Ultrasonographic findings in gastric cancer: In vitro and in vivo studies

1989 ◽  
Vol 17 (5) ◽  
pp. 309-318 ◽  
Author(s):  
Yukio Miyamoto ◽  
Mariko Nakatani ◽  
Masahiro Ida ◽  
Takashi Ishikawa ◽  
Norio Okazawa ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
In Vivo Studies

scholarly journals Pleckstrin-2 as a Prognostic Factor and Mediator of Gastric Cancer Progression

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Jun Wang ◽  
Zhigang He ◽  
Bo Sun ◽  
Wenhai Huang ◽  
Jianbin Xiang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Patients ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
In Vivo Studies ◽  
Vimentin Expression ◽  
Mesenchymal Transition ◽  
Gastric Cancer Patients

Pleckstrin-2 (PLEK2) is a crucial mediator of cytoskeletal reorganization. However, the potential roles of PLEK2 in gastric cancer are still unknown. PLEK2 expression in gastric cancer was examined by western blotting and real-time PCR. Survival analysis was utilized to test the clinical impacts of the levels of PLEK2 in gastric cancer patients. In vitro and in vivo studies were used to estimate the potential roles played by PLEK2 in modulating gastric cancer proliferation, self-renewal, and tumourigenicity. Bioinformatics approaches were used to monitor the effect of PLEK2 on epithelial-mesenchymal transition (EMT) signalling pathways. PLEK2 expression was significantly upregulated in gastric cancer as compared with nontumour samples. Kaplan-Meier plotter analysis revealed that gastric cancer patients with higher PLEK2 levels had substantially poorer overall survival compared with gastric cancer patients with lower PLEK2 levels. The upregulation or downregulation of PLEK2 in gastric cancer cell lines effectively enhanced or inhibited cell proliferation and proinvasive behaviour, respectively. Additionally, we also found that PLEK2 enhanced EMT through downregulating E-cadherin expression and upregulating Vimentin expression. Our findings demonstrated that PLEK2 plays a potential role in gastric cancer and may be a novel therapeutic target for gastric cancer.

Liquid biopsies to track trastuzumab resistance in metastatic HER2-positive gastric cancer

Gut ◽  
2018 ◽  
Vol 68 (7) ◽  
pp. 1152-1161 ◽  
Author(s):  
De-Shen Wang ◽  
Ze-Xian Liu ◽  
Yun-Xin Lu ◽  
Hua Bao ◽  
Xue Wu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
In Situ Hybridisation ◽  
Targeted Sequencing ◽  
In Vivo Studies ◽  
Fluorescence In Situ Hybridisation ◽  
Trastuzumab Resistance ◽  
Liquid Biopsies ◽  
Her2 Positive

ObjectiveTo monitor trastuzumab resistance and determine the underlying mechanisms for the limited response rate and rapid emergence of resistance of HER2+ metastatic gastric cancer (mGC).DesignTargeted sequencing of 416 clinically relevant genes was performed in 78 paired plasma and tissue biopsy samples to determine plasma-tissue concordance. Then, we performed longitudinal analyses of 97 serial plasma samples collected from 24 patients who were HER2+  to track the resistance during trastuzumab treatment and validated the identified candidate resistance genes.ResultsThe results from targeted sequencing-based detection of somatic copy number alterations (SCNA) of HER2 gene were highly consistent with fluorescence in situ hybridisation data, and the detected HER2 SCNA was better than plasma carcinoembryonic antigen levels at predicting tumour shrinkage and progression. Furthermore, most patients with innate trastuzumab resistance presented high HER2 SCNA during progression compared with baseline, while HER2 SCNA decreased in patients with acquired resistance. PIK3CA mutations were significantly enriched in patients with innate resistance, and ERBB2/4 genes were the most mutated genes, accounting for trastuzumab resistance in six (35.3%) and five (29.4%) patients in baseline and progression plasma, respectively. Patients with PIK3CA/R1/C3 or ERBB2/4 mutations in the baseline plasma had significantly worse progression-free survival. Additionally, mutations in NF1 contributed to trastuzumab resistance, which was further confirmed through in vitro and in vivo studies, while combined HER2 and MEK/ERK blockade overcame trastuzumab resistance.ConclusionLongitudinal circulating tumour DNA sequencing provides novel insights into gene alterations underlying trastuzumab resistance in HER2+mGC.

scholarly journals Yiqi Huayu Jiedu Decoction Inhibits the Invasion and Metastasis of Gastric Cancer Cells through TGF-β/Smad Pathway

