STING agonist and IDO inhibitor combination therapy inhibits tumor progression in murine models of colorectal cancer

2021 ◽  
pp. 104384
Author(s):  
Jiaqi Shi ◽  
Caiqi Liu ◽  
Shengnan Luo ◽  
Tingyu Cao ◽  
Binlin Lin ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Combination Therapy ◽  
Tumor Progression ◽  
Murine Models ◽  
Inhibitor Combination

Development of a novel dalotuzumab/AKT inhibitor combination therapy for the treatment of cetuximab refractory colorectal cancer (CRC).

2011 ◽  
Vol 29 (15_suppl) ◽  
pp. e13590-e13590
Author(s):  
G. Naumov ◽  
E. Valentine ◽  
S. Howard ◽  
A. Seeley ◽  
S. Jha ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Combination Therapy ◽  
Akt Inhibitor ◽  
Inhibitor Combination

scholarly journals Knockout of c-mos gene does not affect tumor progression in murine models of lung and colorectal cancer

2017 ◽  
Author(s):  
Zhengxi Chen ◽  
Ju Qiao ◽  
Zhenqi Chen ◽  
Qian Xiao
Keyword(s):  
Colorectal Cancer ◽  
Lung Cancer ◽  
Tumor Progression ◽  
Cancer Patients ◽  
Survival Rates ◽  
Intestinal Cancer ◽  
Murine Models ◽  
Cancer Model ◽  
Poor Survival ◽  
Lung Cancer Model

Background. The c-mos proto-oncogene was one of the first proto-oncogenes to be cloned. Apart from its role in meiosis, many efforts have been made to illuminate the mechanisms by which c-mos acts as an oncogene. c-mos or its coding messenger RNA have been confirmed in most somatic tissues at low levels. However, a detailed role of c-mos as an oncogene in somatic cells remains unknown. Methods. In this study, we analyzed online databases to find out the correlation between Mos expression and poor survival rates in human cancer patients. Then, we investigated whether the involvement of c-mos in tumor progression via applying Apcmin intestinal cancer model and KrasG12D lung cancer model. Results. First, we found the expression of Mos differed between human and mice, and a significant correlation between high Mos expression and poor survival rates in lung cancer patients. Interestingly, we tested that the effects of deficient c-mos in both Apcmin intestinal cancer model and KrasG12D lung cancer model. Despite the abovementioned significant correlation, the results did not show a strong inhibitory effect on murine models of lung and intestine tumors. We find no evidence of a direct role for c-mos in tumor progression in abovementioned mice models. Discussion. It indicated that functions of c-mos gene might be species-specific and that c-mos involvement in tumor progression was circumstantial and it probably depended on other oncogene activation. Keywords: c-mos, Kras, Apc, survival rate, murine model, lung cancer, colorectal cancer

scholarly journals Anti-IL-6 and PD-L1 antibody combination therapy reduces tumor progression in murine models of pancreatic cancer

2015 ◽  
Vol 3 (S2) ◽  
Author(s):  
Thomas Mace ◽  
Reena Shakya ◽  
Jason Pitarresi ◽  
Shannon Loftus ◽  
Benjamin Swanson ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Combination Therapy ◽  
Tumor Progression ◽  
Murine Models

scholarly journals Data on tumor progression of c-mos deficiency in murine models of Kras lung and Apc colorectal cancer

Data in Brief ◽  
2018 ◽  
Vol 20 ◽  
pp. 1124-1132 ◽  
Author(s):  
Zhengxi Chen ◽  
Ju Qiao ◽  
Qirui Wang ◽  
Qian Xiao
Keyword(s):  
Colorectal Cancer ◽  
Tumor Progression ◽  
Murine Models

scholarly journals Knockout of c-mos gene does not affect tumor progression in murine models of lung and colorectal cancer

2017 ◽  
Author(s):  
Zhengxi Chen ◽  
Ju Qiao ◽  
Zhenqi Chen ◽  
Qian Xiao
Keyword(s):  
Colorectal Cancer ◽  
Lung Cancer ◽  
Tumor Progression ◽  
Cancer Patients ◽  
Survival Rates ◽  
Intestinal Cancer ◽  
Murine Models ◽  
Cancer Model ◽  
Poor Survival ◽  
Lung Cancer Model

