The relationship between serosal types, pathological characteristics and free cancer cells in the peritoneal cavity of gastric cancer patients

1989 ◽  
Vol 1 (3) ◽  
pp. 58-61 ◽  
Author(s):  
Qinghua Liu ◽  
Junqing Chen
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Peritoneal Cavity ◽  
Pathological Characteristics ◽  
Gastric Cancer Patients ◽  
The Relationship

Regulation of miR-596 on the Apoptosis of Gastric Cancer Cells through Its Targeting Inhibition of BCL-2

2020 ◽  
Author(s):  
Jianmiao WANG ◽  
Jing YANG ◽  
Ji QIU ◽  
Taoyan SONG
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Mechanism Of Action ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Cell Lines ◽  
Gastric Cancer Patients ◽  
Cancer Tissues ◽  
The Relationship

Background: We aimed to investigate the relationship between miR-596, BCL-2, and apoptosis of gastric cancer cells, and to explore the mechanism of miR-596 in gastric cancer. Besides, this study aimed to find the target of miR-596 and explore the mechanism of action of miR-596 in gastric cancer. Methods: Eighteen samples of gastric cancer tissues and 18 samples of corresponding tumor-adjacent tissues were collected from 18 gastric cancer patients (aged from 40 to 55 yr) admitted to Zhuji People's Hospital, Zhuji, China from March 2017 to May 2018. The expression levels of miR-596 and BCL-2 were detected to verify the regulation of miR-596 on the apoptosis and proliferation of gastric cancer cell lines MKN-45 and HGC-27 and its effect on BCL-2 expression. Results: The expression level of miR-596 was notably lower in gastric cancer tissues than in adjacent tissues, and BCL-2 level was notably higher in gastric cancer tissues than in adjacent tissues. After the up-regulation of miR-596 expression, the proliferation of MKN-45 and HGC-27 cells was significantly decreased, the level of apoptosis was significantly increased (P<0.05), and the expression of BCL-2 was decreased. The dual-luciferase report showed that miR-596 had a targeting inhibition of BCL-2. Gastric cancer cells with up-regulated miR596 and BCL-2 had significantly higher proliferation and lower apoptosis than cells with up-regulated miR-596. Conclusions: miR-596 can inhibit the proliferation of gastric cancer cells and promote the apoptosis through its targeting inhibition of BCL-2 expression.

Surgery-induced peritoneal metastasis and its intraoperative treatment.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 4092-4092
Author(s):  
Satoshi Murata ◽  
Katsushi Takebayashi ◽  
Masatsugu Kojima ◽  
Hiroshi Yamamoto ◽  
Tsuyoshi Yamaguchi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Advanced Gastric Cancer ◽  
Cancer Patients ◽  
Peritoneal Cavity ◽  
Peritoneal Metastasis ◽  
Curative Gastrectomy ◽  
Ki 67 ◽  
D2 Gastrectomy ◽  
Gastric Cancer Patients

4092 Background: A large number of advanced gastric cancer patients undergoing curative gastrectomy with D2 lymph node dissection (D2 gastrectomy) show peritoneal metastasis. The source of these metastatic cells and their treatment remain unclear. We examined the mechanism of surgery-induced peritoneal metastasis and determined the appropriate intraoperative treatment. Methods: (1) Curative gastrectomy was performed for 102 gastric cancer patients. Peritoneal lavage fluid was collected before and after gastrectomy. Cytology, RT-PCR, and cell culture were used to determine the presence of cancer cells. Proliferative potential of tumor cells was evaluated using Ki-67 staining. Tumorigenic capacity was assessed by cell injection into the peritoneal cavity of NOD/ShiJic-scid mice. (2) Fifty clinical T3(SE) or T4(SI) advanced gastric cancer patients undergoing curative D2 gastrectomy prospectively received intraoperative hyperthermic intraperitoneal chemotherapy (HIPEC) in a phase II trial. HIPEC comprised 50 mg CDDP, 10 mg MMC, and 1000 mg 5-FU in 5 L saline maintained at 42–43C° for 30 min. Results: (1) Of 102 peritoneal lavage fluid samples obtained before gastrectomy, 57 from both early and advanced cancer patients did not contain CEA or CK20 mRNA amplification products or cancer cells. Of these 57 samples, CEA or CK20 mRNA was detected in 35 and viable cancer cells were identified in 24 after gastrectomy. Viable cancer cells in all 24 cases showed Ki-67 positivity, indicating proliferative activity. Cultured viable cancer cells developed into peritoneal tumor nodules after spill over into the peritoneal cavity in NOD/ShiJic-scid mice. (2) Fifty patients were eligible for the phase II clinical trial. The overall 5-year survival rate for all patients was 92.4%. This rate in patients with pT2(ss) (n = 12), pT3(se) (n = 35), and pT4(si) (n = 3) disease was 90.0%, 92.3%, and 100%, respectively. Only 2 patients (4%) showed peritoneal relapse. Conclusions: Viable tumorigenic cancer cells spilled over the peritoneal cavity during curative gastrectomy. Intraoperative HIPEC following curative D2 gastrectomy effectively prevented peritoneal metastasis, thereby potentially improving the prognosis of patients with advanced gastric cancer.

