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IVIM-DWI for Early Therapeutic Effect Assessment of Chemotherapy Combined With Anti-Angiogenic Drugs for Colorectal Cancer Liver Metastases

ABSTRACT: Interventions: CapeOX + Bevacizumab Chemotherapy Response Group:None;CapeOX + Bevacizumab Chemotherapy Non-response Group:None Primary outcome(s): perfusion fraction (f);true diffusion coefficient (D);true diffusion coefficient (D);false diffusion coefficient (D*);false diffusion coefficient (D*) Study Design: Factorial

DISEASE(S): Colorectal Cancer

PROVIDER: 35217 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Fibrocyte-like cells mediate acquired resistance to anti-angiogenic therapy with bevacizumab

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Evaluation of Diffusion Weighted Imaging -MRI in Patients With Resectable Liver Metastases From Colorectal Cancer

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REAL-TIME VASCULAR ANATOMICAL IMAGE NAVIGATION FOR LAPAROSCOPIC SURGERY: A RETROSPECTIVE FEASIBILITY STUDY

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Transcription profiling by array of mouse primary hepatocytes under treatment of genotoxic compounds.

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Transcription profiling in primary mouse hepatocytes discriminates between true and false genotoxic compounds

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Dissociation of β2m from MHC Class I triggers formation of noncovalent, transient heavy chain dimers

Project description:At the plasma membrane of mammalian cells, major histocompatibility complex class I molecules (MHC-I) present antigenic peptides to cytotoxic T cells. Following the loss of the peptide and the light chain beta-2 microglobulin (beta2m), the resulting free heavy chains (FHCs) can associate into homotypic complexes in the plasma membrane. Here, we investigate the stoichiometry and dynamics of MHC-I FHCs assemblies by combining a micropattern assay with fluorescence recovery after photobleaching (FRAP) and with single molecule co-tracking. We identify non-covalent MHC-I FHC dimers mediated by the alpha-3 domain as the prevalent species at the plasma membrane, leading a moderate decrease in the diffusion coefficient. MHC-I FHC dimers show increased tendency to cluster into higher order oligomers as concluded from an increased immobile fraction with higher single molecule colocalization. In vitro studies with isolated proteins in conjunction with molecular docking and dynamics simulations suggest that in the complexes, the alpha-3 domain of one FHC binds to another FHC in a manner similar to the beta2m light chain.

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Functional imaging-guided radiotherapy dose escalation in rectal adenocarcinoma: a feasibility study

Project description:Interventions: This study will evaluate the feasibility of a diffusion-weighted magnetic resonance imaging (DW-MRI) guided radiotherapy boost for locally advanced rectal cancer. Patients will undergo pre-treatment MRI in the fortnight prior to commencing radiotherapy (+/- chemotherapy). Boost volume will be defined quantitatively according to intratumoural apparent diffusion coefficient (ADC) value. This volume will be targeted for a single-fraction 5-10Gy boost 3-5 days prior to commencing standard radiotherapy (50Gy delivered in 25 fractions). Treatment will be administered by the Radiation Oncology department at Sunshine Coast University Hospital (SCUH), Birtinya. Each treatment takes approximately 15 minutes per day. Patients will be reviewed once per week by radiation oncology medical staff as per normal practice. Patients will also be asked to complete a quality of life questionnaire at several timepoints prior to, during and following completion of the treatment course, which will take an additional 5-10 minutes on each occasion. Primary outcome(s): Rate of radiotherapy-related treatment toxicity as per Common Terminology Criteria for Adverse Events v5.0[Acute toxicity: throughout and up to 3 months after treatment Late toxicity: assessed at 3-12 monthly intervals after completion of treatment] Study Design: Purpose: Treatment; Allocation: Non-randomised trial; Masking: Open (masking not used);Assignment: Single group;Type of endpoint: Safety/efficacy

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Three-dimensional CRISPR screening reveals epigenetic interaction with anti-angiogenic therapy

Project description:Angiogenesis underlies development, physiology and pathogenesis of cancer, eye and cardiovascular diseases. Inhibiting aberrant angiogenesis using anti-angiogenic therapy (AAT) has been successful in the clinical treatment of cancer and eye diseases. However, resistance to AAT inevitably occurs and its molecular basis remains poorly understood. Here, we identify novel molecular modifiers of the blood endothelial cell (EC) response to a widely used AAT bevacizumab by performing a pooled genetic screen using three-dimensional microcarrier-based cell culture and CRISPR–Cas9. Functional inhibition of the epigenetic reader BET family of proteins BRD2/3/4 shows unexpected mitigating effects on EC survival and/or proliferation upon VEGFA blockade. Moreover, transcriptomic and pathway analyses reveal an interaction between epigenetic regulation and anti-angiogenesis, which may affect chromosomal structure and activity in ECs via the cell cycle regulator CDC25B phosphatase. Collectively, our findings provide insight into epigenetic regulation of the EC response to VEGFA blockade and may facilitate development of quality biomarkers and strategies to overcome resistance to AAT.

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Gene expression analysis of sanroque mouse strain, a model for human follicular helper (Tfh) T-cells lymphoma

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