Clinics and research in hepatology and gastroenterology最新文献

{"title":"Targeting SMOX for the treatment of hepatocellular carcinoma?","authors":"Yulei Tao,&nbsp;Chunming Cheng","doi":"10.1016/j.clinre.2024.102429","DOIUrl":"10.1016/j.clinre.2024.102429","url":null,"abstract":"<div><p>Dysregulation of the polyamine metabolism is common in different cancer types. SMOX is upregulated in hepatocellular carcinoma (HCC) but the relationship between SMOX and liver inflammation and fibrosis, remains unclear. In this issue of <em>Clin Res Hepatol Gastroenterol</em>, Hu and colleagues find targeting SMOX can alleviate liver cancer progression.</p></div>","PeriodicalId":10424,"journal":{"name":"Clinics and research in hepatology and gastroenterology","volume":"48 8","pages":"Article 102429"},"PeriodicalIF":2.6,"publicationDate":"2024-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141765699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Patients with chronic liver diseases are at risk for diabetes even before development of cirrhosis","authors":"Georgia Bale ,&nbsp;Frédéric Clarembeau ,&nbsp;Peter Stärkel ,&nbsp;Géraldine Dahlqvist ,&nbsp;Yves Horsmans ,&nbsp;Nicolas Lanthier","doi":"10.1016/j.clinre.2024.102428","DOIUrl":"10.1016/j.clinre.2024.102428","url":null,"abstract":"<div><h3>Background and aims</h3><p>The prevalence of insulin resistance (IR) and type 2 diabetes mellitus (T2DM) is higher in patients with cirrhosis, compared to control patients without liver disease. The exact mechanism for this is unknown but could include liver inflammation. In this study we investigate whether cirrhosis is the <em>primum movens</em> of IR or if impaired insulin sensitivity is already present in non-cirrhotic patients with chronic liver diseases.</p></div><div><h3>Methods</h3><p>Patients were recruited and divided into three groups: control (CTL), chronic liver disease without cirrhosis (CLD) and cirrhosis (CIR). In patients not taking pharmacological treatment for T2DM, IR was quantified using the homeostasis model assessment of insulin resistance (HOMA-IR). The proportion of patients with T2DM as well as HOMA-IR levels among different disease etiologies were recorded and compared.</p></div><div><h3>Results</h3><p>532 patients were included in our study. Median glycemia and insulinemia and therefore HOMA-IR values were significantly different between the three cohorts (p-value &lt;0.001): IR levels in CLD subjects lie between those seen in CTL and CIR subjects. The proportion of diabetic patients in the two case categories also differs (p-value = 0.027): one quarter of CLD subjects and one third of CIR patients suffer from T2DM. Finally, HOMA-IR levels vary according to disease etiology (p-value &lt;0.001): metabolic steatosis and chronic viral hepatitis C are at greater risk than alcohol and other disease causes.</p></div><div><h3>Conclusion</h3><p>CLD is already a predisposing factor to T2DM, regardless of the presence of CIR. CIR is a factor which elicits additional increase in insulin levels. Metabolic steatosis and hepatitis C are associated with more severe IR.</p></div>","PeriodicalId":10424,"journal":{"name":"Clinics and research in hepatology and gastroenterology","volume":"48 8","pages":"Article 102428"},"PeriodicalIF":2.6,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141757525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silymarin suppresses proliferation and PD-L1 expression in colorectal cancer cells and increases inflammatory CD8+ cells in tumor-bearing mice","authors":"Maysoon Al-Haideri","doi":"10.1016/j.clinre.2024.102425","DOIUrl":"10.1016/j.clinre.2024.102425","url":null,"abstract":"<div><h3>Introduction</h3><p>Silymarin as an herbal medicine has shown anticancer effects on tumor cells, while having low toxicity in normal cells. In this study, the effects of Silymarin on proliferation and apoptosis of colorectal cancer cells and its impact on immune response against cancer cells were evaluated in vitro and in vivo.