Phase II study of intraperitoneal paclitaxel plus S-1/paclitaxel for gastric cancer with positive peritoneal cytology: CY-PHOENIX trial.

2017 ◽  
Vol 35 (4_suppl) ◽  
pp. 96-96 ◽  
Author(s):  
Masaki Aizawa ◽  
Hironori Ishigami ◽  
Hiroshi Yabusaki ◽  
Atsushi Nashimoto ◽  
Haruhiko Imamoto ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Peritoneal Cavity ◽  
Peritoneal Metastasis ◽  
Phase Ii Study ◽  
Peritoneal Cytology ◽  
Positive Peritoneal Cytology ◽  
Grade 3 ◽  
Gastric Cancer Patients

96 Background: The presence of free cancer cells in the peritoneal cavity has been known as a poor prognostic factor in gastric cancer patients. Intraperitoneal (IP) paclitaxel (PTX) provides powerful local effects in the peritoneal cavity, and we previously reported the efficacy and safety of a regimen combining IP PTX with S-1/PTX in gastric cancer patients with peritoneal metastasis. This multicenter phase II study was conducted to evaluate the efficacy of IP PTX plus S-1/PTX for gastric cancer with positive peritoneal cytology. Methods: Eligibility criteria included pathologically confirmed gastric adenocarcinoma, intraperitoneal free cancer cells confirmed by peritoneal washing cytology, and no evidence of overt distant metastasis including macroscopic peritoneal metastasis. Patients were administered IP PTX 20 mg/m2, intravenous PTX 50 mg/m2 on days 1 and 8, and S-1 80 mg/m2/day on days 1-14, q3 weeks. The primary endpoint was the 1-year overall survival (OS) rate. Secondary endpoints were response rate, negative conversion rate on peritoneal cytology and safety. Results: Thirty eight patients were enrolled and fully evaluated for OS and toxicity. The median number of courses was 12.5 (range 2-35). The 1-year OS rate was 84.2% (95 % confidence interval, 68.2-92.6%). Of 3 patients with target lesions, partial response and stable disease were obtained in 2 and 1 patient(s), respectively. The peritoneal cytology findings converted from positive to negative in 36 (94.7 %) patients. The incidences of grade 3/4 hematological and non-hematological toxicities were 45 % and 26 %, respectively. The frequent grade 3/4 toxicities included neutropenia (23%), leukopenia (7%) and anemia (8%). Regarding adverse events related to IP port, 2 patients developed swelling around the port site. Conclusions: IP PTX with S-1/PTX was suggested to be a promising option for gastric cancer with positive peritoneal cytology through the clearance of cancer cells in the peritoneal cavity. Clinical trial information: UMIN000002850.

scholarly journals Extracellular vesicles shed from gastric cancer mediate protumor macrophage differentiation

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Atene Ito ◽  
Shunsuke Kagawa ◽  
Shuichi Sakamoto ◽  
Kazuya Kuwada ◽  
Hiroki Kajioka ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Ascitic Fluid ◽  
Extracellular Vesicles ◽  
Peritoneal Cavity ◽  
Peritoneal Dissemination ◽  
Tumor Associated Macrophages ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Patients

Abstract Background Peritoneal dissemination often develops in gastric cancer. Tumor-associated macrophages (TAMs) are present in the peritoneal cavity of gastric cancer patients with peritoneal dissemination, facilitating tumor progression. However, the mechanism by which macrophages differentiate into tumor-associated macrophages in the peritoneal cavity is not well understood. In this study, the interplay between gastric cancer-derived extracellular vesicles (EVs) and macrophages was investigated. Methods The association between macrophages and EVs in peritoneal ascitic fluid of gastric cancer patients, or from gastric cancer cell lines was examined, and their roles in differentiation of macrophages and potentiation of the malignancy of gastric cancer were further explored. Results Immunofluorescent assays of the ascitic fluid showed that M2 macrophages were predominant along with the cancer cells in the peritoneal cavity. EVs purified from gastric cancer cells, as well as malignant ascitic fluid, differentiated peripheral blood mononuclear cell-derived macrophages into the M2-like phenotype, which was demonstrated by their morphology and expression of CD163/206. The macrophages differentiated by gastric cancer-derived EVs promoted the migration ability of gastric cancer cells, and the EVs carried STAT3 protein. Conclusion EVs derived from gastric cancer play a role by affecting macrophage phenotypes, suggesting that this may be a part of the underlying mechanism that forms the intraperitoneal cancer microenvironment.

