Carnitines slow down tumor development of colon cancer in the DMH-chemical carcinogenesis mouse model

2013 ◽  
Vol 114 (7) ◽  
pp. 1665-1673 ◽  
Author(s):  
Giuseppe Roscilli ◽  
Emanuele Marra ◽  
Federica Mori ◽  
Arianna Di Napoli ◽  
Rita Mancini ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Mouse Model ◽  
Tumor Development ◽  
Chemical Carcinogenesis

Abstract B017: Bacterial minicells decrease tumor development and modulate immunity in a mouse mouse model of colon cancer

2016 ◽  
Author(s):  
Mengxi Tian ◽  
Mohammad W. Khan ◽  
Shea Grenier ◽  
Shingo Tsuji ◽  
Matthew A. Giacalone ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Mouse Model ◽  
Tumor Development

scholarly journals The neurotensin receptor-1 promotes tumor development in a sporadic but not an inflammation-associated mouse model of colon cancer

2011 ◽  
Vol 130 (8) ◽  
pp. 1798-1805 ◽  
Author(s):  
James M. Bugni ◽  
Leina Al- Rabadi ◽  
Kevin Jubbal ◽  
Iordanis Karagiannides ◽  
Gregory Lawson ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Mouse Model ◽  
Tumor Development ◽  
Neurotensin Receptor ◽  
Neurotensin Receptor 1

scholarly journals Losartan and Vitamin D Inhibit Colonic Tumor Development in a Conditional Apc-Deleted Mouse Model of Sporadic Colon Cancer

2019 ◽  
Vol 12 (7) ◽  
pp. 433-448 ◽  
Author(s):  
Urszula Dougherty ◽  
Reba Mustafi ◽  
Haider I. Haider ◽  
Abdurahman Khalil ◽  
Jeffrey S. Souris ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Vitamin D ◽  
Mouse Model ◽  
Tumor Development ◽  
Colonic Tumor ◽  
Sporadic Colon Cancer

Sa1108 SERUM AMYLOID A PROMOTES INFLAMMATION-ASSOCIATED DAMAGE, MACROPHAGE INFILTRATION AND TUMORIGENESIS IN A MOUSE MODEL OF COLITIS-ASSOCIATED COLON CANCER

2020 ◽  
Vol 158 (6) ◽  
pp. S-278
Author(s):  
Tanja Davis ◽  
Daleen Conradie ◽  
Preetha Shridas ◽  
Marcielle C. de Beer ◽  
Frederick c. de Beer ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Mouse Model ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Macrophage Infiltration ◽  
Amyloid A

scholarly journals Apolipoprotein A-I (apoA-I) and apoA-I mimetic peptides inhibit tumor development in a mouse model of ovarian cancer

2010 ◽  
Vol 107 (46) ◽  
pp. 19997-20002 ◽  
Author(s):  
F. Su ◽  
K. R. Kozak ◽  
S. Imaizumi ◽  
F. Gao ◽  
M. W. Amneus ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Mouse Model ◽  
Tumor Development ◽  
Apolipoprotein A ◽  
Mimetic Peptides

Mouse model and human patient data suggest critical roles for Pten and p53 in suppressing POLE mutant tumor development

2021 ◽  
Author(s):  
Vivian S Park ◽  
Meijuan JS Sun ◽  
Wesley D Frey ◽  
Leonard G Williams ◽  
Karl P Hodel ◽  
...  
Keyword(s):  
Dna Damage ◽  
Mouse Model ◽  
Genome Stability ◽  
Nuclear Dna ◽  
Tumor Development ◽  
Base Substitution ◽  
Human Patient ◽  
Mutation Burden ◽  
P53 Activation ◽  
Subsequent Loss

Mutations in the exonuclease domain of POLE are associated with tumors harboring very high mutation burdens. The mechanisms linking this significant mutation accumulation and tumor development remain poorly understood. Pole+/P286R;Trp53+/- mice showed accelerated cancer mortality compared to Pole+/P286R;Trp53+/+ mice. Cells from Pole+/P286R mice showed increased p53 activation, and subsequent loss of p53 permitted rapid growth, implicating canonical p53 loss of heterozygosity in POLE mutant tumor growth. Somewhat surprisingly, however, p53 status had no effect on tumor mutation burden or single base substitution signatures in POLE mutant tumors from mice or humans. Pten has important roles in maintaining genome stability. We find that PTEN mutations are highly enriched in human POLE mutant tumors, including many in POLE signature contexts. One such signature mutation, PTEN-F341V, was previously shown in a mouse model to specifically decrease nuclear Pten and lead to increased DNA damage. We found tumors in Pole+/P286R mice that spontaneously acquired PtenF341V mutations and were associated with significantly reduced nuclear Pten and elevated DNA damage. Taken together with recent published work, our results support the idea that POLE-mediated hypermutagenesis is necessary, but not entirely sufficient, for tumorigenesis. Disabling surveillance of nuclear DNA damage is a likely sufficient factor.

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