</p></div><div><h3>Methods and materials</h3><p>The effect of Silymarin on CT-26 and Caco-2 cells proliferation and apoptosis were demonstrated by MTT assay and PI staining. A subcutaneous tumor of colorectal cancer was developed. Silymarin and Doxorubicin were administrated by intravenous injection. qRT-PCR analyses was performed on blood samples and tumor tissues. Spleen tissue was used to evaluate CD8+ T cell immune responses. Histological study was carried out on tumor tissues.</p></div><div><h3>Results</h3><p>Silymarin showed anti-proliferative effects on CT-26 and Caco-2 cells. The markers of immunogenic cell death (Calreticulin exposure, ATP secretion, and HMGB1 secretion) significantly increased in both cell lines in the presence of silymarin. The expression of genes related to cell proliferation particularly β-Catenin and Cycline D1, and also anti-apoptotic ones such as Bcl-2 significantly reduced in mice treated with Silymarin while the expression of pro-apoptotic Bax increased. The RNA level of PD-L1 decreased in tumor tissues exposed by Silymarin. Moreover, the number of CTLs increased in the spleen of mice treated with Silymarin in comparison with untreated mice. Decreased tumor size and also survival of colorectal cancer cells in Silymarin-treated mice were observed in histological analysis.</p></div><div><h3>Conclusion</h3><p>Silymarin treatment showed a suppressive role on colorectal cancer cells almost as much as Doxorubicin. Our study indicated that having a low toxicity profile, cost-effectiveness, and availability of raw materials, plant-derived Silymarin can be a good candidate for further investigation to treat CRC.</p></div>","PeriodicalId":10424,"journal":{"name":"Clinics and research in hepatology and gastroenterology","volume":"48 8","pages":"Article 102425"},"PeriodicalIF":2.6,"publicationDate":"2024-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141757526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nationwide trends over 10 years in epidemiology and management of pancreatic ductal adenocarcinoma: A real-world study from the French administrative database","authors":"Léo Mas ,&nbsp;Christel Castelli ,&nbsp;Amandine Coffy ,&nbsp;Brigitte Tretarre ,&nbsp;David Piquemal ,&nbsp;Jean-Baptiste Bachet","doi":"10.1016/j.clinre.2024.102426","DOIUrl":"10.1016/j.clinre.2024.102426","url":null,"abstract":"<div><h3>Background &amp; aims</h3><p>Significant progress has been made in the management of pancreatic ductal adenocarcinoma (PDAC) in recent years. In this population-based study, we aimed to compare incidence, therapeutic strategies, and survival outcomes of PDAC patients in France over a decade.</p></div><div><h3>Methods</h3><p>This study was performed using a nationwide French database. All patients receiving care for PDAC during years 2009, 2014 and 2018 were included. Treatment modalities and survival outcomes were analyzed.</p></div><div><h3>Results</h3><p>A total of 8143/8771/10494 patients were considered in 2009/2014/2018, respectively. Incidence increased mainly among patients aged &gt;60 years. In localized PDAC, the proportion of patients receiving best supportive care (BSC) only decreased at 43.6/36.4/32.4 % and 27.8/29.1/34.3 % received chemo(radio)therapy alone. The rate of upfront surgery remained stable while 3/8/18 % of operated patients received neoadjuvant therapy. Median overall survival (OS) was 7.0/7.9/8.5 months in the overall population. Among treated patients, 1-year OS was 61.4/67.7/68.8 % and 30.3/36.3/38.8 % for localized and metastatic PDAC, respectively.</p></div><div><h3>Conclusions</h3><p>This study confirms the rising incidence of PDAC. Improved outcomes were seen in localized PDAC, with a wider use of chemotherapy and neoadjuvant strategies, and in treated metastatic patients. A modest survival gain was seen overall, hindered by the still high rate of patients receiving BSC only.