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Correlation of Twist upregulation and senescence bypass during the progression and metastasis of cervical

null

《医学前沿（英文）》 2014年 第8卷 第1期   页码 106-112 doi: 10.1007/s11684-014-0307-5

摘要：

Cervical carcinoma is associated with high propensity for local invasion and lymph node metastasis. However, the molecular alterations that drive progression and metastasis of cervical cancer remain unclear. Cellular senescence has been proposed as the mechanism that protects an organism against cancer progression and metastasis. In addition, Twist, a basic helix-loop-helix transcription factor, has been suggested as an oncogene because it is overexpressed in many types of human cancer. This gene also exhibits a positive function in regulating invasion and metastasis. In this study, Twist was strongly and positively expressed in normal tissue, squamous cell carcinoma (SCC) IA--IIA, and SCC IIB--IIIB (4.3%, 44%, and 88.9%, respectively). The strong positive expressions of the senescence marker CBX3 were 39.1%, 32%, and 15.6%, respectively. The strong positive expressions of Twist in the SCC groups with or without lymph node metastasis were 80.8% and 50%. For CBX3, such expressions were 7.7% and 29.5%, respectively. Results also showed that the expression of Twist was inversely correlated with that of CBX3. Moreover, the knockdown of Twist with target siRNA in SiHa triggered the induction of the chromatin marker of the cellular senescence CBX3 and senescence-associated β-galactosidase activity. Our results suggested that the expression of Twist increased during the progression and metastasis of cervical cancer. Furthermore, Twist-induced senescence bypass is important in this process.

关键词： cervical cancer     senescence     Twist     CBX3     lymph node metastasis    

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Superenhancers activate the autophagy-related genes Beclin1 and LC3B to drive metastasis and drug resistance

《医学前沿（英文）》 2022年 第16卷 第6期   页码 883-895 doi: 10.1007/s11684-022-0919-0

摘要： Metastasis and drug resistance are the leading causes of poor prognosis in patients with osteosarcoma. Identifying the relevant factors that drive metastasis and drug resistance is the key to improving the therapeutic outcome of osteosarcoma. Here, we reported that autophagy was highly activated in metastatic osteosarcoma. We found increased autophagolysosomes in metastatic osteosarcoma cell lines by using electron microscopy, Western blot, and immunofluorescence experiments. We further examined the expression of the autophagy-related genes Beclin1 and LC3B in 82 patients through immunohistochemistry and found that Beclin1 and LC3B were highly related to unfavorable prognosis of osteosarcoma. Knockdown of Beclin1 and LC3B reduced invasion, metastasis, and proliferation in metastatic osteosarcoma cells. In vitro and in vivo studies also demonstrated that inhibiting by 3-MA inhibited cell growth and metastasis. Moreover, we demonstrated that autophagy-related genes were activated by SEs and that the inhibition of SEs by JQ-1 decreased the metastasis of osteosarcoma. Overall, our findings highlighted the association of autophagy with osteosarcoma progression and shed new light on autophagy-targeting therapy for osteosarcoma.

关键词： osteosarcoma     autophagy     metastasis     drug resistance     Beclin1     LC3B    

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Osteopontin is a promoter for hepatocellular carcinoma metastasis: a summary of 10 years of studies

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《医学前沿（英文）》 2014年 第8卷 第1期   页码 24-32 doi: 10.1007/s11684-014-0312-8

摘要：

In this review, we summarize the novel findings from our series of studies on the leading metastasis-related gene, osteopontin (OPN). In our previous gene expression profiling study, OPN was identified as one of the leading genes associated with the metastasis of hepatocellular carcinoma (HCC). We focused on OPN to evaluate its prognostic values and important roles in HCC metastasis. A retrospective study of large cohorts of HCC patients demonstrated that plasma OPN level was one of the leading independent prognostic factors for HCC patients, even in the early stage of HCC, and could serve as a surrogate serologic biomarker for monitoring the treatment response and tumor recurrence after HCC resection. Using both in vitro and in vivoinvestigations, we found that OPN has an important role in metastasis and tumor growth of HCC and is an attractive potential therapeutic target for combating HCC metastasis. We also found that OPN+ HCC cells have much more amplifications at chromosomal regions, and promoter polymorphisms are important in the regulation of OPN expression and tumor growth and lung metastasis of HCC.