DETERMINATION OF P53 GENE CODON 72 POLYMORPHISMS IN PATIENTS WITH GASTRIC CANCER

2013 ◽  
pp. 11-17
Author(s):  
Thi Tuy Ha Nguyen ◽  
Thi Minh Thi Ha
Keyword(s):  
Gastric Cancer ◽  
Cancer Patients ◽  
P53 Gene ◽  
Diffuse Gastric Cancer ◽  
Codon 72 ◽  
Cancer Group ◽  
Pcr Rflp ◽  
Gastric Cancer Patients ◽  
The Relationship

Background: The role of p53 gene in the gastric cancer is still controversial. This study is aimed at determining the rate of the p53 gene codon 72 polymorphisms in gastric cancer patients and evaluating the relationship between these polymorphisms and endoscopic and histopathological features of gastric cancer. Patients and methods: Sixty eight patients with gastric cancer (cases) and one hundred and thirty six patients without gastric cancer (controls) were enrolled. p53 gene codon 72 polymorphisms were determined by PCR-RFLP technique with DNA extracted from samples of gastric tissue. Results: In the group of gastric cancer, Arginine/Argnine, Arginine/Proline and Proline/Proline genotypes were found in 29.4%, 42.7% and 27.9%, respectively. The differences of rates were not statistically significant between cases and controls (p > 0,05). In males, the Proline/Proline genotype was found in 38.1% in patients with gastric cancer and more frequent in patients without gastric cancer (15.7%, p = 0,01). An analysis of ROC curve showed that the cut-off was the age of 52 in the Proline/Proline genotype, but it was 65 years old in the Arginine/Proline genotype. The Proline/Proline genotype was found in 41.9% in Borrmann III/IV gastric cancer, this rate was higher than Borrmann I/II gastric cancer (16.2%, p = 0.037) and also higher than controls (18.4%, p = 0,01). The rate of Proline/Proline genotype was 41.7% in the diffuse gastric cancer, it was higher than in controls (p = 0,023). Conclusion: No significative difference of rate was found in genotypes between gastric cancer group and controls. However, there was the relationship between Proline/Proline genotype and gastric cancer in males, Borrmann types of gastric cancer, the diffuse gastric cancer. Key words: polymorphism, codon 72, p53 gene, PCR - RFLP, gastric cancer.

scholarly journals Down-regulation of HIF-1α inhibits the proliferation, migration, and invasion of gastric cancer by inhibiting PI3K/AKT pathway and VEGF expression

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Jingjing Zhang ◽  
Jun Xu ◽  
Yonghong Dong ◽  
Bo Huang
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Vegf Expression ◽  
Gastric Cancer Cells ◽  
Tumor Tissues ◽  
Sirna Silencing ◽  
Gastric Cancer Patients

In view of the high incidence of gastric cancer and the functions of hypoxia-inducible factor 1α (HIF-1α), our study aimed to investigate the functionality of HIF-1α in gastric cancer, and to explore the diagnostic and prognostic values of HIF-1α for this disease. Expression of HIF-1α in tumor tissues and adjacent healthy tissues as well as serum collected from both gastric cancer patients and normal healthy controls was detected by qRT-PCR. Survival analysis was performed using Kaplan–Meier method. HIF-1α siRNA silencing cell lines were established. Effects of HIF-1α siRNA silencing as well as PI3K activator sc3036 on proliferation, migration, and invasion of gastric cancer cells were detected by Cell counting kit (CCK-8) assay, and Transwell migration and invasion assay. Effects of HIF-1α siRNA silencing on AKT and VEGF were detected by Western blot. Expression of HIF-1α was significantly down-regulated in tumor tissues than in adjacent healthy tissues in most gastric cancer patients. Serum levels of HIF-1α were also higher in gastric cancer patients than in normal healthy people. Serum HIF-1α showed promising diagnostic and prognostic values for gastric cancer. HIF-1α siRNA silencing inhibited the proliferation, migration, and invasion of gastric cancer cells, while PI3K activator sc3036 treatment reduced those inhibitory effects. Down-regulation of HIF-1α can inhibit the proliferation, migration, and invasion of gastric cancer possibly by inhibiting PI3K/AKT pathway and VEGF expression.

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