</p></div>","PeriodicalId":10424,"journal":{"name":"Clinics and research in hepatology and gastroenterology","volume":"48 8","pages":"Article 102426"},"PeriodicalIF":2.6,"publicationDate":"2024-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141751297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A laterally spreading tumor surrounding a barely visible appendiceal orifice","authors":"Flore de Castelbajac,&nbsp;Salome Ouazana,&nbsp;Xavier Dray","doi":"10.1016/j.clinre.2024.102424","DOIUrl":"10.1016/j.clinre.2024.102424","url":null,"abstract":"","PeriodicalId":10424,"journal":{"name":"Clinics and research in hepatology and gastroenterology","volume":"48 8","pages":"Article 102424"},"PeriodicalIF":2.6,"publicationDate":"2024-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141751296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular mechanism of portal hypertensive gastropathy: An update","authors":"Siwei Tan","doi":"10.1016/j.clinre.2024.102423","DOIUrl":"10.1016/j.clinre.2024.102423","url":null,"abstract":"<div><p>Portal hypertensive gastropathy (PHG) is a serious complication and the most common gastric mucosal injury amongst patients afflicted with cirrhotic or non-cirrhotic portal hypertension (PHT). The pathogenesis of PHG is not completely understood and is likely to be complex. The roles of portal hypertension pressure, parenchymal liver disease, Child-Pugh classification, variceal pressure and <em>Helicobacter pylori</em> infection in the development of PHG are controversial. Splanchnic blood flow, the distribution of mucosal blood, vascular ectasia, local disturbances, inflammatory cell infiltration and increased cytokine production have also been examined to elucidate the underlying mechanisms of PHG. Moreover, various other elements, including prostaglandin E₂ (PGE₂), endothelin-1 (ET-1), tumour necrosis factor-α (TNF-α), Fas ligand (FasL)/Fas, nitric oxide (NO), oxygen free radicals and vascular endothelial growth factor (VEGF), have also been revealed to participate in the pathogenesis of PHG. This review provides an overview of the risk factors, classification and potential molecular processes involved in PHG, followed by a concise summary of our and other studies. This review aims to integrate information to deepen our understanding of the interplay between different signalling pathways involved the pathogenesis of PHG and provides insights into how these signalling pathways are regulated to control the development of PHG.</p></div>","PeriodicalId":10424,"journal":{"name":"Clinics and research in hepatology and gastroenterology","volume":"48 8","pages":"Article 102423"},"PeriodicalIF":2.6,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141733707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Remifentanil represses oxidative stress to relieve hepatic ischemia/reperfusion injury via regulating BACH1/PRDX1 axis","authors":"Yujuan You ,&nbsp;Shoulin Chen ,&nbsp;Huanling Deng ,&nbsp;Xianliang Xing ,&nbsp;Binquan Tang ,&nbsp;Yiguo Wu ,&nbsp;Enjun Lei","doi":"10.1016/j.clinre.2024.102422","DOIUrl":"10.1016/j.clinre.2024.102422","url":null,"abstract":"<div><h3>Background</h3><p>Hepatic ischemia-reperfusion injury (HIRI) is a major cause of liver dysfunction after clinical liver surgery, which seriously affects the prognosis of patients. Remifentanil (RE) has been verified to attenuate HIRI. However, its therapeutic mechanism is still unclear. This study aimed to explore the protective mechanism of RE against HIRI.</p></div><div><h3>Methods</h3><p>A mouse HIRI model and an <em>in vitro</em> model of hypoxia/reoxygenation (H/R)-stimulated AML12 hepatocytes were established. Liver histopathological changes were evaluated by hematoxylin and eosin (HE) staining. Oxidative stress damage was assessed by malondialdehyde (MDA), superoxide dismutase (SOD), and reactive oxygen species (ROS) levels. Liver function was determined by serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH). and adenosine triphosphate (ATP) levels. Cell counting kit-8 (CCK-8) assessed cell viability. Apoptosis was measured by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) and flow cytometry. The levels of inflammatory factors were detected by enzyme-linked immunosorbent assay (ELISA) kits. The differentially expressed genes were evaluated by mRNA microarray analysis. Western blotting and real-time quantitative polymerase chain reaction (RT-qPCR) were conducted to detect molecule expression. The binding of BTB and CNC homology 1 (BACH1) to peroxiredoxin 1 (PRDX1) was validated by chromatin immunoprecipitation (ChIP) and dual luciferase reporter assay.