关键词： osteopontin (OPN)     hepatocellular carcinoma     metastasis     prognosis     therapeutic target     biomarker     genetic polymorphism    

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Bone metastasis of hepatocellular carcinoma: facts and hopes from clinical and translational perspectives

《医学前沿（英文）》 2022年 第16卷 第4期   页码 551-573 doi: 10.1007/s11684-022-0928-z

摘要： Patients with hepatocellular carcinoma (HCC) and bone metastasis (BM) suffer from greatly reduced life quality and a dismal prognosis. However, BM in HCC has long been overlooked possibly due to its relatively low prevalence in previous decades. To date, no consensus or guidelines have been reached or formulated for the prevention and management of HCC BM. Our narrative review manifests the increasing incidence of HCC BM to sound the alarm for additional attention. The risk factors, diagnosis, prognosis, and therapeutic approaches of HCC BM are detailed to provide a panoramic view of this disease to clinicians and specialists. We further delineate an informative cancer bone metastatic cascade based on evidence from recent studies and point out the main factors responsible for the tumor-associated disruption of bone homeostasis and the formation of skeletal cancer lesions. We also present the advances in the pathological and molecular mechanisms of HCC BM to shed light on translational opportunities. Dilemmas and challenges in the treatment and investigation of HCC BM are outlined and discussed to encourage further endeavors in the exploration of underlying pathogenic and molecular mechanisms, as well as the development of novel effective therapies for HCC patients with BM.

关键词： HCC     bone     osteotropism     clinical     basic researches     advances    

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Effect of atorvastatin on tumor growth and metastasis in a breast cancer cell xenograft model and its

Liu LIU MD, PhD, Yaogui NING MM, Chen CHEN MD, Daowen WANG MD, PhD,

《医学前沿（英文）》 2009年 第3卷 第4期   页码 443-446 doi: 10.1007/s11684-009-0079-5

摘要： This paper aims to evaluate the effects and the possible mechanisms of atorvastatin on tumor growth and metastasis in a xenograft tumor model. Twenty-four female athymic BALB/C mice with MDA-MB-435 xenograft tumors were randomly assigned to three groups: a control group, a low-dose atorvastatin treatment group, and a high-dose atorvastatin treatment group. The mice in the treatment groups began to be administered with atorvastatin (10 or 20 mg/kg per day) when the xenograft tumors reached 1 cm in diameter. At the end of the experiment, the tumor volume and weight and the lung metastasis colonies of each mouse were measured. Western blotting was applied to detect phosphorylation of protein kinase B (PKB, Akt), extracellular signal regulated kinase (ERK), c-Jun N-terminal Kinase (JNK), and the expression of cytochrome P450 (CYP) subtype CYP2J2. Atorvastatin suppressed xenograft tumor growth and metastasis both in the low-dose and the high-dose treatment groups ( < 0.05). Atorvastatin also decreased the phosphorylated Akt (p-Akt) and p-ERK but increased p-JNK expression. However, atorvastatin did not alter the expression of CYP2J2 in tumor tissue. This suggests that atorvastatin has the efficacy of suppressing tumor growth and metastasis . These effects were not dependent on down-regulation of CYP2J2 expression.

关键词： atorvastatin     xenograft tumor     metastasis     CYP2J2    

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Overexpressed miR-9 promotes tumor metastasis via targeting E-cadherin in serous ovarian cancer

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《医学前沿（英文）》 2017年 第11卷 第2期   页码 214-222 doi: 10.1007/s11684-017-0518-7

