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Percutaneous radiofrequency ablation with artificial hydrothorax for liver cancer in the hepatic dome.

Yue HAN ; Lei YU ; Yu-zhi HAO ; Min YANG ; Shan LIU ; Ying-bing DENG ; Lian-fang HE ; Jian-qiang CAI ; Min-hua CHEN

Chinese Journal of Oncology.2012;34(11):846-849. doi:10.3760/cma.j.issn.0253-3766.2012.11.011

OBJECTIVETo assess the value of application of percutaneous radiofrequency ablation (RFA) with artificial hydrothorax for liver cancer in the hepatic dome.

METHODSThirty-two patients with 43 lesions of hepatic malignant tumors in the hepatic dome underwent ultrasound-guided percutaneous radiofrequency ablation (RFA) with artificial hydrothorax. Artificial hydrothorax was created by infusion of saline via an intrathoracically placed 14-G central venous catheter, which was ultrasound-guided percutaneously inserted before RFA, separating the right lung from the hepatic dome. The adverse reaction and therapeutic efficacy were also analyzed.

RESULTSIn the 32 patients with 43 lesions in the hepatic dome (4 tumors in segment IV 21 tumors in segment VII and 18 tumors in segment VIII), 18 lesions of 14 patients were not observed by ultrasound before the operation. Thirty-two patients received the ultrasound-guided placement of intrathoracical catheter, and (1606.3 ± 485.9) ml (1000 - 2500 ml) saline solution was infused successfully. After obtaining an image of the whole tumor, 31 patients received percutaneous RFA therapy on schedule, and 22 patients received percutaneous transdiaphragmatic RFA therapy. One patient with 2 lesions gave up the treatment, because one of his tumors was not detectable by ultrasound. Diaphragmatic muscle hemorrhage was seen in two patients, subcutaneous edema in two patients, and pneumothorax in one patient. All the complications were cured, and no serious complications or related death occurred. 1-month follow-up with contrast-enhanced CT/MRI images showed that 29 patients had complete ablation, and the effective rate of this technique was 93.5% (29/31).

CONCLUSIONSArtificial hydrothorax helps us not only to visualize the whole tumor in the hepatic dome, but also offers a transdiaphragmatic route for therapy. Ultrasound-guided percutaneous RFA with artificial hydrothorax is a feasible, safe, and effective technique for treating liver cancer in the hepatic dome and worthy of being promoted.

Adult ; Aged ; Carcinoma, Hepatocellular ; diagnostic imaging ; surgery ; Catheter Ablation ; methods ; Female ; Follow-Up Studies ; Humans ; Hydrothorax ; Liver Neoplasms ; diagnostic imaging ; surgery ; Male ; Middle Aged ; Sodium Chloride ; Ultrasonography, Interventional

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Subcarinal lymph node metastasis and strategy of lymphadenectomy in thoracic esophageal carcinoma.

Zhen-jun MIAO ; Wen-ping WANG ; Kang-ning WANG ; Kun ZHANG ; Long-qi CHEN

Chinese Journal of Oncology.2012;34(11):842-845. doi:10.3760/cma.j.issn.0253-3766.2012.11.010

OBJECTIVETo assess the metastatic frequency of subcarinal lymph nodes of thoracic esophageal carcinoma and its influencing factors, in order to determine the adequate range of lymph node dissection during esophagectomy.

METHODSThe clinical data from a cohort of 782 patients with thoracic esophageal carcinoma who underwent esophagectomy with lymphadenectomy were analyzed retrospectively with respect to the impact of subcarinal lymph nodes dissection or no dissection on the incidence of postoperative complications.

RESULTSThe metastasis rate of subcarinal lymph nodes was 17.5%. The metastasis rates in the upper, middle and lower esophageal carcinomas were 8.3%, 19.1% and 16.2%, respectively (P > 0.05). For T1, T2, T3 and T4, they were 0, 4%, 22.2% and 34%, respectively (P < 0.05). The overall incidence of postoperative complications with and without subcarinal lymph nodes dissection was 19.0% versus 14.6% (P > 0.05), and the incidence of pulmonary complications was 10.3% versus 7.3% (P > 0.05).

CONCLUSIONSThoracic esophageal carcinomas have a high metastasis rate of subcrinal lymph nodes, and subcarinal lymph nodes dissection is not associated with increasing perioperative complications. Therefore, for the thoracic esophageal carcinoma, no matter the tumor site, esophageal cancer length or size, once the tumor invades the outer membrane, routine subcarinal lymph node dissection should be done.

