Reduced Fusiform Gyrus Activation During Face Processing in Pediatric Brain Tumor Survivors

Author(s):  
Matthew C. Hocking ◽  
Robert T. Schultz ◽  
Jane E. Minturn ◽  
Cole Brodsky ◽  
May Albee ◽  
...  

Abstract Objective: The neural mechanisms contributing to the social problems of pediatric brain tumor survivors (PBTS) are unknown. Face processing is important to social communication, social behavior, and peer acceptance. Research with other populations with social difficulties, namely autism spectrum disorder, suggests atypical brain activation in areas important for face processing. This case-controlled functional magnetic resonance imaging (fMRI) study compared brain activation during face processing in PBTS and typically developing (TD) youth. Methods: Participants included 36 age-, gender-, and IQ-matched youth (N = 18 per group). PBTS were at least 5 years from diagnosis and 2 years from the completion of tumor therapy. fMRI data were acquired during a face identity task and a control condition. Groups were compared on activation magnitude within the fusiform gyrus for the faces condition compared to the control condition. Correlational analyses evaluated associations between neuroimaging metrics and indices of social behavior for PBTS participants. Results: Both groups demonstrated face-specific activation within the social brain for the faces condition compared to the control condition. PBTS showed significantly decreased activation for faces in the medial portions of the fusiform gyrus bilaterally compared to TD youth, ps ≤ .004. Higher peak activity in the left fusiform gyrus was associated with better socialization (r = .53, p < .05). Conclusions: This study offers initial evidence of atypical activation in a key face processing area in PBTS. Such atypical activation may underlie some of the social difficulties of PBTS. Social cognitive neuroscience methodologies may elucidate the neurobiological bases for PBTS social behavior.

2017 ◽  
Vol 25 (12) ◽  
pp. 3749-3757 ◽  
Author(s):  
Matthew C. Hocking ◽  
Lauren F. Quast ◽  
Cole Brodsky ◽  
Janet A. Deatrick

2014 ◽  
Vol 40 (3) ◽  
pp. 297-308 ◽  
Author(s):  
C. G. Salley ◽  
L. L. Hewitt ◽  
A. F. Patenaude ◽  
M. W. Vasey ◽  
K. O. Yeates ◽  
...  

2010 ◽  
Vol 31 (Abstracts) ◽  
pp. E19
Author(s):  
Jennifer C. Acker ◽  
Christina G. Salley ◽  
Larissa L. Hewitt ◽  
Keith O. Yeates ◽  
Andrea Farkas Patenaude ◽  
...  

2012 ◽  
Vol 224 (06) ◽  
Author(s):  
T Milde ◽  
M Zucknick ◽  
M Kool ◽  
A Korshunov ◽  
H Witt ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yiqun Zhang ◽  
Fengju Chen ◽  
Lawrence A. Donehower ◽  
Michael E. Scheurer ◽  
Chad J. Creighton

AbstractThe global impact of somatic structural variants (SSVs) on gene expression in pediatric brain tumors has not been thoroughly characterised. Here, using whole-genome and RNA sequencing from 854 tumors of more than 30 different types from the Children’s Brain Tumor Tissue Consortium, we report the altered expression of hundreds of genes in association with the presence of nearby SSV breakpoints. SSV-mediated expression changes involve gene fusions, altered cis-regulation, or gene disruption. SSVs considerably extend the numbers of patients with tumors somatically altered for critical pathways, including receptor tyrosine kinases (KRAS, MET, EGFR, NF1), Rb pathway (CDK4), TERT, MYC family (MYC, MYCN, MYB), and HIPPO (NF2). Compared to initial tumors, progressive or recurrent tumors involve a distinct set of SSV-gene associations. High overall SSV burden associates with TP53 mutations, histone H3.3 gene H3F3C mutations, and the transcription of DNA damage response genes. Compared to adult cancers, pediatric brain tumors would involve a different set of genes with SSV-altered cis-regulation. Our comprehensive and pan-histology genomic analyses reveal SSVs to play a major role in shaping the transcriptome of pediatric brain tumors.


2021 ◽  
Vol 37 (3) ◽  
pp. 204-206
Author(s):  
Carolina Nör ◽  
Vijay Ramaswamy

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