</p></div><div><h3>Results</h3><p>RE treatment improved liver function, and repressed oxidative stress damage and apoptosis in HIRI mice. Nine differentially expressed genes in the liver tissues of HIRI mice were selected by microarray analysis, among which BACH1 was down-regulated and PRDX1 was up-regulated after RE treatment. In addition, BACH1 directly bound to the promoter region of PRDX1 to inhibit its transcription and expression, which led to oxidative stress injury. BACH1 overexpression or PRDX1 silencing could counteract the beneficial effects of RE against HIRI.</p></div><div><h3>Conclusion</h3><p>RE suppressed oxidative stress injury and inflammation via inactivation of the BACH1/PRDX1 axis, thereby ameliorating HIRI. Our findings enrich the understanding of the protective mechanisms of RE against HIRI, and provide novel evidence for its clinical application.</p></div>","PeriodicalId":10424,"journal":{"name":"Clinics and research in hepatology and gastroenterology","volume":"48 8","pages":"Article 102422"},"PeriodicalIF":2.6,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141696359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ZNF300 promotes proliferation and migration of hepatocellular carcinoma by upregulating c-MYC gene expression","authors":"Wei Xiang,&nbsp;Junwei Ni,&nbsp;Liyang Dong,&nbsp;Guoqing Zhu","doi":"10.1016/j.clinre.2024.102415","DOIUrl":"10.1016/j.clinre.2024.102415","url":null,"abstract":"<div><h3>Background</h3><p>Hepatocellular carcinoma (HCC) is the most common primary malignant tumor of the liver. Currently, the treatments of HCC are limited to surgical resection and liver transplantation, and there is no effective systemic therapy.</p></div><div><h3>Objectives</h3><p>To investigate the regulatory mechanism of zinc finger protein 300 (ZNF300) in hepatocellular carcinoma (HCC).</p></div><div><h3>Methods</h3><p>The expressions of ZNF300 in HCC tissue samples and HCC cell lines (Hep3B, Huh7, SNU-387) were detected. ZNF300 overexpression vector (ZNF300) or shRNAZNF300 (shZNF300) was transfected into HCC cells to increase or inhibit ZNF300 expression. 5‐Ethynyl‐2′‐deoxyuridine assay (EdU), cell counting kit‐8 assay (CCK‐8) and transwell invasion assay were conducted to evaluate the proliferation, viability, migration, and invasion of HCC cells respectively. The expressions of tumor migration and invasion related proteins (matrix metallopeptidase 2 (MMP-2) and MMP-9), c-MYC, and MAPK/ERK signaling pathway related molecules (p-ERK1/2, ERK1/2, p-P38, P38) were determined by western blotting. Hep3B cells transfected with shZNF300 were subcutaneously injected into nude mice to perform tumor xenograft experiment. Tumor volume and weight were measured.</p></div><div><h3>Results</h3><p>ZNF300 was upregulated in HCC tissues and cells. The expressions of MMP-2 and MMP-9 were increased in HCC cells after transfecting with ZNF300 but reduced in HCC cells transfected with shZNF300. Downregulation of ZNF300 inhibited HCC cell proliferation, migration, and invasion, while overexpression of ZNF300 showed the opposite effects. Moreover, the expressions of c-MYC and MAPK/ERK signaling pathway related molecules were increased after overexpression of ZNF300 but reduced after downregulating ZNF300. In tumor xenograft experiment, downregulation of ZNF300 reduced tumor volume and weight.</p></div><div><h3>Conclusion</h3><p>The present study proved that downregulation of ZNF300 inhibited HCC growth by reducing c-MYC expression and MAPK/ERK signaling pathway.</p></div>","PeriodicalId":10424,"journal":{"name":"Clinics and research in hepatology and gastroenterology","volume":"48 7","pages":"Article 102415"},"PeriodicalIF":2.6,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141630445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preclinical human and murine models of hepatocellular carcinoma (HCC)","authors":"Pharidah Rajan Ibrahim Omar Sundi ,&nbsp;Velaphi C. Thipe ,&nbsp;Mohamed Abdullahi Omar ,&nbsp;Temitope Isaac Adelusi ,&nbsp;Jalene Gedefa ,&nbsp;Olamide T. Olaoba","doi":"10.1016/j.clinre.2024.102418","DOIUrl":"10.1016/j.clinre.2024.102418","url":null,"abstract":"<div><p>Hepatocellular