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Molecular alterations and clinical relevance in esophageal squamous cell carcinoma

null

《医学前沿（英文）》 2013年 第7卷 第4期   页码 401-410 doi: 10.1007/s11684-013-0286-y

摘要：

Esophageal squamous cell carcinoma (ESCC) is one of the most common types of gastrointestinal cancers, and the fourth leading cause of cancer-related deaths in China. Early detection and intervention in time may dramatically increase the survival of the patients by initiating treatment regimens during earlier stages of ESCC or even during precancerous stages. Molecular classification will be useful for subtyping esophageal tumors or precancerous lesions to improve current therapeutics or early intervention of the disease. In this review, we summarize the findings in investigating the molecular alterations and clinical relevance of ESCC.

关键词： esophageal squamous cell carcinoma (ESCC)     early detection     molecular classification     molecular markers    

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Repurposed benzydamine targeting CDK2 suppresses the growth of esophageal squamous cell carcinoma

《医学前沿（英文）》 2023年 第17卷 第2期   页码 290-303 doi: 10.1007/s11684-022-0956-8

摘要： Esophageal squamous cell carcinoma (ESCC) is one of the leading causes of cancer death worldwide. It is urgent to develop new drugs to improve the prognosis of ESCC patients. Here, we found benzydamine, a locally acting non-steroidal anti-inflammatory drug, had potent cytotoxic effect on ESCC cells. Benzydamine could suppress ESCC proliferation in vivo and in vitro. In terms of mechanism, CDK2 was identified as a target of benzydamine by molecular docking, pull-down assay and in vitro kinase assay. Specifically, benzydamine inhibited the growth of ESCC cells by inhibiting CDK2 activity and affecting downstream phosphorylation of MCM2, c-Myc and Rb, resulting in cell cycle arrest. Our study illustrates that benzydamine inhibits the growth of ESCC cells by downregulating the CDK2 pathway.

关键词： benzydamine     cyclin-dependent kinase 2     patient-derived xenograft     esophageal squamous cell carcinoma    

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p53 functional activation is independent of its genotype in five esophageal squamous cell carcinoma cell

Junfang JI, Kun WU, Min WU, Qimin ZHAN,

《医学前沿（英文）》 2010年 第4卷 第4期   页码 412-418 doi: 10.1007/s11684-010-0260-x

摘要： mutations have been found in many esophageal squamous cell carcinoma (ESCC) clinical specimens and cell lines. We reasoned that functional inactivation of wild-type or the functional activation of mutant-type might exist in these specimens and cell lines. In this study, we identified the correlation between p53 functional activation and its genotype in five different ESCC cell lines. To examine the potential p53 activation in a certain ESCC cell line, DNA damage methods including X-ray exposure and cisplatin treatment were employed to treat cells. Further, the expression of p53 protein and four transcripts of well-known p53 target genes were investigated using Western blot and reverse transcription-polymerase chain reaction (RT-PCR) after cell exposure to DNA damage. The results showed that in KYSE 30 cell line with mutant and KYSE 150 with wild-type , p53 could be activated by DNA damages. However, p53 could not be activated following the DNA damages in YES 2 with wild-type , KYSE 70 with mutant , and EC9706 with unknown genotype. All our data indicated that p53 function in certain cells is not closely correlated with its genotype. To judge p53 function in a particular cell line, it is important to examine the p53 functional activation, but not to simply rely on the genotype.

关键词： p53     esophageal squamous cell carcinoma     DNA damage    

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U-shaped association between telomere length and esophageal squamous cell carcinoma risk: a case-control

