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genetic alterations in hepatocellular carcinoma: An update

World Journal of Gastroenterology 2016年第41期22卷 9069-9095页

作者： Zhao-Shan Niu Xiao-Jun Niu Wen-Hong Wang Laboratory of Micromorphology School of Basic Medicine Medical Department of Qingdao University Oncology Specialty Medical Department of Qingdao University Department of Pathology School of Basic Medicine Medical Department of Qingdao University

Hepatocellular carcinoma(HCC) is one of the leading causes of cancer-related deaths worldwide. Although recent advances in therapeutic approaches for treating HCC have improved the prognoses of patients with HCC, this cancer is still associated with a poor survival rate mainly due to late diagnosis. Therefore, a diagnosis must be made sufficiently early to perform curative and effective treatments. There is a need for a deeper understanding of the molecular mechanisms underlying the initiation and progression of HCC because these mechanisms are critical for making early diagnoses and developing novel therapeutic strategies. Over the past decade, much progress has been made in elucidating the molecular mechanisms underlying hepatocarcinogenesis. In particular, recent advances in next-generation sequencing technologies have revealed numerous genetic alterations, including recurrently mutated genes and dysregulated signaling pathways in HCC. A better understanding of the genetic alterations in HCC could contribute to identifying potential driver mutations and discovering novel therapeutic targets in the future. In this article, we summarize the current advances in research on the genetic alterations, including genomic instability, single-nucleotide polymorphisms, somatic mutations and deregulated signaling pathways, implicated in the initiation and progression of HCC. We also attempt to elucidate some of the genetic mechanisms that contribute to making early diagnoses of and developing molecularly targeted therapies for HCC.

关键词： genetic alterations Chromosomal instability Somatic mutations Signaling pathways Hepatocellular carcinoma

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Prognostic value of BCL2 and TP53 genetic alterations for diffuse large B-cell lymphoma patients treated with R-CHOP

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Cancer Biology & Medicine 2022年第6期19卷 893-909页

作者： Yan Qin Haizhu Chen Peng Liu Changgong Zhang Jianliang Yang Lin Gui Xiaohui He Liqiang Zhou Shengyu Zhou Shiyu Jiang Hongxin Jiang Yuankai Shi Department of Medical Oncology National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences&Peking Union Medical CollegeBeijing Key Laboratory of Clinical Study on Anticancer Molecular Targeted DrugsBeijing 100021China Department of Medical Oncology Suzhou Municipal HospitalAffiliated Suzhou Hospital of Nanjing Medical UniversitySuzhou 215001China

Objective:Limited data about the prognostic significance of BCL2 mutations and BCL2 copy number variations in diffuse large B-cell lymphoma(DLBCL)are *** study aimed to comprehensively describe BCL2 genetic alterations in DLBCL patients,and examine correlation of BCL2,TP53 and other genetic alterations with outcomes in patients treated with ***:Probe capture-based high-resolution sequencing was performed on 191 patients diagnosed with de novo ***,BCL2,and BCL6 protein expressions were detected by ***:The presence of BCL2 alterations significantly correlated with poor progression-free survival(PFS)(5-year PFS:13.7%vs.40.8%;P=0.003)and overall survival(OS)(5-year OS:34.0%vs.70.9%;P=0.036).Importantly,patients who harbored BCL2 gain/amplifications(BCL2GA/AMP)also had a remarkably inferior 5-year PFS(11.1%vs.38.3%;Palterations,especially BCL2GA/AMP,TP53 mutations,and International Prognostic Index(IPI)were significantly associated with inferior PFS and *** prognostic models for OS were constructed based on 3 risk factors,including BCL2 alterations(Model 1)or BCL2GA/AMP(Model 2),TP53 mutations,and IPI,to stratify patients into 4 risk groups with different survival ***:This study showed that DLBCL patients treated with R-CHOP,BCL2 alterations,especially BCL2GA/AMP and TP53 mutations were significantly associated with inferior outcomes,which were independent of the *** novel prognostic models we proposed predicted outcomes for DLBCL patients treated with R-CHOP,but further validation of the prognostic models is still warranted.

