Gene/Protein Disease Symptom Drug Enzyme Compound
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This paper describes a voxel-based method for coregistering microPET [(18)F]FDG emission images and MRI data without the need for fiducial markers. [(18)F]FDG has a well-characterized biodistribution in normal mice and thus may be useful for image registration. Female BALB/c mice were implanted with EMT-6 mouse mammary carcinoma 1 week prior to imaging. Three imaging sessions were performed in which a [(18)F]FDG microPET-R4 emission scan was taken followed by small-animal MRI with and without Gd-based contrast agent. MicroPET and MR images were registered using a voxel-based algorithm that computes rigid-body image transformations based on the alignment of intensity gradients. Registration accuracy was assessed on the basis of dual-modality external fiducial line sources incorporated into the mouse bed. The root mean square (rms) registration errors were 0.74 mm translation and 1.44 degrees rotation without contrast and 0.72 mm translation and 0.89 degrees rotation with contrast. Generally, good registration was evident upon inspection of fused microPET/MR images. Accurate automated, voxel-based microPET-MR image coregistration, utilizing image intensity gradients, is feasible. Our technique requires no manual identification of image features and makes no use of surgically implanted or external fiducial markers or stereotactic apparatus.
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PMID:Registration of [18F]FDG microPET and small-animal MRI. 1602 3

Glioblastoma multiforme (GBM) has been considered the most aggressive glioma type. Temozolomide (TMZ) is the main first-line chemotherapeutic agent for GBM. Decreased mutS homolog 6 (MSH6) expression is clinically recognized as one of the principal reasons for GBM resistance to TMZ. However, the specific functions of MSH6 in GBM, in addition to its role in mismatch repair, remain unknown. Methods: Bioinformatics were employed to analyze MSH6 mRNA and protein levels in GBM clinical samples and to predict the potential cancer-promoting functions and mechanisms of MSH6. MSH6 levels were silenced or overexpressed in GBM cells to assess its functional effects in vitro and in vivo. Western blot, qRT-PCR, and immunofluorescence assays were used to explore the relevant molecular mechanisms. Cu2(OH)PO4@PAA nanoparticles were fabricated through a hydrothermal method. Their MRI and photothermal effects as well as their effect on restraining the MSH6-CXCR4-TGFB1 feedback loop were investigated in vitro and in vivo. Results: We demonstrated that MSH6 is an overexpressed oncogene in human GBM tissues. MSH6, CXCR4 and TGFB1 formed a triangular MSH6-CXCR4-TGFB1 feedback loop that accelerated gliomagenesis, proliferation (G1 phase), migration and invasion (epithelial-to-mesenchymal transition; EMT), stemness, angiogenesis and antiapoptotic effects by regulating the p-STAT3/Slug and p-Smad2/3/ZEB2 signaling pathways in GBM. In addition, the MSH6-CXCR4-TGFB1 feedback loop was a vital marker of GBM, making it a promising therapeutic target. Notably, photothermal therapy (PTT) mediated by Cu2(OH)PO4@PAA + near infrared (NIR) irradiation showed outstanding therapeutic effects, which might be associated with a repressed MSH6-CXCR4-TGFB1 feedback loop and its downstream factors in GBM. Simultaneously, the prominent MR imaging (T1WI) ability of Cu2(OH)PO4@PAA could provide visual guidance for PTT. Conclusions: Our findings indicate that the oncogenic MSH6-CXCR4-TGFB1 feedback loop is a novel therapeutic target for GBM and that PTT is associated with the inhibition of the MSH6-CXCR4-TGFB1 loop.
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PMID:Oncogenic MSH6-CXCR4-TGFB1 Feedback Loop: A Novel Therapeutic Target of Photothermal Therapy in Glioblastoma Multiforme. 3086 43