scholarly journals Collaborating genomic, transcriptomic and microbiomic alterations lead to canine extreme intestinal polyposis

Oncotarget ◽  
2018 ◽  
Vol 9 (49) ◽  
pp. 29162-29179 ◽  
Author(s):  
Jin Wang ◽  
Tianfang Wang ◽  
Micah A. Bishop ◽  
John F. Edwards ◽  
Hang Yin ◽  
...  
Keyword(s):  
Intestinal Polyposis

Differentiated Thyroid Carcinoma and Intestinal Polyposis Syndromes

2012 ◽  
Vol 12 (4) ◽  
pp. 377-381 ◽  
Author(s):  
Vincenzo Triggiani ◽  
Vito Angelo Giagulli ◽  
Angela Tafaro ◽  
Francesco Resta ◽  
Carlo Sabba ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Differentiated Thyroid Carcinoma ◽  
Intestinal Polyposis ◽  
Polyposis Syndromes

Intestinal Polyposis Associated with Oral Pigmentation

BMJ ◽  
1953 ◽  
Vol 1 (4817) ◽  
pp. 993-993
Author(s):  
R. D. G. Creery
Keyword(s):  
Intestinal Polyposis

scholarly journals Intestinal Polyposis associated with Pigmentation of Oral Mucosa

BMJ ◽  
1954 ◽  
Vol 1 (4871) ◽  
pp. 1132-1133 ◽  
Author(s):  
R. M. T. Walker-Brash
Keyword(s):  
Oral Mucosa ◽  
Intestinal Polyposis

Familial Intestinal Polyposis

1955 ◽  
Vol 35 (5) ◽  
pp. 1277-1281 ◽  
Author(s):  
C.E. Dukes ◽  
H.E. Lockhart-Mummery
Keyword(s):  
Intestinal Polyposis

scholarly journals PTEN-deficient intestinal stem cells initiate intestinal polyposis

2007 ◽  
Vol 39 (2) ◽  
pp. 189-198 ◽  
Author(s):  
Xi C He ◽  
Tong Yin ◽  
Justin C Grindley ◽  
Qiang Tian ◽  
Toshiro Sato ◽  
...  
Keyword(s):  
Stem Cells ◽  
Intestinal Stem Cells ◽  
Intestinal Polyposis

Abstract 53: Ablation of Thrombin Signaling in Platelets but Not in Endothelial Cells Impairs Hemostasis in a Mouse Model of Spontaneous Gastrointestinal Bleeding

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Stephen J Wilson ◽  
Maria M Stevens ◽  
Shaun R Coughlin
Keyword(s):  
Myocardial Infarction ◽  
Endothelial Cells ◽  
Platelet Activation ◽  
Bleeding Risk ◽  
Arterial Disease ◽  
Gi Bleeding ◽  
Intestinal Polyposis ◽  
Wild Type ◽  
Spontaneous Bleeding ◽  
Peripheral Arterial

Human PAR1 is expressed in endothelial cells as well as in platelets where it facilitates the response to thrombin and platelet activation. Vorapaxar, a PAR1 antagonist, prevents myocardial infarction and stroke in patients with prior MI or peripheral arterial disease at a cost of increased bleeding risk. Par1 is also highly expressed in endothelial cells in mice, and Par1-deficiency is associated with bleeding in the mouse embryo at midgestation. Additionally, known actions of endothelial PAR1 activation suggest pro-hemostatic functions. This raises the question of whether inhibition of PAR1 function in endothelial cells (in addition to PAR1 inhibition in platelets) contributes to the bleeding risk associated with Vorapaxar treatment. Our previous work demonstrated that Par1 deficiency results in loss of thrombin signaling in mouse endothelial cells but not mouse platelets, while Par4 deficiency ablated thrombin-induced platelet activation in mice. Thus, mice allow us to separate loss of thrombin signaling in platelets from loss of thrombin signaling in endothelial cells. Accordingly, we used Apc min/+ mice, which develop intestinal polyposis and spontaneous GI bleeding, as a model to determine whether loss of thrombin signaling in platelets (Par4 KO) or endothelial and other cells (Par1 KO) exacerbates spontaneous bleeding. Hematocrit and other hematologic parameters were measured biweekly from 7 weeks through 15 weeks of age. Hematocrits in mice wild-type for Apc were stable over this period (41.48 ± 0.48 at 7 weeks; 40.48 ± 0.37 at 15 weeks, n=15). Hematocrits in Apc min/+ mice fell approximately linearly from 37.06 ± 0.82 at 7 weeks to 14.39 ± 1.12 at 15 weeks (n=15). Hematocrits in Par1-deficient Apc min/+ mice were indistinguishable from those in Apc min/+ without Par deficiency (14.39 ± 1.12 vs 14.47 ± 1.66 at 15 weeks; n=6-15). By contrast, Par4-deficient Apc min/+ mice were already severely anemic at 7 weeks compared to Apc min/+ mice (19 ± 2.0 vs 39 ± 3.6; p<0.01, n=4). Par-dependent differences in polyp count and size were not detected. Taken together, our results suggest that loss of thrombin signaling in platelets promotes spontaneous GI bleeding in the Apc min model while loss of thrombin signaling in endothelial cells is without effect in this system.

Nonfamilial Intestinal Polyposis and Brain Tumor in a 5-Year-Old Girl

1987 ◽  
Vol 4 (3) ◽  
pp. 247-260 ◽  
Author(s):  
Manuel A. Castello ◽  
Patrizia Operamolla ◽  
Anna Clerico ◽  
Mauro Taucci ◽  
Guglielmo Mazzoni ◽  
...  
Keyword(s):  
Brain Tumor ◽  
Intestinal Polyposis

scholarly journals Genetic Factors in Hereditary Intestinal Polyposis and Oral Pigmentation

1959 ◽  
Vol 52 (1_suppl) ◽  
pp. 123-125
Author(s):  
James A. Ferguson ◽  
Anne Van Der Woude
Keyword(s):  
Genetic Factors ◽  
Intestinal Polyposis

An overview of inherited intestinal polyposis syndromes

2014 ◽  
Vol 12 (1) ◽  
pp. 31-35 ◽  
Author(s):  
Kay Neale ◽  
Vicky Cuthill
Keyword(s):  
Intestinal Polyposis ◽  
Polyposis Syndromes
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