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Ting-Ting Wu ◽  
Jun Lu ◽  
Pei-Qiu Zheng ◽  
Shen-Lin Liu ◽  
Jian Wu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
In Vivo Studies ◽  
Migration And Invasion ◽  
Invasion And Metastasis ◽  
Gastric Cancer Cells ◽  
Smad Pathway ◽  
Immunohistochemical Assay

Background.Yiqi Huayu Jiedu Decoction (YHJD) can obviously improve the quality of life of those patients with gastric cancer and prolong their survival.Methods. In vitro experiments, we observe YHJD’s effect on the cells’ proliferation by MTT assay. Cell adhesion assay, wound-healing assay, and Transwell invasion assay serve to detect its influence on cells’ adhesion, migration, and invasion, respectively. Inhibitor (10 μM/L of SB431542) and activator (10 ng/mL of TGF-β) of TGF-β/Smad pathway were used to estimate whether YHJD’s impact on the biological behavior of gastric cancer cells was related to TGF-β/Smad pathway. In in vivo studies, YHJD was administered to the nude mice transplanted with gastric cancer to observe its effect on the tumor. Western blotting and immunohistochemical assay were used to test relevant cytokines of TGF-β/Smad pathway and epithelial-mesenchymal transition (EMT) in MGC-803 cells and the tumor bearing nude mice.Results.YHJD inhibited proliferation, adhesion, migration, and invasion of MGC-803 gastric cancer cells in vitro. In in vivo studies, YHJD reduced the volume of the transplanted tumors. It also enhanced the expression of E-cadherin and decreased the levels of N-cadherin, TGF-β, Snail, and Slug in both MGC-803 cells and the transplanted tumor by western blot assay. The immunohistochemical assay revealed that YHJD raised E-cadherin in the tumors of the mice; on the contrary, the expression of N-cadherin, Twist, vimentin, TGF-βR I, p-Smad2, p-Smad3, Snail, and Slug reduced.Conclusion. YHJD can effectively inhibit the invasion and metastasis of gastric cancer cells. The mechanism may be related to TGF-β/Smad pathway.

scholarly journals Linc01133 contributes to gastric cancer growth by enhancing YES1-dependent YAP1 nuclear translocation via sponging miR-145-5p

2022 ◽  
Vol 13 (1) ◽  
Author(s):  
Yujing Sun ◽  
Yuan Tian ◽  
Junyi He ◽  
Yaru Tian ◽  
Guohao Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Nuclear Translocation ◽  
In Vivo Studies ◽  
Cancer Growth ◽  
Cell Cycle Regulators ◽  
Gastric Cancer Patients

AbstractThe long intergenic non-coding RNA linc01133 is reported to be oncogenic in various malignancies. However, the role and mechanism of linc01133 in regulating gastric cancer growth is still not clear. In the present study, we found that linc01133 was significantly upregulated in gastric cancer tissues compared to non-tumorous gastric tissues. Linc01133 over-expression significantly correlated with tumor size and tumor differentiation in gastric cancer patients. The expression of linc01133 was regulated by c-Jun and c-Fos collaboratively. In both in vitro and in vivo studies, linc01133 was shown to promote gastric cancer cell growth. Linc01133 localized in the cytoplasm and functioned as an endogenous competing RNA of miR-145-5p to upregulate the expression of YES1, which was proved to be the target gene of miR-145-5p. By promoting YES1-dependent YAP1 nuclear translocation, linc01133 upregulated the expression of the key cell cycle regulators CDK4, CDK6 and cyclin D1 to promote G1-S phase transition. Thus, our study unveiled the function and mechanism of linc01133 regulating cell cycle progression in gastric cancer.

Positron emission tomography (PET) with 89Zr-labeled trastuzumab (89Zr-trastuzumab): Monitoring HER2 expression in HER2-positive gastric cancer in vivo.

2011 ◽  
Vol 29 (4_suppl) ◽  
pp. 35-35
Author(s):  
Y. Y. Janjigian ◽  
N. T. Villegas ◽  
J. P. Holland ◽  
M. A. Shah ◽  
V. Divilov ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Specific Activity ◽  
Gastric Cancer Cell Line ◽  
In Vivo Studies ◽  
In Vitro Assays ◽  
Organ Distribution ◽  
Her2 Positive ◽  
Bibw 2992

