Abstract 503: Prostaglandin E2 produced by tumor cells or by the host tumor microenvironment is not completely abolished by aspirin or celecoxib and limits the ability of the host immune system to control tumor growth

2019 ◽  
Author(s):  
John N. Snouwaert ◽  
Leigh Jania ◽  
MyTrang Nguyen ◽  
Pragnya Dontu ◽  
Jérôme Besse ◽  
...  
Keyword(s):  
Immune System ◽  
Tumor Microenvironment ◽  
Tumor Growth ◽  
Prostaglandin E2 ◽  
Tumor Cells ◽  
Host Immune System ◽  
Control Tumor Growth ◽  
Control Tumor

A MATHEMATICAL MODEL OF IMMUNE RESPONSE TO TUMOR INVASION INCORPORATED WITH DANGER MODEL

2015 ◽  
Vol 23 (03) ◽  
pp. 505-526 ◽  
Author(s):  
XUEFANG LI ◽  
JIAN-XIN XU
Keyword(s):  
Mathematical Model ◽  
Immune Response ◽  
Immune System ◽  
Tumor Cells ◽  
Tumor Invasion ◽  
Interleukin 12 ◽  
Specific System ◽  
Control Tumor Growth ◽  
Control Tumor ◽  
Broad Understanding

In this paper, a new mathematical model of the interactions between a growing tumor and an immune system is presented by incorporating the danger model. The populations involved are tumor cells, CD8+T-cells, natural killer cells (NK-cells), dendritic cells (DCs) and cytokine interleukin-12 (IL-12). A key feature of this work is the inclusion of the danger model into the dynamics of the immune system, which is rarely considered by previous works. Regarding the constructed mathematical model, both the location of equilibria and their stability properties are discussed, which are useful not only to gain a broad understanding of the specific system dynamics, but also to help guide the development of therapies. Moreover, numerical simulations of the system with chemotherapy and immunotherapy by using specific parameters are presented to illustrate that proper therapy is able to eliminate the entire tumor. In addition, we illustrate cases for which neither chemotherapy nor immunotherapy alone are able to control tumor growth, but a combination treatment is sufficient to eliminate the tumor cells.

IL-6-transfected tumor cells modulate the status of CD8+ and CD4+ T cells to control tumor growth

Immunobiology ◽  
2010 ◽  
Vol 215 (6) ◽  
pp. 486-491 ◽  
Author(s):  
Chia-Ling Hsieh ◽  
Shih-Jen Liu ◽  
Chia-Rui Shen ◽  
Mei-Yu Chen ◽  
Shu-Ching Hsu ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Growth ◽  
Tumor Cells ◽  
Cd4 T Cells ◽  
Control Tumor Growth ◽  
The Status ◽  
Control Tumor

scholarly journals RUNX3 methylation drives hypoxia-induced cell proliferation and antiapoptosis in early tumorigenesis

2020 ◽  
Author(s):  
Sun Hee Lee ◽  
Do Young Hyeon ◽  
Soo-Hyun Yoon ◽  
Ji-Hak Jeong ◽  
Saeng-Myung Han ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Growth ◽  
Posttranslational Modifications ◽  
Nucleocytoplasmic Transport ◽  
Cancer Cell Proliferation ◽  
Runt Domain ◽  
Transactivation Activity ◽  
Control Tumor Growth ◽  
Related Transcription Factor ◽  
Control Tumor

Abstract Inactivation of tumor suppressor Runt-related transcription factor 3 (RUNX3) plays an important role during early tumorigenesis. However, posttranslational modifications (PTM)-based mechanism for the inactivation of RUNX3 under hypoxia is still not fully understood. Here, we demonstrate a mechanism that G9a, lysine-specific methyltransferase (KMT), modulates RUNX3 through PTM under hypoxia. Hypoxia significantly increased G9a protein level and G9a interacted with RUNX3 Runt domain, which led to increased methylation of RUNX3 at K129 and K171. This methylation inactivated transactivation activity of RUNX3 by reducing interactions with CBFβ and p300 cofactors, as well as reducing acetylation of RUNX3 by p300, which is involved in nucleocytoplasmic transport by importin-α1. G9a-mediated methylation of RUNX3 under hypoxia promotes cancer cell proliferation by increasing cell cycle or cell division, while suppresses immune response and apoptosis, thereby promoting tumor growth during early tumorigenesis. Our results demonstrate the molecular mechanism of RUNX3 inactivation by G9a-mediated methylation for cell proliferation and antiapoptosis under hypoxia, which can be a therapeutic or preventive target to control tumor growth during early tumorigenesis.

scholarly journals Targeting COX-2 and EP4 to control tumor growth, angiogenesis, lymphangiogenesis and metastasis to the lungs and lymph nodes in a breast cancer model

2012 ◽  
Vol 92 (8) ◽  
pp. 1115-1128 ◽  
Author(s):  
Xiping Xin ◽  
Mousumi Majumder ◽  
Gannareddy V Girish ◽  
Vik Mohindra ◽  
Takayuki Maruyama ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Lymph Nodes ◽  
Cancer Model ◽  
Breast Cancer Model ◽  
Control Tumor Growth ◽  
Control Tumor ◽  
Cox 2
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