关键词： BCL2 TP53 genetic alterations diffuse large B-cell lymphoma prognosis

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genetic alterations of hepatocellular carcinoma by random amplified polymorphic DNA analysis and cloning sequencing of tumor differential DNA fragment

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World Journal of Gastroenterology 2005年第26期11卷 4102-4107页

作者： Zhi-HongXian Wen-MingCong Shu-HuiZhang Meng-ChaoWu DepartmentofPathology EasternHepatobiliarySurgeryHospitalSecondMilitaryMedicalUniversityShanghai200438China

AIM: To study the genetic alterations and their association with clinicopathological characteristics of hepatocellular carcinoma (HCC), and to find the tumor related DNA ***: DNA isolated from tumors and corresponding noncancerous liver tissues of 56 HCC patients was amplified by random amplified polymorphic DNA (RAPD)with 10 random 10-mer arbitrary primers. The RAPD bands showing obvious differences in tumor tissue DNA corresponding to that of normal tissue were separated,purified, cloned and sequenced. DNA sequences were analyzed and compared with GenBank ***: A total of 56 cases of HCC were demonstrated to have genetic alterations, which were detected by at least one primer. The detestability of genetic alterations ranged from 20% to 70% in each case, and 17.9% to 50% in each primer. Serum HBV infection, tumor size,histological grade, tumor capsule, as well as tumor intrahepatic metastasis, might be correlated with genetic alterations on certain primers. A band with a higher intensity of 480 bp or so amplified fragments in tumor DNA relative to normal DNA could be seen in 27 of 56 tumor samples using primer 4. Sequence analysis of these fragments showed 91% homology with Homo sapiens double homeobox protein DUX10 ***: genetic alterations are a frequent event in HCC, and tumor related DNA fragments have been found in this study, which may be associated with hepatocarcinogenesis. RAPD is an effective method for the identification and analysis of genetic alterations in HCC, and may provide new information for further evaluating the molecular mechanism of hepatocarcinogenesis.

关键词： genetic alterations Hepatocellular carcinoma DNA fragment

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Mediator complex components are frequent targets for genetic alterations in various types of human cancer

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Journal of genetics and Genomics 2017年第12期44卷 587-591页

作者： Libin Deng Cheng Zhang Duling Miao Xiaoli Tang Shiwen Luo Hong-Bo Xin Huidong Shi Institute of Translational Medicine Nanchang UniversityNanchang 330031China Medical School of Nanchang University Nanchang 330031China Center for Experimental Medicine The First Affiliated Hospital of Nanchang UniversityNanchang 330006China Department of Biochemistry and Molecular Biology Medical College of GeorgiaAugusta UniversityAugustaGA 30912USA Georgia Cancer Center Augusta UniversityAugustaGA 30912USA

The Mediator co-activator complex is a highly conserved,multisubunit protein complex required for gene transcription by RNA polymerase Ⅱ（RNAPⅡ）in all eukaryotes（Allen and Taatjes,2015）.This complex,which consists of at least 30 polypeptides,can be divided into four structurally distinct sub-modules including the head,middle,tail,and cyclin-dependent kinase 8（CDK8）modules （CKM）（Fig. 1A）（Yin and Wang, 2014; Allen and Taatjes, 2015）.

关键词： Mediator complex component frequent targets genetic alterations

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SOX11 as a potential prognostic biomarker in hepatocellular carcinoma linked to immune infiltration and ferroptosis

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Chinese Journal of Cancer Research 2024年第4期36卷 378-397页

作者： Hongyu Chen Qiangguo Ao Yueling Wang Yue Qian Qingli Cheng Wei Zhang Department of Nephrology the Second Medical Center of PLA General HospitalNational Clinical Research Center for Geriatric DiseasesBeijing 100853China Clinical Laboratory the First Affiliated Hospital of Henan UniversityKaifeng 475000China Cell Biology Department Wuxi School of MedicineJiangnan UniversityWuxi 214122China Department of Pathogen Biology Guizhou Nursing Vocational CollegeGuiyang 550000China

