GPR40 {FFAR1 [non-esterified ('free') fatty acid receptor 1]} is a G-protein-coupled receptor expressed preferentially in pancreatic beta-cells. GPR40 functions as a receptor for medium and long-chain fatty acids, and has been implicated in mediating both physiological and pathological effects of fatty acids on beta-cells. The GPR40 gene is encoded at an interesting chromosomal locus that contains several genes: at the 5'-end of the locus, located approximately 4 kb upstream of GPR40, is CD22, a gene encoding a receptor expressed selectively in lymphocytes and involved in B-lymphocyte maturation and function. At the 3'-end of the locus are the GPR41 (FFAR3) and GPR43 (FFAR2) genes encoding receptors activated by short-chain fatty acids. The intergenic region between CD22 and GPR40 contains several evolutionarily conserved sequence blocks, among them HR2 and HR3. beta-Cell-specific expression of GPR40 is controlled at the transcriptional level through HR2, a potent beta-cell-specific enhancer. The mechanisms controlling cell-specific expression of the remaining genes in the cluster are unknown. Given the divergent modes of expression of the genes within the locus and their demonstrated physiological significance, it is important to analyse further the locus with a view to fully understanding the basis for transcriptional regulation of the encoded genes.
e14149 Background: Oncologists often need an objective, quantitative assessment of a patient's response to therapy. Lacking a standardized format, the oncologist may request a RECIST (Response Evaluation Criteria in Solid Tumors) analysis. RECIST, however, was developed to provide standardized assessment in the context of randomized clinical trials. RECIST is based on the prospective analysis of a limited sample of tumor lesions or lymph nodes, whereas the clinician naturally makes clinical decisions retrospectively. Furthermore, RECIST has definitions, rules, and criteria for classifying responses that may not apply in the clinical setting, and it does not include consistent rules for merging or splitting lymph nodes, mixed tumor responses, lesions that may cavitate, and a wide range of individualistic responses encountered in clinical practice. Methods: To address these issues, we have modified our working Excel-based template for RECIST 1.1 assessment to include a "myRECIST" feature, so that the radiologist can enter data and examine a range of pre-defined or customizable scenarios, including RECIST1.1, iRECIST, Lugano, volumetric and other parametric protocols. With a few interactions, this template can produce exportable tables and graphs of tumor responses that can guide therapy, as shown in the attached image. Definitions are standardized and linked to RADLEX ontology for specificity and subsequent analysis. Results: This template has been developed for clinical use and is available for downloading from our institutional web-site. Conclusions: We have developed, for public use, a free, easy-to-use, down-loadable Excel template for evaluating prospective or retrospective scenarios of tumor response to therapy that avoids the restrictions of the RECIST methodology. This template may prove useful to oncologists both in and out of the context of randomized clinical trials. We call this "myRECIST."
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