Adult ; Aged ; Aged, 80 and over ; Esophageal Neoplasms ; pathology ; surgery ; Esophagectomy ; Female ; Humans ; Lymph Node Excision ; methods ; Lymphatic Metastasis ; Male ; Middle Aged ; Neoplasm Staging ; Postoperative Complications ; Retrospective Studies

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Expression and significance of Rab5a and APPL1 in breast cancer.

Qian CHEN ; Wei-yan LIU ; Zhen ZHAO ; Yun XIE ; Bao-san HAN

Chinese Journal of Oncology.2012;34(11):838-841. doi:10.3760/cma.j.issn.0253-3766.2012.11.009

OBJECTIVETo investigate the expression of Rab5a and APPL1 in breast cancer and fibroma, and analyze their correlation with HER-2 expression, metastasis and development of breast cancer.

METHODSRab5a and APPL1 in paraffin embedded tissues of 74 breast carcinomas and 40 breast fibromas were detected by immunohistochemistry. Their relationship with metastasis, pathological grade, and HER-2 expression in breast cancer was determined by statistical analysis.

RESULTSThere was no expression or low expression of Rab5a and APPL1 in the breast fibroma, but the positive expression rate of Rab5a and APPL1 in the breast carcinomas were 91.9% and 83.8%, respectively. No significant difference in expression of Rab5a and APPL1 was found between metastatic and non-metastatic groups, and pathological grade I/II and grade III groups. But Rab5a was overexpressed in HER-2-positive group compared with that in the HER-2-negative group.

CONCLUSIONSRab5a and APPL1 are overexpressed in breast cancer, and are positively correlated with the HER-2 expression. These proteins may influence the growth and proliferation of breast cancer cells by HER-2 signal transduction.

Adaptor Proteins, Signal Transducing ; metabolism ; Adult ; Aged ; Aged, 80 and over ; Breast Neoplasms ; metabolism ; pathology ; Carcinoma, Ductal, Breast ; metabolism ; pathology ; Carcinoma, Intraductal, Noninfiltrating ; metabolism ; pathology ; Carcinoma, Squamous Cell ; metabolism ; pathology ; Female ; Fibroma ; metabolism ; pathology ; Humans ; Immunohistochemistry ; Lymphatic Metastasis ; Middle Aged ; Neoplasm Grading ; Paraffin Embedding ; Receptor, ErbB-2 ; metabolism ; Young Adult ; rab5 GTP-Binding Proteins ; metabolism

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SNP rs16917496 within SET8 3'UTR is associated with the age of onset of breast cancer.

Bai-lin ZHANG ; Feng-ju SONG ; Hong ZHENG ; Li-na ZHANG ; Yan-rui ZHAO ; Ke-xin CHEN

Chinese Journal of Oncology.2012;34(11):835-837. doi:10.3760/cma.j.issn.0253-3766.2012.11.008

OBJECTIVEWe have identified a SNP within the seed-binding region for miR-502 in the 3'-UTR of the SET8 gene that codes for a methyltransferase for histone H4. SET8 methylates TP53 and thus regulates cell proliferation and genome stability. This study is to investigate the role for this SNP and its interaction with the TP53 codon 72 SNP in the age of onset of breast cancer.

METHODSWe conducted a case-only study of 1, 110 breast cancer cases. PCR-RFLP was used for SNP genotyping. Ages of onset of breast cancer among different genotypes were analyzed using SAS software.

RESULTSOur analysis revealed that the SET8 CC and TP53 GG genotypes were independently associated with earlier age of onset of breast cancer in an allele-dose dependent manner. Moreover, individuals with both SET8 CC and p53 GG genotypes developed cancer at age of 47.74 years, compared with 54.55 years for individuals with both SET8 TT and TP53 CC genotypes.

CONCLUSIONSmiR-502-binding SNP in SET8 may modulate SET8 expression and contribute to early development of breast cancer either independently or together with the TP53 codon 72 SNP.

3' Untranslated Regions ; genetics ; Adult ; Age of Onset ; Aged ; Aged, 80 and over ; Binding Sites ; genetics ; Breast Neoplasms ; genetics ; Codon ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Histone-Lysine N-Methyltransferase ; genetics ; Humans ; MicroRNAs ; genetics ; Middle Aged ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Polymorphism, Single Nucleotide ; Tumor Suppressor Protein p53 ; genetics ; Young Adult

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Effects of Tiam1 on invasion and metastasis of breast carcinoma and its mechanisms.