Objective:SOX11 is expressed in numerous malignancies,including hepatocellular carcinomas(HCC),but its oncogenic function has not been ***,we performed a comprehensive bioinformatics analysis of the Liver Hepatocellular Carcinoma(LIHC)dataset to investigate the function of SOX11 in ***:SOX11 expression data from The Cancer Genome Atlas(TCGA)and Gene Expression Omnibus(GEO)were validated by immunohistochemistry(IHC).Co-expression,differential expression,and functional analyses utilized TCGA-LIHC,Timer 2.0,Metascape,GTEx,and LinkedOmics *** with immune infiltration,ferroptosis,and immune checkpoint genes were *** changes were explored via *** regression,receiver operating characteristic curve(ROC),Kaplan-Meier analysis,and nomogram modeling evaluated associations with HCC clinicopathological ***11’s impact on proliferation and migration was studied in HepG2 and HuH7 cell ***:SOX11 was significantly elevated in HCC tumors compared to ***11-associated genes exhibited differential expression in pathways involving extracellular membrane ion *** associations were found between SOX11 levels,immune infiltration,ferroptosis,and immune checkpoint genes in HCC ***11 levels correlated with HCC stage,histologic grade,and tumor status,and independently predicted overall and disease-specific ***11 expression effectively distinguished between tumor and normal liver *** correlations highlighted a significant relationship between SOX11 and ferroptosis-associated *** SOX11 levels in HepG2 and HuH7 cells resulted in reduced proliferation and ***:SOX11 was found to represent a promising biomarker within HCC diagnosis and prognosis together with being a possible drug-target.

关键词： SOX11 biomarker HCC prognosis genetic alterations tumor-immune infiltration ferroptosis

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Risk stratification for radioactive iodine refractoriness using molecular alterations in distant metastatic differentiated thyroid cancer

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Chinese Journal of Cancer Research 2024年第1期36卷 25-35页

作者： Zhuanzhuan Mu Xin Zhang Dongquan Liang Jugao Fang Ge Chen Wenting Guo Di Sun Yuqing Sun Zhentian Kai Lisha Huang Jun Liang Yansong Lin Department of Nuclear Medicine State Key Laboratory of Complex Severe and Rare DiseasesPeking Union Medical College(PUMC)HospitalChinese Academy of Medical Sciences&PUMCBeijing 100730China Beijing Key Laboratory of Molecular Targeted Diagnosis and Therapy in Nuclear Medicine Beijing 100730China Pepperdine University Graduate School of Education and Psychology Los Angeles 90045USA Department of Head and Neck Surgery Affiliated Beijing Tongren HospitalCapital Medical UniversityBeijing 100730China Department of General Surgery State Key Laboratory of Complex Severe and Rare DiseasesPeking Union Medical College(PUMC)HospitalChinese Academy of Medical Sciences&PUMCBeijing 100730China Central Laboratory State Key Laboratory of Complex Severe and Rare DiseasesPeking Union Medical College(PUMC)HospitalChinese Academy of Medical Sciences&PUMCBeijing 100730China Department of Bioinformatics Zhejiang Shaoxing Topgen Biomedical Technology Co.LtdShanghai 201321China Department of Medicine Zhejiang Shaoxing Topgen Biomedical Technology Co.LtdShanghai 201321China Department of Oncology Peking University International HospitalBeijing 102206China

Objective: Patients with radioactive iodine-refractory differentiated thyroid cancer(RAIR-DTC) are often diagnosed with delay and constrained to limited treatment options. The correlation between RAI refractoriness and the underlying genetic characteristics has not been extensively ***: Adult patients with distant metastatic DTC were enrolled and assigned to undergo next-generation sequencing of a customized 26-gene panel(Thyro Lead). Patients were classified into RAIR-DTC or non-RAIR groups to determine the differences in clinicopathological and molecular characteristics. Molecular risk stratification(MRS) was constructed based on the association between molecular alterations identified and RAI refractoriness, and the results were classified as high, intermediate or low ***: A total of 220 patients with distant metastases were included, 63.2% of whom were identified as RAIRDTC. genetic alterations were identified in 90% of all the patients, with BRAF(59.7% vs. 17.3%), TERT promoter(43.9% vs. 7.4%), and TP53 mutations(11.5% vs. 3.7%) being more prevalent in the RAIR-DTC group than in the non-RAIR group, except for RET fusions(15.8% vs. 39.5%), which had the opposite pattern. BRAF and TERT promoter are independent predictors of RAIR-DTC, accounting for 67.6% of patients with RAIR-DTC. MRS was strongly associated with RAI refractoriness(Palterations were associated with RAI refractoriness, with BRAF and TERT promoter mutations being the predominant contributors, followed by TP53 and DICER1 mutations. MRS might serve as a valuable tool for both prognosticating clinical outcomes and directing precision-based therapeutic interventions.

