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Private somatic mutations identified with liquid biopsy lead tumor progression in solid cancers

Journal of Cancer Metastasis and Treatment 2020年第1期6卷 718-725页

作者： maria Palmieri Margherita Baldassarri Nicola Iuso Francesca Fava Alessandra Fabbiani Francesco Cetta Chiara Fallerini Rossella Tita maria antonietta mencarelli Alessandra Renieri Elisa Frullanti Medical Genetics University of SienaSiena 53100Italy Department of Medical Biotechnologies Med Biotech Hub and Competence CenterUniversity of SienaSiena 53100Italy Genetica Medica Azienda Ospedaliera Universitaria SeneseSiena 53100Italy

Aim:Primary tumors can be divided into oncogene-addicted(e.g.,lung)and non-oncogene addicted(e.g.,breast).Only the former group has an Achilles-heel single gene for successful target therapy,whereas the latter has mutations of multiple causative ***,tissue biopsy used for genetic surveys do not give a complete picture of the molecular profile and clonal evolution,but only provide static information over ***:A series of 133 patients with 16 different solid tumors were *** samples were collected and cell-free DNA(cfDNA)was *** libraries were analyzed using AVENIO circulating tumor DNA(ctDNA)Expanded Kit and Illumina NextSeq 550 for sequencing was *** order to evaluate the clinical evolution over time,a second cfDNA analysis was performed after a mean interval of 2 ***:Through the cfDNA liquid biopsy,we found 89 pathogenic variants in 54 ***,lung,and prostate cancers showed the largest number of mutated ***53,PIK3CA,FGFR3,KRAS,and ERBB2 were the most frequently mutated genes among 16 different *** distribution didn’t show any type of *** particular,every patient with disease progression seems to have a“private”combination of gene pair mutations,with TP53 as the most frequently mutated ***:We showed that the clonal evolution of tumors includes a private combination of genes,regardless of tumor *** the future,the cancer treatment can be the targeted therapy against specific tumor mutation(s).The present approach seems promising to both identify key cancer genes and follow clonal evolution over time.

关键词： Cell-free DNA liquid biopsy solid tumors advanced tumors private mutations targeted-therapy

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Bile-acid-activated farnesoid X receptor regulates hydrogen sulfide production and hepatic microcirculation

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World Journal of Gastroenterology 2009年第17期15卷 2097-2108页

作者： Barbara Renga Andrea mencarelli Marco Migliorati Eleonora Distrutti Stefano Fiorucci Department of Clinical and Experimental Medicine University of Perugia Via E dal Pozzo 06122 Perugia Italy Azienda Ospedaliera di Perugia Ospedale Santa Maria della Misericordia 06122 Perugia Italy

AIM: To investigate whether the farnesoid X receptor (FXR) regulates expression of liver cystathionase (CSE), a gene involved in hydrogen sulfi de (H2S) generation. METHODS: The regulation of CSE expression in response to FXR ligands was evaluated in HepG2 cells and in wild-type and FXR null mice treated with 6-ethyl chenodeoxycholic acid (6E-CDCA), a synthetic FXR ligand. The analysis demonstrated an FXR responsive element in the 5'-flanking region of the human CSE gene. The function of this site was investigated by luciferase reporter assays, chromatin immunoprecipitation and electrophoretic mobility shift assays. Livers obtained from rats treated with carbon tetrachloride alone, or in combination with 6-ethyl chenodeoxycholic acid, were studied for hydrogen sulphide generation and portal pressure measurement. RESULTS: Liver expression of CSE is regulated by bile acids by means of an FXR-mediated mechanism. Western blotting, qualitative and quantitative polymerase chain reaction, as well as immunohistochemical analysis, showed that expression of CSE in HepG2 cells and in mice is induced by treatment with an FXR ligand. Administration of 6E-CDCA to carbon tetrachloride treated rats protected against the down-regulation of CSE expression, increased H2S generation, reduced portal pressure and attenuated the endothelial dysfunction of isolated and perfused cirrhotic rat livers. CONCLUSION: These results demonstrate that CSE is an FXR-regulated gene and provide a new molecular explanation for the pathophysiology of portal hypertension.

关键词： Nuclear receptor Farnesoid X receptor Cystathionase Hydrogen sulfide Portal hypertension

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