Yuan-qing WU ; Yue-ying XIE ; Gang PENG

Chinese Journal of Oncology.2012;34(11):831-834. doi:10.3760/cma.j.issn.0253-3766.2012.11.007

OBJECTIVETo investigate the significance of Tiam1 in invasion and metastasis of breast carcinoma and its mechanisms.

METHODSImmunohistochemistry was used to detect Tiam1 expression in tumor tissue of 126 breast carcinomas. Tiam1 was silenced by siRNA in breast carcinoma cell line MDA-MB-435, then the expressions of phosphor-ERK 1, ERK 2 and VEGF were detected, and electrophoretic mobility shift assay (EMSA) was used to examine the transcription activiy of AP-1.

RESULTSThere was a significant relationship between Tiam1 expression and lymph node metastasis (P < 0.05). Furthermore, after silencing of Tiam1, the expressions of phosphor-ERK 1, ERK 2 and VEGF were decreased, and the transcription activity of AP-1 was down-regulated in the MDA-MB-435 cells.

CONCLUSIONTiam1 is closely related with invasion and metastasis of breast carcinoma, and the cascade Tiam1 through ERK, AP-1 and VEGF pathways may play an important role in enhancing angiogenesis, therefore, to promote invasion and metastasis of breast carcinoma.

Breast Neoplasms ; metabolism ; pathology ; Cell Line, Tumor ; Female ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Guanine Nucleotide Exchange Factors ; genetics ; metabolism ; Humans ; Lymphatic Metastasis ; Mitogen-Activated Protein Kinase 1 ; metabolism ; Mitogen-Activated Protein Kinase 3 ; metabolism ; Neoplasm Invasiveness ; RNA, Messenger ; metabolism ; RNA, Small Interfering ; genetics ; Signal Transduction ; T-Lymphoma Invasion and Metastasis-inducing Protein 1 ; Transcription Factor AP-1 ; metabolism ; Vascular Endothelial Growth Factor A ; metabolism

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Differentiation of rat bone marrow mesenchymal stem cells into adipocytes and blockage of the differentiation.

Xue-zhong CHEN ; Jie-yu ZHANG ; Jia-yu ZENG ; Rong YANG ; Fang LIU ; Jing ZHAO ; Wei-bo ZHANG ; Yu-xian WANG ; Ai-hong MAO ; Wen-ru TANG ; Shi-qi LIAO

Chinese Journal of Oncology.2012;34(11):826-830. doi:10.3760/cma.j.issn.0253-3766.2012.11.006

OBJECTIVETo explore the pathogenesis of tumors by blocking the normal differentiation process of stem cells.

METHODSBone marrow mesenchymal stem cells (BMSCs) from rats were isolated, cultured and purified by whole bone marrow adherence method. The rat BMSCs were induced to differentiate into adipocytes with dexamethasone, insulin and indomethacin. Blockage of the differentiation process was induced by 3-methylcholanthrene (3-MC).

RESULTSThe differentiation experiment showed that at 30 days after the induction, oil red O staining-positive cells occurred with increased intracytolasmic lipid droplets, characteristic for adipocytes. The differentiation blockage experiment showed that at 30 days after induction, the deposits of oil red O staining-cytoplasmic lipid droplets was significantly reduced, indicating that the blocked cells were adipocytes, but not fully differentiated. Morphological identification showed that cell contact inhibition disappeared, abnormal cell nuclei, increased number of micronucleus aberration and karyotype abnormalities, indicating that malignant transformation of the stem cells occurred after the differentiation blockage.

CONCLUSIONSThe results of this study show a blockage of the differentiation of that stem cells at the intermediate phase, and a tendency of malignant transformation of the stem cells. The results of our study provide new evidence that cancer stem cells may be originated by suppression of stem cell differentiation.

Adipocytes ; cytology ; Animals ; Bone Marrow Cells ; cytology ; drug effects ; Cell Differentiation ; drug effects ; Cell Transformation, Neoplastic ; Cells, Cultured ; Dexamethasone ; pharmacology ; Drug Combinations ; Female ; Indomethacin ; pharmacology ; Insulin ; pharmacology ; Mesenchymal Stromal Cells ; cytology ; drug effects ; Methylcholanthrene ; pharmacology ; Rats ; Rats, Wistar

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Inhibitory effect of compound cantharides capsule on the proliferation of xenografts of human hepatocellular carcinoma HepG(2)215 in mice.

