mortality/aging
• mice with DSS-induced colitis show more than 80% mortality rate compared to 30% of wild-type mice
(J:248779)
• DSS-treated mice exhibit increased weight loss, colon shortening and mortality with more severe diarrhea and hematochezia compared with wild-type mice
(J:280467)
• AOM/DSS-treated mice exhibit increased weight loss and higher tumor burdens and tumor size with more severe diarrhea and hematochezia compared with wild-type mice
(J:280467)
|
• DSS and AOM treated mice show earlier and higher mortality than wild-type mice
|
• after DSS treatment
|
digestive/alimentary system
• decreased in AOM/DSS-treated mice
|
• increased in AOM/DSS-treated mice
|
• DSS and AOM treated mice exhibit reduced colon length
|
• mice exhibit increased susceptibility to DSS-induced colitis, showing sustained weight loss, rectal bleeding and diarrhea after removal of DSS compared to wild-type mice which start recovering
• DSS-induced mice show increased damage and delayed recovery of the epithelial layer, characterized by more infiltrating inflammatory cells, ulceration, and hyperplasia
• DSS-induced mice show increased inflammatory cytokines and chemokines which remain elevated during the recovery phase
|
• mice with DSS-induced colitis show more than 80% mortality rate compared to 30% of wild-type mice
(J:248779)
• DSS-treated mice exhibit increased weight loss, colon shortening and mortality with more severe diarrhea and hematochezia compared with wild-type mice
(J:280467)
• AOM/DSS-treated mice exhibit increased weight loss and higher tumor burdens and tumor size with more severe diarrhea and hematochezia compared with wild-type mice
(J:280467)
|
neoplasm
• mice treated with both DSS and AOM show increased colitis-associated colorectal tumorigenesis, having a higher tumor burden in the colon and increased tumor size
(J:248779)
• DSS and AOM treated mice develop aberrant crypt focus which progresses into tubular adenoma and adenocarcinoma
(J:248779)
• tumors from DSS and AOM treated mice exhibit a higher proliferation rate and undergo less apoptosis than wild-type tumor cells
(J:248779)
• higher tumor burdens, increased tumor size and high-grade dysplasia in AOM/DSS-treated mice
(J:280467)
|
growth/size/body
• in DSS-treated mice
(J:248779)
• in DSS-treated mice
(J:280467)
|
cellular
• decreased in AOM/DSS-treated mice
|
• increased in AOM/DSS-treated mice
|
homeostasis/metabolism
• DSS-induced mice show increased inflammatory cytokines and chemokines which remain elevated during the recovery phase
|
• after DSS treatment
|
• mice treated with both DSS and AOM show increased colitis-associated colorectal tumorigenesis, having a higher tumor burden in the colon and increased tumor size
(J:248779)
• DSS and AOM treated mice develop aberrant crypt focus which progresses into tubular adenoma and adenocarcinoma
(J:248779)
• tumors from DSS and AOM treated mice exhibit a higher proliferation rate and undergo less apoptosis than wild-type tumor cells
(J:248779)
• higher tumor burdens, increased tumor size and high-grade dysplasia in AOM/DSS-treated mice
(J:280467)
|
immune system
• mice exhibit increased susceptibility to DSS-induced colitis, showing sustained weight loss, rectal bleeding and diarrhea after removal of DSS compared to wild-type mice which start recovering
• DSS-induced mice show increased damage and delayed recovery of the epithelial layer, characterized by more infiltrating inflammatory cells, ulceration, and hyperplasia
• DSS-induced mice show increased inflammatory cytokines and chemokines which remain elevated during the recovery phase
|
• mice with DSS-induced colitis show more than 80% mortality rate compared to 30% of wild-type mice
(J:248779)
• DSS-treated mice exhibit increased weight loss, colon shortening and mortality with more severe diarrhea and hematochezia compared with wild-type mice
(J:280467)
• AOM/DSS-treated mice exhibit increased weight loss and higher tumor burdens and tumor size with more severe diarrhea and hematochezia compared with wild-type mice
(J:280467)
|
• DSS-induced mice show increased inflammatory cytokines and chemokines which remain elevated during the recovery phase
|