摘要：

MicroRNAs (miRNAs) play critical roles in the development and progression in various cancers. Dysfunctional miR-9 expression remains ambiguous, and no consensus on the metastatic progression of ovarian cancer has been reached. In this study, results from the bioinformatics analysis show that the 3′-UTR of the E-cadherin mRNA was directly regulated by miR-9. Luciferase reporter assay results confirmed that miR-9 could directly target this 3′-UTR. miR-9 and E-cadherin expression in ovarian cancer tissue was quantified by qRT-PCR. Migration and invasion were detected by wound healing and Transwell system assay in SKOV3 and A2780. qRT-PCR and Western blot were performed to detect the epithelial?mesenchymal transition-associated mRNA and proteins. Immunofluorescence technique was used to analyze the expression and subcellular localization of E-cadherin, N-cadherin, and vimentin. The results showed that miR-9 was frequently upregulated in metastatic serous ovarian cancer tissue compared with paired primary ones. Upregulation of miR-9 could downregulate the expression of E-cadherin but upregulate the expression of mesenchymal markers (N-cadherin and vimentin). Overexpression of miR-9 could promote the cell migration and invasion in ovarian cancer, and these processes could be effectively inhibited via miR-9 inhibitor. Thus, our study demonstrates that miR-9 may promote ovarian cancer metastasis via targeting E-cadherin and a novel potential therapeutic approach to control metastasis of ovarian cancer.

关键词： ovarian cancer     metastasis     miR-9     E-cadherin    

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Epithelial-to-mesenchymal transition in cancer: complexity and opportunities

Yun Zhang, Robert A. Weinberg

《医学前沿（英文）》 2018年 第12卷 第4期   页码 361-373 doi: 10.1007/s11684-018-0656-6

摘要：

The cell-biological program termed the epithelial-to-mesenchymal transition (EMT) plays an important role in both development and cancer progression. Depending on the contextual signals and intracellular gene circuits of a particular cell, this program can drive fully epithelial cells to enter into a series of phenotypic states arrayed along the epithelial-mesenchymal phenotypic axis. These cell states display distinctive cellular characteristics, including stemness, invasiveness, drug-resistance and the ability to form metastases at distant organs, and thereby contribute to cancer metastasis and relapse. Currently we still lack a coherent overview of the molecular and biochemical mechanisms inducing cells to enter various states along the epithelial-mesenchymal phenotypic spectrum. An improved understanding of the dynamic and plastic nature of the EMT program has the potential to yield novel therapies targeting this cellular program that may aid in the management of high-grade malignancies.

关键词： epithelial-to-mesenchymal transition     cancer     metastasis     cancer stem cell    

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Data mining of microarray for differentially expressed genes in liver metastasis from gastric cancer

Ling XU MM, Feng WANG MM, Xuan-Fu XU MD, Wen-Hui MO BM, Rong WAN MD, Chuan-Yong GUO MD, Xing-Peng WANG MD,

《医学前沿（英文）》 2010年 第4卷 第2期   页码 247-253 doi: 10.1007/s11684-010-0027-4

摘要： Tumor metastasis is the leading cause of death for gastric cancer. Metastasis is the main reason for the failure of clinical treatment for gastric cancer. In order to find metastasis-related genes and abnormal signal transduction pathway of high-invasive gastric cancer, samples of gastric cancer with liver metastasis were collected for microarray detection; up-regulated or down-regulated genes in all three cases were simultaneously screened out. Subsequently, from the preliminary screened genes, molecular pathways possibly impacting liver metastasis from gastric cancer were investigated by the Gene Cluster with Literature Profiles (GenCLip) analysis software. Many biological effects including apoptosis have been validated. Functional analysis of differentially expressed genes revealed that a variety of biological pathways, such as blood circulation and gas exchange, vasodilation and vasoconstriction regulation, and immune defense, could be significantly activated. Besides, gene sequences, specific keywords or gene regulatory networks were further searched by GenCLiP. We conclude that data mining allows to quickly identify a series of special signal transduction pathways involving abnormally expressed genes.