Jian-jun HAN ; Jin-ming YU ; Hui-yong WU ; Ji-bing LIU ; Bao SONG ; De-wen XUE

Chinese Journal of Oncology.2012;34(11):821-825. doi:10.3760/cma.j.issn.0253-3766.2012.11.005

OBJECTIVETo investigate the inhibitory effect of compound cantharides capsules on the proliferation of xenografts of human hepatocellular carcinoma HepG(2215) in mice and their mechanism of action.

METHODSOne hundred healthy Balb/c mice (5-week old, male:female 1:1) were used in this study. Mouse models of human HepG(2215) hepatocarcinoma were established. The tumor-bearing mice were divided into five groups randomly. The control group A received daily intragastric administration of physiologic saline. The intervention groups B1, B2 and B3 were treated with compound cantharides capsule in a dose of 12.5 mg×kg(-1)×d(-1), 25 mg×kg(-1)×d(-1) and 37.5 mg×kg(-1)×d(-1), respectively, for 10 consecutive days. The group C had intraperitoneal injection of cyclophosphamide (25 mg×kg(-1)×d(-1)) for 10 consecutive days. The mice were sacrificed after the completion of administration. The tumors were taken out, the tumor volume was measured, the inhibitory rate of body weight was calculated, and the serum AFP concentration and the level of HBV DNA were determined. The survival of each group mice was analyzed. The levels of mRNA expression of apoptosis-related genes were assayed by quantitative RT-PCR. Apoptosis in the tumor cells was assayed with TUNEL staining. Flow cytometry was used to detect the levels of CD3(+), CD19(+), CD4(+) and CD8(+), and microvessel density (MVD) of the tumors was assessed by immunohistochemistry.

RESULTSAfter completion of the treatment, the inhibition rate of tumor growth of the groups B1, B2 and B3 was 29.8%, 38.7% and 48.1%, respectively, and that of the group C was 52.4%, with a significant difference among the groups (P < 0.05). The median survival time of the groups A, B1, B2, B3 and C was (30.0 ± 3.2) days, (49.0 ± 5.1) days, (50.0 ± 5.2) days, (57.5 ± 6.5) days and (49.0 ± 4.7) days, respectively. The median survival time of the group B3 was significantly longer than that of other groups (P < 0.05). The serum AFP level in the groups A, B1, B2, B3 and C was (492.7 ± 48.5) ng/ml, (281.2 ± 25.6) ng/ml, (194.3 ± 18.7) ng/ml, (170.1 ± 15.8) ng/ml and (138.7 ± 12.5) ng/ml, respectively, indicating that it was significantly inhibited in the group C. The inhibition rate of HBV DNA replication of the groups B1, B2, B3 and C was (46.0 ± 5.1)%, (65.5 ± 6.9)%, (81.3 ± 7.8)% and (19.5 ± 2.1)%, respectively, showing that compound cantharides capsules inhibited HBV DNA replication in a dose-dependent manner. The apoptosis rate of the groups A, B1, B2, B3 and C was (0.27 ± 0.03)%, (7.18 ± 2.12)%, (9.17 ± 2.42)%, (11.27 ± 3.03)% and (5.44 ± 2.45)%, respectively, and that of the group B3 was significantly higher than that of the groups A, B1, B2 and C (P < 0.05). The expression level of bax mRNA was significantly higher than that of the group C (P < 0.05). The drug could significantly decrease the bcl-2 mRNA expression level, more remarkably along with the increasing dose of cantharides, and it was significantly lower than that in the group C (P < 0.05). The levels of CD4(+), CD8(+), CD3(+) and CD19(+) were significantly higher than that in the groups A and C (P < 0.05). The value of MVD of the group B3 was significantly lower that that of groups A and C (P < 0.05).

CONCLUSIONCompound cantharides capsules may inhibit the replication of HBV DNA in HepG(2215) cells, inducing apoptosis in the tumor cells, enhancing the immune function to inhibit the growth of liver cancer cells in mice, and significantly prolong the median survival time of tumor-bearing mice.