null

《医学前沿（英文）》 2015年 第9卷 第4期   页码 478-486 doi: 10.1007/s11684-015-0420-0

摘要：

Telomeres play a critical role in biological ageing by maintaining chromosomal integrity and preventing chromosome ends fusion. Epidemiological studies have suggested that inter-individual differences of telomere length could affect predisposition to multiple cancers, but evidence regarding esophageal squamous cell carcinoma (ESCC) was still uncertain. Several telomere length-related single nucleotide polymorphisms (TL-SNPs) in Caucasians have been reported in genome-wide association studies. However, the effects of telomere length and TL-SNPs on ESCC development are unclear. Therefore, we conducted a case-control study (1045 ESCC cases and 1433 controls) to evaluate the associations between telomere length, TL-SNPs, and ESCC risk in Chinese population. As a result, ESCC cases showed overall shorter relative telomere length (RTL) (median: 1.34) than controls (median: 1.50, P<0.001). More interestingly, an evident nonlinear U-shaped association was observed between RTL and ESCC risk (P<0.001), with odds ratios (95% confidence interval) equal to 2.40 (1.84–3.14), 1.36 (1.03–1.79), 1.01 (0.76–1.35), and 1.37 (1.03–1.82) for individuals in the 1st (the shortest), 2nd, 3rd, and 5th (the longest) quintile, respectively, compared with those in the 4th quintile as reference group. No significant associations were observed between the eight reported TL-SNPs and ESCC susceptibility. These findings suggest that either short or extremely long telomeres may be risk factors for ESCC in the Chinese population.

关键词： esophageal squamous cell carcinoma     telomere length     genetic variants     susceptibility     genome-wide association study    

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GDF15 negatively regulates chemosensitivity via TGFBR2-AKT pathway-dependent metabolism in esophagealsquamous cell carcinoma

《医学前沿（英文）》 2023年 第17卷 第1期   页码 119-131 doi: 10.1007/s11684-022-0949-7

摘要： Treating patients with esophageal squamous cell carcinoma (ESCC) is challenging due to the high chemoresistance. Growth differentiation factor 15 (GDF15) is crucial in the development of various types of tumors and negatively related to the prognosis of ESCC patients according to our previous research. In this study, the link between GDF15 and chemotherapy resistance in ESCC was further explored. The relationship between GDF15 and the chemotherapy response was investigated through in vitro and in vivo studies. ESCC patients with high levels of GDF15 expression showed an inferior chemotherapeutic response. GDF15 improved the tolerance of ESCC cell lines to low-dose cisplatin by regulating AKT phosphorylation via TGFBR2. Through an in vivo study, we further validated that the anti-GDF15 antibody improved the tumor inhibition effect of cisplatin. Metabolomics showed that GDF15 could alter cellular metabolism and enhance the expression of UGT1A. AKT and TGFBR2 inhibition resulted in the reversal of the GDF15-induced expression of UGT1A, indicating that TGFBR2-AKT pathway-dependent metabolic pathways were involved in the resistance of ESCC cells to cisplatin. The present investigation suggests that a high level of GDF15 expression leads to ESCC chemoresistance and that GDF15 can be targeted during chemotherapy, resulting in beneficial therapeutic outcomes.

关键词： GDF15     esophageal squamous cell carcinoma     chemoresistance     cellular metabolism     TGFBR2     AKT    

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功能影像检测食管癌放疗过程中再增殖和乏氧以及预测临床疗效研究

于金明

《中国工程科学》 2012年 第14卷 第7期   页码 9-19

摘要：

18F-FLT PET能监测食管鳞癌放疗过程中肿瘤和正常组织的生物学变化，其较18F-FDG PET能较好区分炎症和肿瘤，能检测食管肿瘤放疗过程中的加速再增殖,18F-FETNIM PET能检测食管鳞癌的乏氧状态,18F-FLT PET和18F-FETNIM PET作为一种非创伤性的影像学技术，能为肿瘤医生提供一个早期评价治疗反应，检测放疗过程中的再增殖克隆源细胞、乏氧和评价新辅助治疗疗效的手段。18F-FLT PET和18F-FETNIM PET能为放射治疗确定“再增殖”和“乏氧”生物学靶区，以通过剂量调强放疗提高再增殖和乏氧区域放疗剂量，提高肿瘤的局部控制率和远期生存。

关键词： 食管肿瘤     放射疗法     正电子发射型     再增殖     乏氧    

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Relative expression of PTTG and bFGF in oral squamous cell carcinoma and Tca8113