carcinoma (HCC) is the most frequent liver cancer, which account for more than 90 % of all liver cancer cases. It is the fifth leading cause of cancer globally and the second leading cause of cancer-related mortality in men. The availability of competent HCC preclinical models is fundamental to the success of mechanistic studies, molecular target identification, and drug testing. However, there are challenges associated with the use of these models. In this review, we provided updates on various cell lines, animals, and human HCC models, their specific preclinic use and associated potential challenges. Overall, the understanding of the merits and demerits of a particular HCC model will improve model selection for various preclinical studies.</p></div>","PeriodicalId":10424,"journal":{"name":"Clinics and research in hepatology and gastroenterology","volume":"48 7","pages":"Article 102418"},"PeriodicalIF":2.6,"publicationDate":"2024-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141616021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liquid biopsy as a tool for KRAS/NRAS/BRAF baseline testing in metastatic colorectal cancer","authors":"Hampig Raphael Kourie ,&nbsp;Joseph Zouein ,&nbsp;Ziad Zalaquett ,&nbsp;Alain Chebly ,&nbsp;Lewis Nasr ,&nbsp;Fadi El Karak ,&nbsp;Maroun Sadek ,&nbsp;Ousama Safar ,&nbsp;Mouin Fouani ,&nbsp;Nizar Bitar ,&nbsp;Kamal Kachmar ,&nbsp;Fady Nasr ,&nbsp;Fadi Farhat ,&nbsp;Jawad Makarem ,&nbsp;Joseph Kattan ,&nbsp;Julien Taieb","doi":"10.1016/j.clinre.2024.102417","DOIUrl":"10.1016/j.clinre.2024.102417","url":null,"abstract":"<div><h3>Background</h3><div>The absence of <em>KRAS</em> and <em>NRAS</em> gene mutations (<em>RAS</em> wild type) in metastatic colorectal cancer (mCRC), is associated with a good response to targeted therapy with anti-<em>EGFR</em> receptor antibodies. The current gold standard for <em>RAS</em> mutational status identification is genetic testing on tissue biopsy samples.</div></div><div><h3>Objective</h3><div>This study aimed to assess the relevance of liquid biopsy as a less invasive alternative to tissue biopsy for detecting <em>KRAS/NRAS</em> and <em>BRAF</em> mutations in patients with metastatic colorectal cancer (mCRC). The study also aimed to determine the concordance between liquid biopsy and tissue biopsy.</div></div><div><h3>Methods</h3><div>This is a phase IV, observational, uncontrolled, non-comparative, non-randomized, open label study. <em>RAS</em>/<em>BRAF</em> status will be tested at baseline using tissue and liquid biopsy using the Idylla/Biocartis PCR-based device. The primary endpoint is the comparison of the <em>RAS</em> status based on liquid biopsy with the <em>RAS</em> status based on tissue biopsy.</div></div><div><h3>Results</h3><div>100 patients with mCRC were included in the study. 75 % of patients showed concordant results between liquid biopsy and tissue biopsy, while 25 % had discordant results. Liquid biopsy demonstrated a sensitivity of 62 % and a specificity of 93 %. The accuracy of liquid biopsy was 75 %, with a moderate agreement between the two tests. The most frequent mutations in concordant cases were in <em>KRAS</em> (41 %), followed by <em>NRAS</em> (4 %) and <em>BRAF</em> (3 %). Mutations were not detected in 42 % of tissue biopsy samples and 60 % of liquid biopsy samples. The presence of hepatic metastases did not significantly affect the concordance between the biopsy methods.</div></div><div><h3>Conclusion</h3><div>Liquid biopsy using the Idylla™ system showed a relatively low sensitivity but high specificity for detecting <em>KRAS</em>/<em>NRAS</em> and <em>BRAF</em> mutations in mCRC patients. Despite some discordant cases, liquid biopsy remains a promising alternative to tissue biopsy due to its non-invasiveness, ability to provide multiple samples, and better representation of tumor heterogeneity.</div></div>","PeriodicalId":10424,"journal":{"name":"Clinics and research in hepatology and gastroenterology","volume":"48 8","pages":"Article 102417"},"PeriodicalIF":2.6,"publicationDate":"2024-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141619537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}