RT and received a lower median RT dose than typically used in cerebral high-grade gliomas, only 55% of patients failed locally. H3K27M mutation may portend worse survival; future studies to improve the therapeutic approach in these patients are warranted.


Sign in / Sign up

Export Citation Format

Share Document