关键词： gastric carcinoma     metastasis     signal transduction     gene chips    

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Tumor growth and metastasis can be inhibited by maintaining genomic stability in cancer cells

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《医学前沿（英文）》 2015年 第9卷 第1期   页码 57-62 doi: 10.1007/s11684-015-0389-8

摘要：

The existence of cancer stem cells, stem-like cancer cells (SLCCs), or tumor-initiating cells is considered as the cause of tumor formation and recurrence, indicating the importance of studying novel therapy that targets SLCCs. The origin of SLCCs is controversial because of two competing hypotheses: SLCCs are either transformed from tissue adult stem cells or dedifferentiated from transformed progenitor cells. Our previous research demonstrates that SLCCs are inducible by increasing genomic instability in cancer cells. In this study, to block the emergence of SLCCs, aminoethyl isothiourea (AET), a compound that clears free radicals and is used to protect patients from radioactive exposure, was used as an agent that maintains genomic stability in combination with mitomycin C (MMC), a commonly used chemotherapeutic drug that damages DNA. Using a rabbit tumor model with VX2 hepatic carcinoma, we found that MMC alone increased lung metastases and disadvantaged survival outcome, but the combination of MMC and AET reversed this effect and even prolonged overall survival. Moreover, in a VX2 xenograft model by immunocompromised mice, MMC alone enriched tumor-initiating cells, but the administration of MMC in combination with AET eliminated tumor cells effectively. Furthermore, MMC alone enhanced genomic instability, but MMC combined with AET attenuated the extent of genomic instability in primary VX2 tumor tissue. Taken together, our data suggest that the genomic protector AET can inhibit the induction of SLCCs, and this combination treatment by AET and cytotoxic agents should be considered as a promising strategy for future clinical evaluation.

关键词： rabbit VX2 liver tumor     mitomycin C     AET     stem-like cancer cells     genomic instability    

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The predictive value of chromosome 8p deletion for metastasis of hepatocellular carcinoma: a summary

QIN Lunxiu, TANG Zhaoyou, GUAN Xinyuan, YE Qinghai, JIA Huliang, REN Ning

《医学前沿（英文）》 2008年 第2卷 第3期   页码 211-215 doi: 10.1007/s11684-008-0041-y

摘要： Hepatocellular carcinoma (HCC) represents an extremely poor prognostic cancer, which is mainly due to the high frequency of metastasis/recurrence after surgical operation. Exploring the molecular mechanisms involved in HCC metastasis could be helpful in the prediction and early diagnosis of HCC recurrence and could also provide new therapeutic targets for HCC metastasis. In the recent decade, we analyzed the genomic aberrations of the clinical specimens, as well as the metastatic models and cell lines of human HCC to identify the genetic markers related to HCC metastasis and to verify their clinical values in the prediction and control of metastasis of HCC. Using the comparative genomic hybridization (CGH) technique, we compared the differences of chromosomal aberrations between primary HCC tumors and their matched metastatic lesions, and found that chromosome 8p deletions might contribute to HCC metastasis. This novel finding was further confirmed by comparison between nude mice models of HCC with different metastatic potentials. By the more sensitive genome-wide microsatellite analysis, 8p deletion was defined to 8p23.3 and 8p11.2, which are two likely regions harboring metastasis-related genes of HCC. Using ‘8p-specific’ microarrays, two novel metastatic suppressors ( and ) were identified, and were proven to suppress invasion and metastasis of HCC. Clinical studies indicate that 8p deletion detected in HCC or circulating plasma DNA of patients is a useful predictor for metastatic recurrence and prognosis, even for patients with early stage HCC. These novel findings are regarded as important advances in the study of the molecular mechanisms of HCC metastasis, which provide not only a holistic view on the molecular cytogenetic bases of HCC metastasis, but also candidate regions for further study to identify metastatic suppressor genes.

关键词： sensitive genome-wide     prediction     genome-wide microsatellite     frequency     Hepatocellular carcinoma    

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Application progress of lymphography in oncology

Yang YU, Jibin LIU, Lixue YIN

《医学前沿（英文）》 2009年 第3卷 第1期   页码 13-19 doi: 10.1007/s11684-009-0016-7

摘要： Lymphography is often used for the diagnosis of lymphatic metastasis in oncology. Determination of lymphatic metastasis is extremely important for accurate cancer staging, which may directly guide the clinical therapeutic scheme. In recent years, the technology of lymphography has developed rapidly on the basis of traditional lymphography, with the appearance of computed tomography (CT) lymphography, nuclear magnetic resonance (MR) lymphography, contrast-enhanced lymphosonography, and so on; the diagnostic accuracy has also been improved. The imaging principles and methods of these various technologies of lymphography are reviewed in this paper, and their applications and significance in oncology are also discussed in detail.