关键词： Differentiated thyroid cancer distant metastases genetic alterations RAI refractoriness molecular risk stratification

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Pathogenetic mechanisms in gastric cancer

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World Journal of Gastroenterology 2014年第38期20卷 13804-13819页

作者： Jing Shi Yi-ping Qu peng Hou Department of Endocrinology The First Affiliated Hospital of Xi’an Jiaotong University School of Medicine

Gastric cancer(GC) is a major public health issue as the fourth most common cancer and the second leading cause of cancer-related death. Recent advances have improved our understanding of its molecular pathogenesis,as best exemplified by elucidating the fundamental role of several major signaling pathways and related molecular derangements. Central to these mechanisms are the genetic and epigenetic alterations in these signaling pathways,such as gene mutations,copy number variants,aberrant gene methylation and histone modification,nucleosome positioning,and microRNAs. Some of these genetic/epigenetic alterations represent effective diagnostic and prognostic biomarkers and therapeutic targets for GC. This information has now opened unprecedented opportunities for better understanding of the molecular mechanisms of gastric carcinogenesis and the development of novel therapeutic strategies for this cancer. The pathogenetic mechanisms of GC are the focus of this review.

关键词： Gastric cancer Risk factors genetic alterations Epigenetic alterations Signaling pathways

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Molecular features of gastroenteropancreatic neuroendocrine carcinoma: A comparative analysis with lung neuroendocrine carcinoma and digestive adenocarcinomas

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Chinese Journal of Cancer Research 2024年第1期36卷 90-102页

作者： Jianwei Zhang Hanxiao Chen Junli Zhang Sha Wang Yanfang Guan Wenguang Gu Jie Li Xiaotian Zhang Jian Li Xicheng Wang Zhihao Lu Jun Zhou Zhi Peng Yu Sun Yang Shao Lin Shen Minglei Zhuo Ming Lu Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education/Beijing) Department of Gastrointestinal OncologyPeking University Cancer Hospital&InstituteBeijing 100142China Department of Radiation Therapy National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital&Shenzhen HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeShenzhen 518172China Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education/Beijing) Department I of Thoracic OncologyPeking University Cancer Hospital&InstituteBeijing 100142China Medical Department Nanjing Geneseeq Technology Inc.Nanjing 210061China Geneplus-Beijing Beijing 102200China State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers Beijing Key Laboratory of Carcinogenesis and Translational ResearchDepartment of Gastrointestinal OncologyPeking University Cancer Hospital&InstituteBeijing 100142China Key Laboratory of Carcinogenesis and Translational Research(Ministry of Education/Beijing) Department of PathologyPeking University Cancer Hospital&InstituteBeijing 100142China

Objective: There is an ongoing debate about whether the management of gastroenteropancreatic(GEP)neuroendocrine carcinoma(NEC) should follow the guidelines of small-cell lung cancer(SCLC). We aim to identify the genetic differences of GEPNEC and its ***: We recruited GEPNEC patients as the main cohort, with lung NEC and digestive adenocarcinomas as comparative cohorts. All patients undergone next-generation sequencing(NGS). Different gene alterations were compared and analyzed between GEPNEC and lung NEC(LNEC), GEPNEC and adenocarcinoma to yield the remarkable ***: We recruited 257 patients, including 99 GEPNEC, 57 LNEC, and 101 digestive *** the mutations, KRAS, RB1, TERT, IL7R, and CTNNB1 were found to have different gene alterations between GEPNEC and LNEC samples. Specific genes for each site were revealed: gastric NEC(TERT amplification),colorectal NEC(KRAS mutation), and bile tract NEC(ARID1A mutation). The gene disparities between small-cell NEC(SCNEC) and large-cell NEC(LCNEC) were KEAP1 and CDH1. Digestive adenocarcinoma was also compared with GEPNEC and suggested RB1, APC, and KRAS as significant genes. The TP53/RB1 mutation pattern was associated with first-line effectiveness. Putative targetable genes and biomarkers in GEPNEC were identified in22.2% of the patients, and they had longer progression-free survival(PFS) upon targetable treatment [12.5 months vs. 3.0 months, HR=0.40(0.21-0.75), P=0.006].Conclusions: This work demonstrated striking gene distinctions in GEPNEC compared with LNEC and adenocarcinoma and their clinical utility.