Background. The c-mos proto-oncogene was one of the first proto-oncogenes to be cloned. Apart from its role in meiosis, many efforts have been made to illuminate the mechanisms by which c-mos acts as an oncogene. c-mos or its coding messenger RNA have been confirmed in most somatic tissues at low levels. However, a detailed role of c-mos as an oncogene in somatic cells remains unknown. Methods. In this study, we analyzed online databases to find out the correlation between Mos expression and poor survival rates in human cancer patients. Then, we investigated whether the involvement of c-mos in tumor progression via applying Apcmin intestinal cancer model and KrasG12D lung cancer model. Results. First, we found the expression of Mos differed between human and mice, and a significant correlation between high Mos expression and poor survival rates in lung cancer patients. Interestingly, we tested that the effects of deficient c-mos in both Apcmin intestinal cancer model and KrasG12D lung cancer model. Despite the abovementioned significant correlation, the results did not show a strong inhibitory effect on murine models of lung and intestine tumors. We find no evidence of a direct role for c-mos in tumor progression in abovementioned mice models. Discussion. It indicated that functions of c-mos gene might be species-specific and that c-mos involvement in tumor progression was circumstantial and it probably depended on other oncogene activation. Keywords: c-mos, Kras, Apc, survival rate, murine model, lung cancer, colorectal cancer

scholarly journals Antioxidants Promote Intestinal Tumor Progression in Mice

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 241
Author(s):  
Zhiyuan V. Zou ◽  
Kristell Le Gal ◽  
Ahmed E. El Zowalaty ◽  
Lara E. Pehlivanoglu ◽  
Viktor Garellick ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Colorectal Cancer ◽  
Tumor Progression ◽  
Human Subjects ◽  
Plasma Concentrations ◽  
Intestinal Tumor ◽  
Adenomatous Polyposis ◽  
Intestinal Tumors ◽  
The Impact

Dietary antioxidants and supplements are widely used to protect against cancer, even though it is now clear that antioxidants can promote tumor progression by helping cancer cells to overcome barriers of oxidative stress. Although recent studies have, in great detail, explored the role of antioxidants in lung and skin tumors driven by RAS and RAF mutations, little is known about the impact of antioxidant supplementation on other cancers, including Wnt-driven tumors originating from the gut. Here, we show that supplementation with the antioxidants N-acetylcysteine (NAC) and vitamin E promotes intestinal tumor progression in the ApcMin mouse model for familial adenomatous polyposis, a hereditary form of colorectal cancer, driven by Wnt signaling. Both antioxidants increased tumor size in early neoplasias and tumor grades in more advanced lesions without any impact on tumor initiation. Importantly, NAC treatment accelerated tumor progression at plasma concentrations comparable to those obtained in human subjects after prescription doses of the drug. These results demonstrate that antioxidants play an important role in the progression of intestinal tumors, which may have implications for patients with or predisposed to colorectal cancer.

scholarly journals Immune checkpoint inhibitor combination therapies very frequently induce secondary adrenal insufficiency

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Katsunori Manaka ◽  
Junichiro Sato ◽  
Maki Takeuchi ◽  
Kousuke Watanabe ◽  
Hidenori Kage ◽  
...  
Keyword(s):  
Combination Therapy ◽  
Adrenal Insufficiency ◽  
Cancer Patients ◽  
Immune Checkpoint ◽  
Checkpoint Inhibitors ◽  
Delayed Diagnosis ◽  
Secondary Adrenal Insufficiency ◽  
Acth Deficiency ◽  
Life Threatening ◽  
Inhibitor Combination

AbstractImmune checkpoint inhibitors (ICIs) are potent therapeutic options for many types of advanced cancer. The expansion of ICIs use however has led to an increase in immune-related adverse events (irAEs). Secondary adrenal insufficiency (AI) can be life-threatening especially in patients with delayed diagnosis. We retrospectively investigated secondary AI in ICI-treated patients. A total of 373 cancer patients treated with ICIs were included and evaluated. An adrenocorticotropic hormone (ACTH) deficiency was described in 13 patients. Among 24 patients with a combination of nivolumab and ipilimumab therapy, 7 patients (29%) developed secondary AI in a median time of 8 weeks during the combination therapy and 2 of 15 patients (13%) developed isolated ACTH deficiency during maintenance nivolumab monotherapy following the combination therapy. More than half of the patients (4/7) with a combination therapy-induced multiple anterior hormone deficiencies was diagnosed as secondary AI based on regular ACTH and cortisol tests with slight subjective symptoms. Secondary AI can arise frequently and rapidly in cancer patients receiving a combination ICI therapy, and thus we speculate active surveillance of AI using regular ACTH and cortisol tests during the combination therapy might be useful for avoiding life-threatening conditions due to secondary AI.

Lipocalin 2 expression promotes tumor progression and therapy resistance by inhibiting ferroptosis in colorectal cancer

2021 ◽  
Author(s):  
Nazia Chaudhary ◽  
Bhagya Shree Choudhary ◽  
Sanket Girish Shah ◽  
Nileema Khapare ◽  
Nehanjali Dwivedi ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Progression ◽  
Therapy Resistance ◽  
Lipocalin 2
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