Animals ; Antineoplastic Agents ; administration & dosage ; pharmacology ; Antiviral Agents ; administration & dosage ; pharmacology ; Apoptosis ; drug effects ; Cantharidin ; administration & dosage ; pharmacology ; Capsules ; DNA Replication ; DNA, Viral ; Drug Combinations ; Female ; Hep G2 Cells ; Hepatitis B virus ; Humans ; Male ; Mice ; Mice, Inbred BALB C ; Microvessels ; pathology ; Neoplasm Transplantation ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; metabolism ; RNA, Messenger ; metabolism ; Tumor Burden ; drug effects ; Virus Replication ; Xenograft Model Antitumor Assays ; alpha-Fetoproteins ; metabolism ; bcl-2-Associated X Protein ; genetics ; metabolism

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Polypeptide P110 enhances the growth-inhibitory effect of cisplatin on colon cancer HCT-116 cells and xenotransplanted tumors in mice.

Zhi-qiang CHEN ; Wei CUI ; Shi-yun TAN ; Jian-hua CHEN ; Jun LIU ; Jian ZHANG ; Cai-hong CHEN

Chinese Journal of Oncology.2012;34(11):816-820. doi:10.3760/cma.j.issn.0253-3766.2012.11.004

OBJECTIVETo observe the growth-inhibitory effect of polypeptide P110, designed with G3BP protein targets, plus cisplatin on human colon cancer HCT-116 cells and mouse colon cancer C26 xenotransplanted tumors in mice.

METHODSThe proliferation inhibition of HCT-116 cells and HUVEC cells in vitro was evaluated by MTT assay. A mouse model of xenotransplanted C26 mouse colon cancer was established. The inhibitory effects of P110 and cisplatin at different concentrations on C26 xenotransplanted tumors were assessed.

RESULTSP110 enhanced the inhibitory effect of cisplatin on proliferation of HCT-116 cells. By treated with 20 µmol/LP110 + 10, 30, 90 µmol/L cisplatin, the proliferation inhibitory rates were (43.3 ± 3.2)%, (46.4 ± 4.6)% and (47.6 ± 5.8)%, respectively, significantly higher than that in the cisplatin group (P < 0.05). 20 µmol/L P110 + 10 µmol/L cisplatin effectively killed HCT-116 cells, whereas with less toxicity to HUVEC cells. The tumor inhibition rates in mice of P110 (25 mg/kg, 50 mg/kg, 100 mg/kg) plus cisplatin (1 mg/kg) were 23.0%, 30.4% and 34.2%, respectively. While, the tumor inhibition rates in mice of the cisplatin group (1 mg/kg) was 22.7%. Compared with cisplatin at the same concentration, the tumor inhibition rates in mice of the P110 plus cisplatin groups were all increased.

CONCLUSIONSP110 can enhance the growth inhibitory effects of cisplatin on HCT-116 cells and C26 xenotransplanted tumors in mice. P110 plus cisplatin can reduce the effective dose of cisplatin and decrease the toxicity of cisplatin.

Animals ; Antineoplastic Agents ; pharmacology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cisplatin ; pharmacology ; Colonic Neoplasms ; pathology ; Drug Synergism ; HCT116 Cells ; Human Umbilical Vein Endothelial Cells ; Humans ; Male ; Mice ; Mice, Inbred BALB C ; Neoplasm Transplantation ; Peptides ; pharmacology ; Random Allocation ; Tumor Burden ; drug effects ; Xenograft Model Antitumor Assays

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High expression of HPV16L2N120E7E6 fusion protein in E. coli and its inhibitory effect on tumor growth in mice.

Li ZHAO ; Meng GAO ; Jian GAO ; Jiao REN ; Hui ZHANG ; Hou-wen TIAN ; Wen-jie TAN ; Li RUAN

Chinese Journal of Oncology.2012;34(11):810-815. doi:10.3760/cma.j.issn.0253-3766.2012.11.003

OBJECTIVETo investigate the high expression of HPV16L2N120E7E6 fusion protein by prokaryotic expression system, and evaluate its immunogenicity and antitumor efficacy in vaccinated mice.

METHODSThe HPV16L2N120E7E6 fusion gene, its codons were optimized to increase the expression of the protein, was constructed by overlap extension PCR and inserted into prokaryotic expression vector pET9a. Then the fusion protein was expressed by inducing with IPTG in E. coli strain BL21 (DE3) harboring with plasmid pETL2N120E7E6, and further detected by SDS-PAGE and Western-blot. Finally, the humoral and cellular immune responses were measured by ELISA and ELISPOT, respectively, in vaccinated mice with the purified HPV16L2N120E7E6 fusion protein, and the antitumor efficacy was assessed in mice using the TC-1 tumor challenge model.