Yumei DING BM , Lili CHEN MD , Bo CHENG PhD , Handong ZHANG MM ,

《医学前沿（英文）》 2009年 第3卷 第3期   页码 357-362 doi: 10.1007/s11684-009-0046-1

摘要： The purpose of this study was to investigate the expression of pituitary tumor transforming gene (PTTG) and basic fibroblast growth factor (bFGF) in oral squamous cell carcinoma (OSCC) and tongue cancer cell line Tca8113, as well as their effects on each other. We detected PTTG protein and bFGF in OSCC tissues from 56 cases using the streptavidin-biotin peroxidase (S-P) method; additionally, after being treated with different concentrations of anti bFGF or PTTG antibody, PTTG or bFGF expression in Tca8113 was examined by immunocytochemistry. The results were as follows: (1) Positive rates of PTTG protein and bFGF were 78.2% and 67.3% in OSCC, respectively, which were significantly higher than those in normal mucosal tissues (<0.05). PTTG protein was significantly up-regulated in poorly and moderately differentiated tumors compared to well differentiated tumors (<0.05), and there was also a significant difference between tumors with lymph node metastasis and tumors without lymph node metastasis (<0.05). PTTG protein expression was positively correlated with bFGF ( = 0.382, <0.05); (2) PTTG protein emitted strong fluorescence in Tca8113, and it decreased after being treated with anti-bFGF antibody. Anti-PTTG antibody also had an inhibitive effect on bFGF expression. In summary, the overexpression of PTTG protein is closely related with OSCC differentiation and lymph node metastasis. PTTG protein expression conforms to bFGF in OSCC tissues and Tca8113 cells. Detection of both PTTG and bFGF may help to judge the degree of malignancy and prognosis of patients with OSCC.

关键词： carcinoma     squamous cell     pituitary tumor transforming gene (PTTG) protein     basic fibroblast growth factor    

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Surgical treatment of hepatocellular carcinoma with cirrhotic esophageal varices and hypersplenism: a

JIANG Bin, CHEN Xiaoping, HUANG Zhiyong, ZHANG Zhiwei, HE Songqing, WANG Shaofa, WU Zaide, QIU Fazu

《医学前沿（英文）》 2007年 第1卷 第1期   页码 24-29 doi: 10.1007/s11684-007-0005-7

摘要： In treating hepatocellular carcinoma (HCC) patients with advanced cirrhosis, one of the most difficult problems is concomitant esophageal varices and hypersplenism. Whether these conditions should be treated surgically in association with HCC resection is still in debate. To elucidate whether esophageal devascularization or splenectomy is beneficial when simultaneously performed with liver resection in HCC patients with both varices and hypersplenism, HCC patients ( = 184) with esophageal varices and hypersplenism received one of the three treatments: simultaneous liver resection and esophageal devascularization (Group I, = 41); simultaneous liver resection and splenectomy (Group II, = 61); liver resection only (Group III, = 82). The incidences of postoperative complications of the three groups were 31.7%, 29.5% and 24.4%, respectively, with no significant difference among them. The 5-year tumor-free survival rates for the group I, group II and group III were 34.1%, 36.1% and 37.8%, respectively. Variceal bleeding caused death by only 4.2% in group I, but by 14.3% in group II and 23.2% in group III. The survival rates in the group I and the group II were comparable to those in the group III, however, the recurrences of postoperative fatal variceal bleeding in group I and group II were significantly lower than those in group III. The results suggest that HCC patients with esophageal varices and hypersplenism should undergo hepatic resection plus esophageal devascularization or splenectomy if radical resection of HCC can be expected.
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Genomic variations in the counterpart normal controls of lung squamous cell carcinomas