35 Background: The ToGA study established HER2 is a target in the treatment of gastric cancer. Trastuzumab pharmacokinetics and organ distribution is varied in each patient and is heavily affected by the extent of tumor load (Oude Munnink, JCO 2010). 89Zr-trastuzumab HER2 PET can be used to image that variability and may aid in detection and staging of HER2-positive tumors. We are implementing 89Zr-radiolabeled trastuzumab PET in vivo for imaging of HER2-positive gastric cancer and for future non-invasive assessment of HER2 inhibition with a dual irreversible HER1/HER2 inhibitor, BIBW-2992. Methods: 89Zr (t1/2 = 3.17 days) was prepared via the 89Y(p,n)89Zr transmutation with high radiochemical yields (1.52±0.11 mCi/μAh) and purity (>99.99%). Trastuzumab was functionalized with the tris-hydroxamate chelate, desferrioxamine B (DFO) and radiolabeled with [89Zr]Zr-oxalate at room temperature. 89Zr-trastuzumab PET experiments in athymic nu/nu mice bearing sub-cutaneous NCI-N87 (HER2+) and/or SNU1 (HER2-) tumors were conducted. NCI-N87 gastric cancer cells were treated with BIBW-2992. Results: 89Zr-trastuzumab radiolabeling proceeded in high radiochemical yield and specific-activity of 2.82±0.05 mCi/mg. In vitro assays demonstrated >99% radiochemical purity with an immunoreactive fraction of 0.87±7. In vivo biodistribution experiments revealed high and specific uptake in HER2-positive tumors after 72 h (85.2±11.1% ID/g) with retention of activity for over 120 h. No uptake was seen in HER2-negative gastric cancer xenografts. In vitro, BIBW-2992 demonstrates dose dependent growth inhibition in the HER2+ gastric cancer cell line. Conclusions: 89Zr-trastuzumab provides quantitative and highly-specific delineation of HER2-positive gastric cancer. In vivo studies of BIBW2-2992 in gastric cancer with 89Zr-trastuzumab HER2 PET response assessment are underway. A Phase I study of 89Zr-trastuzumab PETin HER2-positive patients is to open at MSKCC imminently. No significant financial relationships to disclose.

In vitro and in vivo studies of new cationic Zn(II)‐benzonaphthoporphyrazines as photosensitizers for PDT

2001 ◽  
Vol 5 (8) ◽  
pp. 645-651
Author(s):  
M. Peeva ◽  
M. Shopova ◽  
U. Michelsen ◽  
D. Wöhrle ◽  
G. Petrov ◽  
...  
Keyword(s):  
In Vivo Studies

Effect of caffeine on theophyliine on cerebral blood flow response to brain activation: In vitro and in vivo studies

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S198-S198
Author(s):  
Joseph R Meno ◽  
Thien-son K Nguyen ◽  
Elise M Jensen ◽  
G Alexander West ◽  
Leonid Groysman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Activation ◽  
In Vivo Studies ◽  
Blood Flow Response ◽  
Flow Response

Effects of Unfractionated and Low Molecular Weight Heparins on Platelet Thromboxane Biosynthesis “In Vivo”

1994 ◽  
Vol 72 (06) ◽  
pp. 942-946 ◽  
Author(s):  
Raffaele Landolfi ◽  
Erica De Candia ◽  
Bianca Rocca ◽  
Giovanni Ciabattoni ◽  
Armando Antinori ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Unfractionated Heparin ◽  
Low Molecular Weight Heparin ◽  
Primary Source ◽  
In Vivo Studies ◽  
Low Molecular Weight ◽  
Heparin Administration ◽  
To Receive

SummarySeveral “in vitro” and “in vivo” studies indicate that heparin administration may affect platelet function. In this study we investigated the effects of prophylactic heparin on thromboxane (Tx)A2 biosynthesis “in vivo”, as assessed by the urinary excretion of major enzymatic metabolites 11-dehydro-TxB2 and 2,3-dinor-TxB2. Twenty-four patients who were candidates for cholecystectomy because of uncomplicated lithiasis were randomly assigned to receive placebo, unfractionated heparin, low molecular weight heparin or unfractionaed heparin plus 100 mg aspirin. Measurements of daily excretion of Tx metabolites were performed before and during the treatment. In the groups assigned to placebo and to low molecular weight heparin there was no statistically significant modification of Tx metabolite excretion while patients receiving unfractionated heparin had a significant increase of both metabolites (11-dehydro-TxB2: 3844 ± 1388 vs 2092 ±777, p <0.05; 2,3-dinor-TxB2: 2737 ± 808 vs 1535 ± 771 pg/mg creatinine, p <0.05). In patients randomized to receive low-dose aspirin plus unfractionated heparin the excretion of the two metabolites was largely suppressed thus suggesting that platelets are the primary source of enhanced thromboxane biosynthesis associated with heparin administration. These data indicate that unfractionated heparin causes platelet activation “in vivo” and suggest that the use of low molecular weight heparin may avoid this complication.

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