RESULTSThe codon-optimized HPV16L2N120E7E6 fusion gene was highly expressed in E. coli strain BL21 (DE3) harboring with plasmid pETL2N120E7E6, and the amount of fusion protein was nearly 48.6% of the total bacterial protein. The purified fusion protein could induce high titer of specific antibody against L2, E7 and E6 in vaccinated mice. When accompanied with the adjuvant CpG, the fusion protein was able to elicit strong and moderate cellular immune responses in vaccinated mice against peptide HPV16E7(49-57) and peptide pools of HPV16E6, respectively. Furthermore, the tumor therapeutic experiment showed that HPV16L2N120E7E6 + CpG could prevent the tumor formation in 80.0% (8/10) vaccinated mice.

CONCLUSIONSThe data of this study suggest that HPV16L2N120E7E6 fusion protein could be a promising candidate vaccine for treatment of chronic HPV16 infection and post-operative adjuvant therapy for cervical cancer.

Adjuvants, Immunologic ; pharmacology ; Animals ; Cancer Vaccines ; immunology ; therapeutic use ; Capsid Proteins ; genetics ; immunology ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; Codon ; Escherichia coli ; immunology ; metabolism ; Female ; Humans ; Immunization ; methods ; Immunotherapy ; methods ; Mice ; Mice, Inbred C57BL ; Neoplasm Transplantation ; Oligodeoxyribonucleotides ; immunology ; Oncogene Proteins, Viral ; genetics ; immunology ; metabolism ; Papillomavirus E7 Proteins ; genetics ; immunology ; metabolism ; Papillomavirus Vaccines ; immunology ; therapeutic use ; Plasmids ; Recombinant Fusion Proteins ; genetics ; immunology ; metabolism ; Repressor Proteins ; genetics ; immunology ; metabolism

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Changes of metastatic potential of residual hepatocellular carcinoma in nude mice after in vivo chemotherapy and the corresponding mechanisms.

Wei XIONG ; Zhao-you TANG ; Zheng-gang REN ; Xiao-dong ZHU ; Liang LIU ; Wei ZHANG ; Wen-quan WANG

Chinese Journal of Oncology.2012;34(11):805-809. doi:10.3760/cma.j.issn.0253-3766.2012.11.002

OBJECTIVETo explore the changes of metastatic potential of residual hepatocellular carcinoma (HCC) after in vivo chemotherapy and its mechanism.

METHODSNude mouse models of orthotopic HCC in the nude mouse livers was established using human hepatocellular carcinoma cell line MHCC97L cells. Oxaliplatin (10 mg/kg, once per week) was administered intraperitoneally (i.p.) to mice in the trial group. Mice in the control group received 0.2 ml of 0.9% sodium chloride on the same days. On day 7 after the third injection, all mice were sacrificed and tumor fragments of equal volume (2 mm×2 mm×2 mm) from each mouse of the oxaliplatin-treated and untreated groups were reinoculated into the livers of each new recipient mouse correspondingly. The growth, metastasis and molecular phenotype of the reinoculated tumors in both groups were determined.

RESULTSIn the new recipient mice, compared with untreated tumors, oxaliplatin pre-treated tumors grew significantly slower [(2624.59 ± 491.60) mm(3) vs. (3849.72 ± 827.09) mm(3), P < 0.001], but gave more spontaneous metastasis to the lung (10/12 vs. 3/12, P = 0.012). A decreased expression of E-cadherin and increased expression of N-cadherin, vimentin and transcription factor Snail were detected in the oxaliplatin pre-treated tumors by immunohistochemistry, which provided the evidence of epithelial mesenchymal transition (EMT) in these tumors.

CONCLUSIONResidual hepatocellular carcinomas after in vivo chemotherapy grow slower but gain enhanced metastatic potential to the lung, associated with epithelial mesenchymal transition.

Animals ; Antineoplastic Agents ; therapeutic use ; Apoptosis ; drug effects ; Cadherins ; metabolism ; Carcinoma, Hepatocellular ; drug therapy ; metabolism ; secondary ; Cell Line, Tumor ; Epithelial-Mesenchymal Transition ; Humans ; Liver Neoplasms ; drug therapy ; metabolism ; pathology ; Lung Neoplasms ; drug therapy ; secondary ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Metastasis ; Neoplasm Transplantation ; Neoplasm, Residual ; drug therapy ; metabolism ; secondary ; Organoplatinum Compounds ; therapeutic use ; Snail Family Transcription Factors ; Transcription Factors ; metabolism ; Tumor Burden ; Vimentin ; metabolism ; Xenograft Model Antitumor Assays

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