Sinusoidal Obstruction Syndrome Promotes Liver Metastatic Seeding of Colorectal Cancer Cells in a Rat Model.
Animals
Cell Line, Tumor
Colorectal Neoplasms
/ genetics
Disease Models, Animal
Disease Progression
Gene Expression Regulation, Neoplastic
Hepatic Veno-Occlusive Disease
/ chemically induced
Intercellular Adhesion Molecule-1
/ genetics
Liver Neoplasms
/ genetics
Male
Matrix Metalloproteinase 9
/ genetics
Monocrotaline
Rats, Inbred F344
Tumor Burden
Vascular Endothelial Growth Factor A
/ genetics
Colorectal cancer
cancer microenvironment
liver metastasis
monocrotaline
sinusoidal obstruction syndrome
Journal
Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988
Informations de publication
Date de publication:
Apr 2021
Apr 2021
Historique:
received:
01
02
2021
revised:
13
03
2021
accepted:
16
03
2021
entrez:
4
4
2021
pubmed:
5
4
2021
medline:
14
4
2021
Statut:
ppublish
Résumé
Sinusoidal obstruction syndrome (SOS) after neoadjuvant chemotherapy with oxaliplatin for colorectal liver metastases (CRLM) has been reported to lead to early recurrence. This study investigated the effects of SOS on the development of CRLM in a rat model. RCN-H4 cells were injected into the spleen or liver of ten monocrotaline-treated (SOS group) and ten untreated (control group) rats. The number and size of liver tumors were compared between the groups. The number of liver tumors in the splenic RCN-H4 injection model was significantly higher in the SOS group than in the control group (332±213 vs. 16±5, p=0.029); however, the largest tumor diameter in the hepatic model was similar between groups (6.2±1.8 vs. 6.4±2.4 mm, p=0.87). SOS promotes CRLM development by splenic RCN-H4 cell injection. This might be due to the higher incidence of cancer cell implantation into the liver.
Sections du résumé
BACKGROUND/AIM
OBJECTIVE
Sinusoidal obstruction syndrome (SOS) after neoadjuvant chemotherapy with oxaliplatin for colorectal liver metastases (CRLM) has been reported to lead to early recurrence. This study investigated the effects of SOS on the development of CRLM in a rat model.
MATERIALS AND METHODS
METHODS
RCN-H4 cells were injected into the spleen or liver of ten monocrotaline-treated (SOS group) and ten untreated (control group) rats. The number and size of liver tumors were compared between the groups.
RESULTS
RESULTS
The number of liver tumors in the splenic RCN-H4 injection model was significantly higher in the SOS group than in the control group (332±213 vs. 16±5, p=0.029); however, the largest tumor diameter in the hepatic model was similar between groups (6.2±1.8 vs. 6.4±2.4 mm, p=0.87).
CONCLUSION
CONCLUSIONS
SOS promotes CRLM development by splenic RCN-H4 cell injection. This might be due to the higher incidence of cancer cell implantation into the liver.
Identifiants
pubmed: 33813385
pii: 41/4/1803
doi: 10.21873/anticanres.14946
doi:
Substances chimiques
ICAM1 protein, rat
0
Vascular Endothelial Growth Factor A
0
vascular endothelial growth factor A, rat
0
Intercellular Adhesion Molecule-1
126547-89-5
Monocrotaline
73077K8HYV
Matrix Metalloproteinase 9
EC 3.4.24.35
Mmp9 protein, rat
EC 3.4.24.35
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1803-1810Informations de copyright
Copyright © 2021 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.