关键词： Neuroendocrine carcinoma gastroenteropancreatic lung genetic alterations molecular markers

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Realizing the potential of exploiting human IPSCs and their derivatives in research of Down syndrome

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BIOCELL 2023年第12期47卷 2567-2578页

作者： YAFEI WANG JIELEI NI YUHAN LIU DINGYING LIAO QIANWEN ZHOU XIAOYANG JI GANG NIU YANXIANG NI Nanophotonics Research Center Institute of Microscale Optoelectronics&State Key Laboratory of Radio Frequency Heterogeneous IntegrationShenzhen UniversityShenzhen518060China Phil Rivers Technology Beijing100871China Department of Ophthalmology Peking University Shenzhen HospitalShenzhen518036China

Down syndrome(DS)is a genetic condition characterized by intellectual disability,delayed brain development,and early onset Alzheimer’s *** use of primary neural cells and tissues is important for understanding this disease,but there are ethical and practical issues,including availability from patients and experimental ***,there are significant genetic and physiological differences between animal models and humans,which limits the translation of the findings in animal studies to *** in induced pluripotent stem cells(iPSC)technology have revolutionized DS research by providing a valuable tool for studying the cellular and molecular pathologies associated with *** pluripotent stem cells derived from cells obtained from DS patients contain the patient’s entire genome including trisomy *** iPSCs as well as their derived cells or organoids can be useful for disease modeling,investigating the molecular mechanisms,and developing potential strategies for treating or alleviating *** this review,we focus on the use of iPSCs and their derivatives obtained from DS individuals and healthy humans for DS *** summarize the findings from the past decade of DS studies using iPSCs and their *** also discuss studies using iPSC technology to investigate DS-associated genes(e.g.,APP,OLIG1,OLIG2,RUNX1,and DYRK1A)and abnormal phenotypes(e.g.,dysregulated mitochondria and leukemia risk).Lastly,we review the different strategies for mitigating the limitations of iPSCs and their derivatives,for alleviating the phenotypes,and for developing therapies.

关键词： Down syndrome Induced pluripotent stem cell Trisomy 21 Neurodevelopment genetic alterations Alzheimer’s disease

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Clinical and molecular significance of homologous recombination deficiency positive non-small cell lung cancer in Chinese population:An integrated genomic and transcriptional analysis

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Chinese Journal of Cancer Research 2024年第3期36卷 282-297页

作者： Yifei Wang Yidan Ma Lei He Jun Du Xiaoguang Li Peng Jiao Xiaonan Wu Xiaomao Xu Wei Zhou Li Yang Jing Di Changbin Zhu Liming Xu Tianlin Sun Lin Li Dongge Liu Zheng Wang Department of Pathology Department of Minimally Invasive Tumor Therapies Center Department of Thoracic Surgery Department of Oncology Department of Respiratory and Critical Care Medicine Beijing HospitalNational Center of GerontologyInstitute of Geriatric MedicineChinese Academy of Medical SciencesBeijing 100730China Amoy Diagnostics Co. Ltd.Xiamen 361027China

Objective:The clinical significance of homologous recombination deficiency(HRD)in breast cancer,ovarian cancer,and prostate cancer has been established,but the value of HRD in non-small cell lung cancer(NSCLC)has not been fully *** study aimed to systematically analyze the HRD status of untreated NSCLC and its relationship with patient prognosis to further guide clinical ***:A total of 355 treatment-naïve NSCLC patients were retrospectively *** status was assessed using the AmoyDx Genomic Scar Score(GSS),with a score of≥50 considered ***,transcriptomic,tumor microenvironmental characteristics and prognosis between HRD-positive and HRDnegative patients were ***:Of the patients,25.1%(89/355)were *** to HRD-negative patients,HRDpositive patients had more somatic pathogenic homologous recombination repair(HRR)mutations,higher tumor mutation burden(TMB)(Palterations in HRD

关键词： Non-small cell lung cancer homologous recombination deficiency genetic alterations transcriptional analysis tumor microenvironment prognosis

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