关键词： lymphography     lymphatic metastasis     sentinel lymph node biopsy    

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The impact of hypoxia in hepatocellular carcinoma metastasis

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《医学前沿（英文）》 2014年 第8卷 第1期   页码 33-41 doi: 10.1007/s11684-013-0301-3

摘要：

Hypoxia is a common phenomenon in hepatocellular carcinoma (HCC). Hypoxia stabilizes transcription factor, hypoxia-inducible factor (HIF), to activate gene transcription. Expression of HIF is closely associated with metastasis and poor prognosis in HCC. HIF mediates expression of genes that are involved in every step of HCC metastasis including epithelial-mesenchymal transition, invasion of the extracellular matrix, intravasation, extravasation, and secondar y growth of the metastases. Because HIF is the central regulator of HCC metastasis, HIF inhibitors are attractive tools when used alone or as combined treatment to curb HCC metastasis. This review will summarize the current findings on the impact of hypoxia/HIF in HCC, with a particular focus on cancer metastasis.

关键词： hypoxia     hepatocellular carcinoma (HCC)     metastasis     hypoxia-inducible factor (HIF)    

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Hilar cholangiocarcinoma: Pathology and tumor biology

Dong KUANG, Guo-Ping WANG,

《医学前沿（英文）》 2010年 第4卷 第4期   页码 371-377 doi: 10.1007/s11684-010-0130-6

摘要： Hilar cholangiocarcinoma, first described by Klatskin in 1965, is a relatively rare tumor arising from the bile ducts. The histomorphological features of hilar cholangiocarcinoma are identical with other extra- and intra-hepatic bile duct carcinomas. The most common disease associated with cholangiocarcinoma is primary sclerosing cholangitis. The development of cholangiocarcinoma is a multistep process associated with several mutations in oncogenes and tumor-suppressor genes. Based on macroscopic appearance, three distinct subtypes have been described: sclerosing, nodular, and papillary. Microscopically, more than 95% of tumors are adenocarcinomas. Hilar cholangiocarcinoma is a slowly growing tumor and tends to spread longitudinally along the bile ducts with neural, perineural, and subepithelial extension. Lymph node invasion can be found in 30%–50% patients at the time of diagnosis, but blood-born metastases are rare and usually occur at late stages.

关键词： hilar cholangiocarcinoma     morphology     primary sclerosing cholangitis     metastasis     growth    

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Lymphatic metastasis is related to the epithelial-mesenchymal transition and expressions of VEGF, MMP

Lihui WANG, Lianhong LI, Shen LV, Shujun FAN, Li ZHAN, Bo WANG, Zhong ZHANG

《医学前沿（英文）》 2009年 第3卷 第2期   页码 164-170 doi: 10.1007/s11684-009-0038-1

摘要： The invasion and metastasis of breast cancer are supposed to involve several stages in which epithelial-mesenchymal transition (EMT) is regarded as the mechanistic basis for the behavior of cancer cells. A series of factors related to EMT are apparently involved in such process. The current study aimed to investigate the contributions of EMT and related factors in lymph node metastasis of breast cancer. The expressions of E-cadherin (E-Cad), N-cadherin (N-Cad), vascular endothelial cell growth factor (VEGF), matrix metalloproteinase-9 (MMP-9), cyclooxygenase-2 (COX-2), and CD34 were examined in 74 cases of breast cancer, including 39 cases with lymph node metastasis and 35 cases without lymph node metastasis by immunohistochemistry. Multivariable Cox proportional hazards model was used to analyze the patients’ prognosis. The expressions of N-Cad, VEGF, MMP-9, and COX-2 in cases with lymph node metastasis were significantly higher than those without lymph node metastasis ( <0.05), while the E-Cad level was inversely related to status of lymph node metastasis ( <0.05). The metastasis rate of lymph node in the cases with EMT (lower E-Cad expression and higher N-Cad expression) was 78.3%, while that without EMT (higher E-Cad expression and lower N-Cad expression) was 11.1%. There was a statistical difference in the expression of COX-2 protein between histological grade I and grade II or III, respectively ( <0.05). In the cases with higher grade, the expression of E-Cad was decreased, while that of N-Cad was increased. Higher microvascular density (MVD) was also found to be significantly associated with lymphatic metastasis ( <0.05), and the cases with higher MVD had shorter survival time. This study indicates that EMT and expressions of VEGF, MMP-9 and COX-2, and MVD value are strongly correlated with lymph node metastasis in breast cancer.

