Colonization of the rat liver by syngeneic tumor cells An experimental approach by in vivo and in situ studies

1988 ◽  
Vol 55 (1) ◽  
pp. 111-116
Author(s):  
E. Solberg ◽  
T. Gjøen ◽  
R. Seljelid ◽  
S. O. Kolset
Keyword(s):  
Tumor Cells ◽  
Rat Liver ◽  
Experimental Approach ◽  
In Situ Studies ◽  
Syngeneic Tumor

In vitro and in vivo suppression of growth of rat liver epithelial tumor cells by antisense oligonucleotide against protein kinase C-alpha

2000 ◽  
Vol 33 (4) ◽  
pp. 601-608 ◽  
Author(s):  
Shwu-Bin Lin ◽  
Li-Ching Wu ◽  
Siao-Ling Huang ◽  
Hui-Lun Hsu ◽  
Sung-Hwa Hsieh ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Tumor Cells ◽  
Rat Liver ◽  
Antisense Oligonucleotide ◽  
Epithelial Tumor ◽  
Kinase C ◽  
Epithelial Tumor Cells

Epidermal Growth Factor—Interactions with Normal and Malignant Urothelium: In Vivo and in Situ Studies

1987 ◽  
Vol 138 (5) ◽  
pp. 1329-1335 ◽  
Author(s):  
Edward M. Messing ◽  
Patricia Hanson ◽  
Peter Ulrich ◽  
Edrogen Erturk
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
In Situ Studies ◽  
Epidermal Growth ◽  
Factor Interactions

scholarly journals Application of a simple device for "attracting" and "trapping" glioma cells in situ

2021 ◽  
Author(s):  
Haimin Song ◽  
Runwei Yang ◽  
Runbin Lai ◽  
Kaishu Li ◽  
Bowen Ni ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Cells ◽  
Adult Brain ◽  
Tumor Bed ◽  
In Vivo Experiments ◽  
New Strategy ◽  
New Treatment

Glioblastoma multiforme (GBM) is the most malignant adult brain tumor. The current adjuvant therapies for GBM are disappointing, which are based on cytotoxicity strategy. Thus, other ways should be explored to improve the curative effect. According to the strong invasive ability of GBM cells, we assume a new treatment strategy for GBM by developing a new cell trap device (CTD) with some kind of "attractive" medium loaded in it to attract and capture the tumor cells. The in vitro experiment showed that Hepatocyte Growth Factor（HGF）presented stronger chemotaxis on C6 and U87 cell line than the Epidermal Growth Factor (EGF) and Fibroblast Growth Factor (FGF). A simple in vitro CTD loaded with HGF was made and in vivo experiments results showed that HGF successfully attracted tumor cells from tumor bed in situ into the CTD. This study proposes the new strategy for GBM treatment of "attract and trap" tumor cells is proved to be feasible.

scholarly journals The aberrantly expressed miR-372 partly impairs sensitivity to apoptosis in parathyroid tumor cells

2018 ◽  
Vol 25 (7) ◽  
pp. 761-771 ◽  
Author(s):  
Chiara Verdelli ◽  
Irene Forno ◽  
Annamaria Morotti ◽  
Pasquale Creo ◽  
Vito Guarnieri ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Wnt Pathway ◽  
Mrna Levels ◽  
Parathyroid Tumor ◽  
Protein Levels ◽  
Parathyroid Adenomas ◽  
Tumor Parenchyma ◽  
Induced Apoptosis

Parathyroid tumors deregulate microRNAs belonging to the two clusters on the chromosome 19, the C19MC and miR-371-373 clusters. Here, we report that the embryonic miR-372 is aberrantly expressed in half of parathyroid adenomas (PAds) in most of atypical adenomas and carcinomas (n = 15). Throughin situhybridization, we identified that miR-372-positive parathyroid tumor cells were scattered throughout the tumor parenchyma. In PAd-derived cells, ectopic miR-372 inhibited the expression of its targetsCDKN1A/p21 and LATS2 at both mRNA and protein levels. Although the viability of parathyroid cells was not affected by miR-372 overexpression, the miRNA blunted camptothecin-induced apoptosis in primary PAd-derived cultures. miR-372 overexpression in parathyroid tumor cells increased parathormone (PTH) mRNA levels, and it positively correlatedin vivowith circulating PTH levels. Conversely, the parathyroid-specific genesTBX1andGCM2were not affected by miR-372 mimic transfection. Finally, miR-372 dampened the Wnt pathway in parathyroid tumor cells through DKK1 upregulation. In conclusion, miR-372 is a novel mechanism exploited by a subset of parathyroid tumor cells to partially decrease sensitivity to apoptosis, to increase PTH synthesis and to deregulate Wnt signaling.

scholarly journals In Situ Silver-based Electrochemical Bioreactor In Vivo

2020 ◽  
Author(s):  
Yong Huang ◽  
Liping Zhong ◽  
Zhiming Deng ◽  
Pan Wu ◽  
Jian He ◽  
...  
Keyword(s):  
Silver Nanoparticles ◽  
Graphene Oxide ◽  
Tumor Cells ◽  
Silver Nanoparticle ◽  
A549 Cells ◽  
Induced Apoptosis ◽  
Induced Changes

