| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-169 |
Sentence |
denotes |
Vaccine against MUC1 antigen expressed in inflammatory bowel disease and cancer lessens colonic inflammation and prevents progression to colitis-associated colon cancer. |
| T1 |
0-169 |
Sentence |
denotes |
Vaccine against MUC1 antigen expressed in inflammatory bowel disease and cancer lessens colonic inflammation and prevents progression to colitis-associated colon cancer. |
| TextSentencer_T2 |
170-342 |
Sentence |
denotes |
Association of chronic inflammation with an increased risk of cancer is well established, but the contributions of innate versus adaptive immunity are not fully delineated. |
| T2 |
170-342 |
Sentence |
denotes |
Association of chronic inflammation with an increased risk of cancer is well established, but the contributions of innate versus adaptive immunity are not fully delineated. |
| TextSentencer_T3 |
343-553 |
Sentence |
denotes |
There has furthermore been little consideration of the role played by chronic inflammation-associated antigens, including cancer antigens, and the possibility of using them as vaccines to lower the cancer risk. |
| T3 |
343-553 |
Sentence |
denotes |
There has furthermore been little consideration of the role played by chronic inflammation-associated antigens, including cancer antigens, and the possibility of using them as vaccines to lower the cancer risk. |
| TextSentencer_T4 |
554-744 |
Sentence |
denotes |
We studied the human tumor antigen MUC1 which is abnormally expressed in colon cancers and also in inflammatory bowel disease (IBD) that gives rise to colitis-associated colon cancer (CACC). |
| T4 |
554-744 |
Sentence |
denotes |
We studied the human tumor antigen MUC1 which is abnormally expressed in colon cancers and also in inflammatory bowel disease (IBD) that gives rise to colitis-associated colon cancer (CACC). |
| TextSentencer_T5 |
745-957 |
Sentence |
denotes |
Using our new mouse model of MUC1(+) IBD that progresses to CACC, interleukin-10 knockout mice crossed with MUC1 transgenic mice, we show that vaccination against MUC1 delays IBD and prevents progression to CACC. |
| T5 |
745-957 |
Sentence |
denotes |
Using our new mouse model of MUC1(+) IBD that progresses to CACC, interleukin-10 knockout mice crossed with MUC1 transgenic mice, we show that vaccination against MUC1 delays IBD and prevents progression to CACC. |
| TextSentencer_T6 |
958-1121 |
Sentence |
denotes |
One mechanism is the induction of MUC1-specific adaptive immunity (anti-MUC1 IgG and anti-MUC1 CTL), which seems to eliminate abnormal MUC1(+) cells in IBD colons. |
| T6 |
958-1121 |
Sentence |
denotes |
One mechanism is the induction of MUC1-specific adaptive immunity (anti-MUC1 IgG and anti-MUC1 CTL), which seems to eliminate abnormal MUC1(+) cells in IBD colons. |
| TextSentencer_T7 |
1122-1204 |
Sentence |
denotes |
The other mechanism is the change in the local and the systemic microenvironments. |
| T7 |
1122-1204 |
Sentence |
denotes |
The other mechanism is the change in the local and the systemic microenvironments. |
| TextSentencer_T8 |
1205-1441 |
Sentence |
denotes |
Compared with IBD in vaccinated mice, IBD in control mice is dominated by larger numbers of neutrophils in the colon and myeloid-derived suppressor cells in the spleen, which can compromise adaptive immunity and facilitate tumor growth. |
| T8 |
1205-1441 |
Sentence |
denotes |
Compared with IBD in vaccinated mice, IBD in control mice is dominated by larger numbers of neutrophils in the colon and myeloid-derived suppressor cells in the spleen, which can compromise adaptive immunity and facilitate tumor growth. |
| TextSentencer_T9 |
1442-1642 |
Sentence |
denotes |
This suggests that the tumor-promoting microenvironment of chronic inflammation can be converted to a tumor-inhibiting environment by increasing adaptive immunity against a disease-associated antigen. |
| T9 |
1442-1642 |
Sentence |
denotes |
This suggests that the tumor-promoting microenvironment of chronic inflammation can be converted to a tumor-inhibiting environment by increasing adaptive immunity against a disease-associated antigen. |