关键词： epithelial-mesenchymal transition     vascular endothelial cell growth factor     matrix metalloproteinase-9     cyclooxygenase-2     higher microvascular density     breast cancer    

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Bioinformatic exploration of MTA1-regulated gene networks in colon cancer

null

《医学前沿（英文）》 2016年 第10卷 第2期   页码 178-182 doi: 10.1007/s11684-016-0442-2

摘要：

Metastasis-associated gene 1 (MTA1) controls a series of biological processes in tumor progression. Tumor progression is a complex process regulated by a gene network. The global cancer gene regulatory network must be analyzed to determine the position of MTA1 in the molecular network and its cooperative genes by further exploring the biological functions of this gene. We used TCGA data sets and GeneCards database to screen MTA1-related genes. GO and KEGG pathway analyses were conducted with DAVID and gene network analysis via STRING and Cytoscape. Results showed that in the development of colon cancer, MTA1 is linked to certain signal pathways, such as Wnt/Notch/nucleotide excision repair pathways. The findings also suggested that MTA1 demonstrates the closest relationship in a coregulation process with the key molecules AKT1, EP300, CREBBP, SMARCA4, RHOA, and CAD. These results lead MTA1 exploration to an in-depth investigation in different directions, such as Wnt, Notch, and DNA repair.

关键词： metastasis-associated gene 1     colon cancer     bioinformatics    

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标题 作者 时间 类型 操作

Correlation of Twist upregulation and senescence bypass during the progression and metastasis of cervical

null

期刊论文

Superenhancers activate the autophagy-related genes Beclin1 and LC3B to drive metastasis and drug resistance

期刊论文

Osteopontin is a promoter for hepatocellular carcinoma metastasis: a summary of 10 years of studies

null

期刊论文

Bone metastasis of hepatocellular carcinoma: facts and hopes from clinical and translational perspectives

期刊论文

Effect of atorvastatin on tumor growth and metastasis in a breast cancer cell xenograft model and its

Liu LIU MD, PhD, Yaogui NING MM, Chen CHEN MD, Daowen WANG MD, PhD,

期刊论文

Overexpressed miR-9 promotes tumor metastasis via targeting E-cadherin in serous ovarian cancer

null

期刊论文

Epithelial-to-mesenchymal transition in cancer: complexity and opportunities

Yun Zhang, Robert A. Weinberg

期刊论文

Data mining of microarray for differentially expressed genes in liver metastasis from gastric cancer

Ling XU MM, Feng WANG MM, Xuan-Fu XU MD, Wen-Hui MO BM, Rong WAN MD, Chuan-Yong GUO MD, Xing-Peng WANG MD,

期刊论文

Tumor growth and metastasis can be inhibited by maintaining genomic stability in cancer cells

null

期刊论文

The predictive value of chromosome 8p deletion for metastasis of hepatocellular carcinoma: a summary

QIN Lunxiu, TANG Zhaoyou, GUAN Xinyuan, YE Qinghai, JIA Huliang, REN Ning

期刊论文

Application progress of lymphography in oncology

Yang YU, Jibin LIU, Lixue YIN

期刊论文

The impact of hypoxia in hepatocellular carcinoma metastasis

null

期刊论文

Hilar cholangiocarcinoma: Pathology and tumor biology

Dong KUANG, Guo-Ping WANG,

期刊论文

Lymphatic metastasis is related to the epithelial-mesenchymal transition and expressions of VEGF, MMP

Lihui WANG, Lianhong LI, Shen LV, Shujun FAN, Li ZHAN, Bo WANG, Zhong ZHANG

期刊论文

Bioinformatic exploration of MTA1-regulated gene networks in colon cancer

null

期刊论文