null

《医学前沿（英文）》 2018年 第12卷 第3期   页码 280-288 doi: 10.1007/s11684-017-0580-1

摘要：

Lung squamous cell carcinoma (LUSC) causes approximately 400 000 deaths each year worldwide. The occurrence of LUSC is attributed to exposure to cigarette smoke, which induces the development of numerous genomic abnormalities. However, few studies have investigated the genomic variations that occur only in normal tissues that have been similarly exposed to tobacco smoke as tumor tissues. In this study, we sequenced the whole genomes of three normal lung tissue samples and their paired adjacent squamous cell carcinomas. We then called genomic variations specific to the normal lung tissues through filtering the genomic sequence of the normal lung tissues against that of the paired tumors, the reference human genome, the dbSNP138 common germline variants, and the variations derived from sequencing artifacts. To expand these observations, the whole exome sequences of 478 counterpart normal controls (CNCs) and paired LUSCs of The Cancer Genome Atlas (TCGA) dataset were analyzed. Sixteen genomic variations were called in the three normal lung tissues. These variations were confirmed by Sanger capillary sequencing. A mean of 0.5661 exonic variations/Mb and 7.7887 altered genes per sample were identified in the CNC genome sequences of TCGA. In these CNCs, C:G→T:A transitions, which are the genomic signatures of tobacco carcinogen N-methyl-N-nitro-N-nitrosoguanidine, were the predominant nucleotide changes. Twenty five genes in CNCs had a variation rate that exceeded 2%, including ARSD (18.62%), MUC4 (8.79%), and RBMX (7.11%). CNC variations in CTAGE5 and USP17L7 were associated with the poor prognosis of patients with LUSC. Our results uncovered previously unreported genomic variations in CNCs, rather than LUSCs, that may be involved in the development of LUSC.

关键词： lung cancer     counterpart normal control     genomic variations    

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Knockdown of RFC4 inhibits the cell proliferation of nasopharyngeal carcinoma and

《医学前沿（英文）》 2023年 第17卷 第1期   页码 132-142 doi: 10.1007/s11684-022-0938-x

摘要： Nasopharyngeal carcinoma (NPC) is a malignant tumor that mainly occurs in East and Southeast Asia. Although patients benefit from the main NPC treatments (e.g., radiotherapy and concurrent chemotherapy), persistent and recurrent diseases still occur in some NPC patients. Therefore, investigating the pathogenesis of NPC is of great clinical significance. In the present study, replication factor c subunit 4 (RFC4) is a key potential target involved in NPC progression via bioinformatics analysis. Furthermore, the expression and mechanism of RFC4 in NPC were investigated in vitro and in vivo. Our results revealed that RFC4 was more elevated in NPC tumor tissues than in normal tissues. RFC4 knockdown induced G2/M cell cycle arrest and inhibited NPC cell proliferation in vitro and in vivo. Interestingly, HOXA10 was confirmed as a downstream target of RFC4, and the overexpression of HOXA10 attenuated the silencing of RFC4-induced cell proliferation, colony formation inhibition, and cell cycle arrest. For the first time, this study reveals that RFC4 is required for NPC cell proliferation and may play a pivotal role in NPC tumorigenesis.

关键词： nasopharyngeal carcinoma     WGCNA     RFC4     proliferation    

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Patient-derived xenograft platform of OSCC: a renewable human bio-bank for preclinical cancer research and a new co-clinical model for treatment optimization

null

《医学前沿（英文）》 2016年 第10卷 第1期   页码 104-110 doi: 10.1007/s11684-016-0432-4

摘要：

Advances in next-generation sequencing and bioinformatics have begun to reveal the complex genetic landscape in human cancer genomes, including oral squamous cell carcinoma (OSCC). Sophisticated preclinical models that fully represent intra- and inter-tumoral heterogeneity are required to understand the molecular diversity of cancer and achieve the goal of personalized therapies. Patient-derived xenograft (PDX) models generated from human tumor samples that can retain the histological and genetic features of their donor tumors have been shown to be the preferred preclinical tool in translational cancer research compared with other conventional preclinical models. Specifically, genetically well-defined PDX models can be applied to accelerate targeted antitumor drug development and biomarker discovery. Recently, we have successfully established and characterized an OSCC PDX panel as part of our tumor bio-bank for translational cancer research. In this paper, we discuss the establishment, characterization, and preclinical applications of the PDX models. In particular, we focus on the classification and applications of the PDX models based on validated annotations, including clinicopathological features, genomic profiles, and pharmacological testing information. We also explore the translational value of this well-annotated PDX panel in the development of co-clinical trials for patient stratification and treatment optimization in the near future. Although various limitations still exist, this preclinical approach should be further tested and improved.

