IL-12 inhibits postoperative residual tumor growth in murine models of sarcoma and renal carcinoma

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Huiqin Ding ◽  
Shoujun Yuan ◽  
Jiangang Wang ◽  
Huan Qin ◽  
Yantao Han
Cancer ◽  
1999 ◽  
Vol 85 (10) ◽  
pp. 2249-2254 ◽  
Author(s):  
Hiroshi Nakaguchi ◽  
Takamitsu Fujimaki ◽  
Akira Matsuno ◽  
Reiko Matsuura ◽  
Akio Asai ◽  
...  

1992 ◽  
Vol 10 (4) ◽  
pp. 529-535 ◽  
Author(s):  
G Scambia ◽  
P Benedetti Panici ◽  
F Battaglia ◽  
G Ferrandina ◽  
G Baiocchi ◽  
...  

PURPOSE The purpose of this study was to investigate the significance of epidermal growth factor receptor (EGF-R) expression in a group of advanced ovarian carcinomas. PATIENTS AND METHODS The study was conducted on 72 previously untreated patients with International Federation of Gynecology and Obstetrics (FIGO) stage III-IV disease. The median follow-up was 24 months (range, 4 to 75 months). EGF-R was measured by a radioreceptorial assay. A cutoff of 1.5 fmol per milligram of protein was chosen to define EGF-R positivity. Medians and life tables obtained with the Kaplan and Meier method were analyzed by the log-rank test. The risk of progression was estimated by Cox's proportional hazards model. RESULTS EGF-R was detected in 54% of primary tumors. When EGF-R was analyzed in different tissue specimens of the same tumor, consistent findings were noted in 88% (seven of eight) of cases. A lower concordance rate (nine of 15; 60%) was found between primary tumors and omental metastases, with a tendency toward higher EGF-R levels in the latter. The EGF-R expression did not significantly correlate with age, stage, grading, and residual tumor after primary surgery. In the univariate analysis, stage IV disease, postoperative residual tumor diameter greater than 2 cm, presence of ascites, and EGF-R positivity were found to be significantly associated with a greater risk of disease progression. In the multivariate analysis, only the postoperative residual tumor and the EGF-R expression remained significantly associated with a high risk of progression. CONCLUSION Data reported here suggest that the presence of EGF-R in advanced ovarian tumor at the time of the primary surgery identifies a subset of patients with a particularly poor prognosis.


Neurosurgery ◽  
1991 ◽  
pp. 666 ◽  
Author(s):  
E A Healey ◽  
P D Barnes ◽  
W J Kupsky ◽  
R M Scott ◽  
S E Sallan ◽  
...  

2009 ◽  
Vol 35 (11) ◽  
pp. 1164-1168 ◽  
Author(s):  
C. Ausch ◽  
V. Buxhofer-Ausch ◽  
U. Olszewski ◽  
W. Hinterberger ◽  
E. Ogris ◽  
...  

Cell Reports ◽  
2018 ◽  
Vol 24 (1) ◽  
pp. 47-55 ◽  
Author(s):  
Yongliang Wang ◽  
Ali R. Nasiri ◽  
William E. Damsky ◽  
Curtis J. Perry ◽  
Xian-Man Zhang ◽  
...  

2011 ◽  
Author(s):  
Huang Dachuan ◽  
Ong Choon Kiat ◽  
Teh Bin Tean ◽  
Bernice Wong Huimin ◽  
Waraporn Chan-on ◽  
...  

1993 ◽  
Vol 29 ◽  
pp. S136
Author(s):  
S. Čolaković ◽  
V. Lukić ◽  
Lj. Stamatović ◽  
J. Marinković ◽  
J. Josifovski ◽  
...  

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Hui Yuan ◽  
Zelong Lin ◽  
Yingjun Liu ◽  
Yuchuan Jiang ◽  
Ke Liu ◽  
...  

Abstract Background M2-polarized tumor-associated macrophages (M2-TAMs) have been shown to correlate with the progression of various cancers, including intrahepatic cholangiocarcinoma (ICC). However, the interactions and mechanism between M2 macrophages and ICC are not completely clear. We aimed to clarify whether M2 macrophages promote the malignancy of ICC and its mechanism. Methods Two progressive murine models of ICC were used to evaluate the alterations in different macrophage populations and phenotypes. Furthermore, we assessed M2 macrophage infiltration in 48 human ICC and 15 normal liver samples. The protumor functions and the underlying molecular mechanisms of M2 macrophages in ICC were investigated in an in vitro coculture system. Results We found that the number of M2 macrophages was significantly higher in ICC tissues than in normal bile ducts in the two murine models. M2 macrophage infiltration was highly increased in peritumoral compared with intratumoral regions and normal liver (p < 0.01). ICC cells induced macrophages to differentiate into the M2-TAM phenotype, and coculture with these M2 macrophages promoted ICC cell proliferation, invasion and epithelial–mesenchymal transition (EMT) in vitro. Mechanistically, M2-TAM-derived IL-10 promoted the malignant properties of ICC cells through STAT3 signaling. Furthermore, blockade of IL-10/STAT3 signaling partly rescued the effects of M2 macrophages on ICC. Conclusion Our results indicated that M2-polarized macrophages induced by ICC promote tumor growth and invasiveness through IL-10/STAT3-induced EMT and might be a potential therapeutic target for ICC.


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