Abstract In this study we show for the first time that a reduced graphene oxide (rGO) carrier has a 15-fold higher catalysis rate than graphene oxide (GO) in Ag+ reduction. Based on this, we constructed a tumor microenvironment-enabled in situ silver-based electrochemical oncolytic bioreactor (SEOB) which unlocked an Ag+ prodrug to generate silver nanoparticles and inhibited the growth of various tumors. In this bioreactor system, intratumoral H2O2 acted as the reductant and the rGO carrier acted as the catalyst. Chelation of aptamers to this prodrug increased the production of silver nanoparticles by tumor cells, especially in the presence of Vitamin C, which broke down in tumor cells to supply massive amounts of H2O2. Consequently, highly efficient silver nanoparticle-induced apoptosis was observed in HepG2 and A549 cells in vitro and in HepG2- and A549-derived tumors in vivo. The apoptosis was associated with ROS-induced changes in mitochondrial membrane potential and DNA damage. The specific aptamer targeting and intratumoral silver nanoparticle production guaranteed excellent biosafety, with no damage to normal cells, because the Ag+ prodrug was specifically unlocked in tumors. More significantly, there was no evident tissue damage in monkeys, which greatly increases the clinical translation potential of the SEOB system.

EXPERIMENTAL DETERMINATION OF IN VIVO PRESSURE DISTRIBUTION IN BIOLOGIC JOINTS

2000 ◽  
Vol 04 (01) ◽  
pp. 1-7 ◽  
Author(s):  
W. Herzog ◽  
E. M. Hasler ◽  
T. R. Leonard
Keyword(s):  
Muscle Force ◽  
Experimental Approach ◽  
Pressure Distributions ◽  
Joint Contact ◽  
Hindlimb Movement ◽  
Joint Contact Pressure ◽  
Contact Pressures

The purpose of this communication is to present an idea, and its technical implementation, on how to estimate experimentally in vivo joint contact pressure distributions. The idea is illustrated for the cat patellofemoral joint. For this particular joint, the approach requires muscle force and hindlimb movement measurements during unrestrained locomotion, and the quantification of the joint contact pressures in situ for conditions approximating the in vivo conditions as closely as possible. Although the approach is time-consuming and has its limitations, it is, as far as we know, the first purely experimental approach to determine the in vivo joint contact pressures during normal movement. "Purely experimental" refers to the idea that the required movements, muscle forces and contact pressures are all measured rather than estimated theoretically.

In vitro and in vivo suppression of growth of rat liver epithelial tumor cells by antisense oligonucleotide against protein kinase C-α

2000 ◽  
Vol 33 (4) ◽  
pp. 601-608 ◽  
Author(s):  
Shwu-Bin Lin ◽  
Li-Ching Wu ◽  
Siao-Ling Huang ◽  
Hui-Lun Hsu ◽  
Sung-Hwa Hsieh ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Tumor Cells ◽  
Rat Liver ◽  
Antisense Oligonucleotide ◽  
Epithelial Tumor ◽  
Kinase C ◽  
Epithelial Tumor Cells

Repression of protein synthesis and mTOR signaling in rat liver mediated by the AMPK activator aminoimidazole carboxamide ribonucleoside

2005 ◽  
Vol 288 (5) ◽  
pp. E980-E988 ◽  
Author(s):  
Ali K. Reiter ◽  
Douglas R. Bolster ◽  
Stephen J. Crozier ◽  
Scot R. Kimball ◽  
Leonard S. Jefferson
Keyword(s):  
Protein Synthesis ◽  
Rat Liver ◽  
Translational Control ◽  
Serum Insulin ◽  
Experimental Models ◽  
Mtor Signaling ◽  
Initiation Factor ◽  
Perfused Liver

The studies described herein were designed to investigate the effects of 5-aminoimidazole-4-carboxamide-1-β-d-ribonucleoside (AICAR), an activator of the AMP-activated protein kinase (AMPK), on the translational control of protein synthesis and signaling through the mammalian target of rapamycin (mTOR) in rat liver. Effects of AICAR observed in vivo were compared with those obtained in an in situ perfused liver preparation to investigate activation of AMPK in the absence of accompanying changes in hormones and nutrients. AMPK became hyperphosphorylated, as assessed by a gel-shift analysis, in response to AICAR both in vivo and in situ; however, increased relative phosphorylation at the Thr172 site on the kinase was observed only in perfused liver. Phosphorylation of AMPK either in vivo or in situ was associated with a repression of protein synthesis as well as decreased phosphorylation of a number of targets of mTOR signaling including ribosomal protein S6 kinase 1, eukaryotic initiation factor (eIF)4G, and eIF4E-binding protein (4E-BP)1. The phosphorylation changes in eIF4G and 4E-BP1 were accompanied by a reduction in the amount of eIF4E present in the active eIF4E·eIF4G complex and an increase in the amount present in the inactive eIF4E·4E-BP1 complex. Reduced insulin signaling as well as differences in nutrient availability may have contributed to the effects observed in vivo as AICAR caused a fall in the serum insulin concentration. Overall, however, the results from both experimental models support a scenario in which AICAR directly represses protein synthesis and mTOR signaling in the liver through an AMPK-dependent mechanism.

scholarly journals A preclinical model of hepatocyte gene transfer: the in vivo, in situ perfused rat liver

Gene Therapy ◽  
2000 ◽  
Vol 7 (21) ◽  
pp. 1816-1823 ◽  
Author(s):  
J L De Godoy ◽  
R Malafosse ◽  
M Fabre ◽  
C Mitchell ◽  
M Mehtali ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Rat Liver ◽  
Preclinical Model ◽  
Perfused Rat Liver
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