关键词： patient-derived xenograft models     personalized medicine     co-clinical trial     patient stratification     oral squamous cell carcinoma    

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Aldolase B attenuates clear cell renal cell carcinoma progression by inhibiting CtBP2

《医学前沿（英文）》 2023年 第17卷 第3期   页码 503-517 doi: 10.1007/s11684-022-0947-9

摘要： Aldolase B (ALDOB), a glycolytic enzyme, is uniformly depleted in clear cell renal cell carcinoma (ccRCC) tissues. We previously showed that ALDOB inhibited proliferation through a mechanism independent of its enzymatic activity in ccRCC, but the mechanism was not unequivocally identified. We showed that the corepressor C-terminal-binding protein 2 (CtBP2) is a novel ALDOB-interacting protein in ccRCC. The CtBP2-to-ALDOB expression ratio in clinical samples was correlated with the expression of CtBP2 target genes and was associated with shorter survival. ALDOB inhibited CtBP2-mediated repression of multiple cell cycle inhibitor, proapoptotic, and epithelial marker genes. Furthermore, ALDOB overexpression decreased the proliferation and migration of ccRCC cells in an ALDOB-CtBP2 interaction-dependent manner. Mechanistically, our findings showed that ALDOB recruited acireductone dioxygenase 1, which catalyzes the synthesis of an endogenous inhibitor of CtBP2, 4-methylthio 2-oxobutyric acid. ALDOB functions as a scaffold to bring acireductone dioxygenase and CtBP2 in close proximity to potentiate acireductone dioxygenase-mediated inhibition of CtBP2, and this scaffolding effect was independent of ALDOB enzymatic activity. Moreover, increased ALDOB expression inhibited tumor growth in a xenograft model and decreased lung metastasis in vivo. Our findings reveal that ALDOB is a negative regulator of CtBP2 and inhibits tumor growth and metastasis in ccRCC.

关键词： ALDOB     kidney cancer     cell proliferation    

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Bevacizumab in combination with pemetrexed and platinum for elderly patients with advanced non-squamousnon-small-cell lung cancer: a retrospective analysis

《医学前沿（英文）》 2022年 第16卷 第4期   页码 610-617 doi: 10.1007/s11684-021-0827-8

摘要： Bevacizumab, an anti-VEGF monoclonal antibody, has significantly improved the clinical outcomes of patients with advanced non-squamous NSCLC (ns-NSCLC). However, the safety and efficacy of bevacizumab for elderly patients with advanced NSCLC require further investigation. Thus, 59 patients were included in the present retrospective study, 22 patients in the bevacizumab plus pemetrexed and platinum (B+PP) group, and 37 patients in the pemetrexed and platinum (PP) group. For the entire cohort of patients, the median OS was 33.3 months, and the 1-year and 2-year overall survival rates were 88.5% and 67.8%, respectively. The median OS and 1-year and 2-year OS rates were 20.5 months, 70.3% and 0%, respectively, in the B+PP group and 33.4 months, 97.0% and 89.4%, respectively, in the PP group (P <0.001). The incidence of grade≥3 adverse events was higher in the B+PP group than in the PP group (27.3% vs. 10.8%, respectively; P=0.204). Univariate and multivariate analyses suggested that the receipt of≥5 cycles of first-line chemotherapy was an independent favorable prognostic factor for OS, whereas the addition of bevacizumab was an unfavorable prognostic factor. With increased toxicities, the addition of bevacizumab to PP does not improve the overall survival of elderly patients with advanced ns-NSCLC.

关键词： bevacizumab     elderly patient     advanced non-small-cell lung cancer     overall survival     toxicity    

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Small cell carcinoma of the urinary bladder without gross hematuria: a case report

null

《医学前沿（英文）》 2015年 第9卷 第3期   页码 384-387 doi: 10.1007/s11684-015-0405-z

摘要：

Small cell carcinoma of the urinary bladder (SCCB) is a rare and aggressive form of bladder cancer with poor prognosis. Hematuria is the main symptom of this malignancy, and most patients have a history of smoking. The disease incidence of malignant bladder tumors in China is approximately 0.74%. Early and accurate diagnosis of SCCB can ensure timely and appropriate treatment of this malignant disease. Oncologic surgery is the standard treatment; however, it may not be a curative approach. Chemotherapy and/or radiotherapy should be performed following surgical removal. This case report describes a patient with a single neoplasm diagnosed as SCCB that arose because of recurrence of bladder cancer after bladder tumor resection. In contrast to previously reported cases, this patient had no gross hematuria and no history of smoking.

