Radiation-induced local white matter (WM) damage has been observed by diffusion tensor imaging (DTI) within a priori-defined regions of interest following radiotherapy (RT) for nasopharyngeal carcinoma (NPC). In this study, we aimed to detect WM changes throughout the brain of NPC patients by DTI. Tract-based spatial statistics (TBSS) was used to analyze DTI data from 81 NPC patients. Fractional anisotropy (FA) and mean diffusivity (MD) were quantified across the whole brain in separate groups: pre-RT, and <6, 6-12, and >12 months post-RT. We found that fractional anisotropy values were significantly lower in the right frontal, parietal, and occipital WM <6 months post-RT compared with pre-RT and remained significantly lower in the right frontal and parietal WM at >12 months. MD values were significantly higher in the right occipital, bilateral temporal, right occipital-temporal junction, left parietal, left centrum semiovale, and left frontal-parietal junction WM <6 months post-RT and remained higher in the right occipital WM at >12 months. This study suggests that changes in white matter microstructure following RT for NPC were widespread, complex, and dynamic. Diffusion tensor imaging with TBSS analysis allows for early non-invasive detection of RT-induced WM damage.

These characteristic CT and MR findings, combined with the location of the lesions and the history of a long duration of clinical symptoms, may prove helpful in differentiating intracranial chondromas from other more common tumors.

Purpose: Molecular targeting is a powerful approach for aggressive claudin-low breast cancer (CLBC). Overexpression of PI3K catalytic subunit gamma (PIK3CG) in human CLBC is offering a promising opportunity for targeted therapies. We utilized a specific inhibitor of PIK3CG combined with paclitaxel (PTX) to treat CLBC cells in vitro and in vivo. Patients and Methods: The tumor cells growth and apoptosis in vitro were analyzed by CCK8, plate clone formation assay, tumorsphere assay, Hoechst staining and flow cytometry. The invasion and metastasis ability of tumor cells in vitro were investigated by wound healing and transwell experiments. Critical gene expression levels were checked by qRT-PCR and Western blot. Xenograft models with CLBC cell lines in SCID mice were established to investigate the effect of combined drugs in vivo. Results: We identified that PIK3CG was a potential therapeutic target for CLBC patients. Targeting PIK3CG potentiated CLBC cells growth inhibition in 2D and 3D cultures by PTX. Inhibition of PIK3CG activation could enhance CLBC cells apoptosis and migration suppression induced by PTX. Manipulating autophagy was a validated approach for the use of PIK3CG inhibitor. Using CLBC xenograft mice model, we found that CLBC tumors in vivo could be well treated by combined drugs of PIK3CG inhibitor and PTX. Conclusion: We demonstrated that PIK3CG was a potential target for the therapy of CLBC and inhibition of PIK3CG activation could reinforce the therapeutic effect of this aggressive disease by PTX. The combined use of PIK3CG inhibitor and PTX might be a potential regimen for treating this subtype of breast cancer.

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