关键词： carcinoma     small cell     urinary bladder neoplasms     diagnosis    

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Expression and clinical implication of PRL-1 and PRL-3 in transitional cell carcinoma of bladder

Bin HAO, Changwei LIU, Huixiang LI

《医学前沿（英文）》 2009年 第3卷 第2期   页码 197-203 doi: 10.1007/s11684-009-0036-3

摘要： The mRNA and protein expression of phosphatase of regenerating liver 1 (PRL-1) and phosphatase of regenerating liver 3 (PRL-3) in transitional cell carcinoma of bladder (BTCC) and normal epithelia of bladder was investigated, and the relationship between the BTCC and pathological changes was clarified. The expression of PRL-1 and PRL-3 mRNA was detected by using reverse transcription polymerase chain reaction (RT-PCR) in 30 cases of BTCC and 10 cases of normal bladder, and the expression of PRL-1 and PRL-3 protein was checked by using immunohistochemistry in 30 cases of BTCC and 15 cases of normal bladder. The expression levels of PRL-1 and PRL-3 mRNA and protein were higher in BTCC than those in normal bladder epithelia ( <0.05). The increased expression of PRL-1 and PRL-3 mRNA and protein was detectable in deep invasion and metastasis of BTCC ( <0.05). There was no correlation between the expression of PRL-1 and PRL-3 and gender, age or recurrence of BTCC (all >0.05). A significantly positive correlation was found between PRL-1 and PRL-3 in BTCC ( <0.05). PRL-1 and PRL-3 are expressed consistently and may contribute to the growth, differentiation, invasion and metastasis of BTCC.

关键词： transitional cell carcinoma of bladder     phosphatase of regenerating liver 1     phosphatase of regenerating liver 3     reverse transcription polymerase chain reaction     immunohistochemistry    

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标题 作者 时间 类型 操作

Molecular alterations and clinical relevance in esophageal squamous cell carcinoma

null

期刊论文

Repurposed benzydamine targeting CDK2 suppresses the growth of esophageal squamous cell carcinoma

期刊论文

p53 functional activation is independent of its genotype in five esophageal squamous cell carcinoma cell

Junfang JI, Kun WU, Min WU, Qimin ZHAN,

期刊论文

U-shaped association between telomere length and esophageal squamous cell carcinoma risk: a case-control

null

期刊论文

GDF15 negatively regulates chemosensitivity via TGFBR2-AKT pathway-dependent metabolism in esophagealsquamous cell carcinoma

期刊论文

功能影像检测食管癌放疗过程中再增殖和乏氧以及预测临床疗效研究

于金明

期刊论文

Relative expression of PTTG and bFGF in oral squamous cell carcinoma and Tca8113

Yumei DING BM , Lili CHEN MD , Bo CHENG PhD , Handong ZHANG MM ,

期刊论文

Surgical treatment of hepatocellular carcinoma with cirrhotic esophageal varices and hypersplenism: a

JIANG Bin, CHEN Xiaoping, HUANG Zhiyong, ZHANG Zhiwei, HE Songqing, WANG Shaofa, WU Zaide, QIU Fazu

期刊论文

Genomic variations in the counterpart normal controls of lung squamous cell carcinomas

null

期刊论文

Knockdown of RFC4 inhibits the cell proliferation of nasopharyngeal carcinoma and

期刊论文

Patient-derived xenograft platform of OSCC: a renewable human bio-bank for preclinical cancer research and a new co-clinical model for treatment optimization

null

期刊论文

Aldolase B attenuates clear cell renal cell carcinoma progression by inhibiting CtBP2

期刊论文

Bevacizumab in combination with pemetrexed and platinum for elderly patients with advanced non-squamousnon-small-cell lung cancer: a retrospective analysis

期刊论文

Small cell carcinoma of the urinary bladder without gross hematuria: a case report

null

期刊论文

Expression and clinical implication of PRL-1 and PRL-3 in transitional cell carcinoma of bladder

Bin HAO, Changwei LIU, Huixiang LI

期刊论文