Reviewer's report
Title:The role of prostaglandin E2 (PGE2) in toll-like receptor 4 (TLR4)-mediated
colitis-associated neoplasia
Version: 1Date:26 February 2010
Reviewer: Naofumi Mukaida
Reviewer's report:
Major comment
There are numerous reports, which indicate the indispensable roles of
COX-2-mediated prostaglandin E2 in colon carcinogenesis. The authors
demonstrated that COX-2 is present downstream TLR-4. Thus, the data in the
present paper seems to be confirmatory. The authors also tried to elucidate the
molecular mechanisms underlying prostaglandin E2-induced acceleration of
colon carcinogenesis. Low dose of prostaglandin increased the amount of
amphiregulin and phosphorylated EGF receptor without enhancing cell
proliferation. Thus, it is unlikely that amphiregulin and EGF receptor system can
be involved in prostaglandin E2-induced acceleration of colon carcinogenesis.
Thus, the authors are encouraged to provide mechanistic insights on the effects
of prostaglandin E2.
Specific comments
#1. Table 1. Tumor incidence in WT mice was calculated as 92.3 %, although the
authors used only 7 WT mice. The calculation seems to be wrong. The range of
percentage of mucosal surface with tumor is 1-40 and 1-5, in WT and
PBS-treated TLR4 KO mice, respectively. However, the incidence of these two
groups is not 100 %. Thus, the lower range of these two groups should be 0.
#2. Figure 3 B and C. The authors should describe the dose of prostaglandin E2
used in these experiments. In Fig. 3C, 15-d-PGJ2 levels should be compared
with untreated group.
#3. Figure 6A. The used dose of prostaglandin E2 should be described.
Level of interest: An article of limited interest
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Reviewer's report
Title:The role of prostaglandin E2 (PGE2) in toll-like receptor 4 (TLR4)-mediated
colitis-associated neoplasia
Version: 1Date:26 February 2010
Reviewer: Naofumi Mukaida
Reviewer's report:
Major comment
There are numerous reports, which indicate the indispensable roles of
COX-2-mediated prostaglandin E2 in colon carcinogenesis. The authors
demonstrated that COX-2 is present downstream TLR-4. Thus, the data in the
present paper seems to be confirmatory. The authors also tried to elucidate the
molecular mechanisms underlying prostaglandin E2-induced acceleration of
colon carcinogenesis. Low dose of prostaglandin increased the amount of
amphiregulin and phosphorylated EGF receptor without enhancing cell
proliferation. Thus, it is unlikely that amphiregulin and EGF receptor system can
be involved in prostaglandin E2-induced acceleration of colon carcinogenesis.
Thus, the authors are encouraged to provide mechanistic insights on the effects
of prostaglandin E2.
Specific comments
#1. Table 1. Tumor incidence in WT mice was calculated as 92.3 %, although the
authors used only 7 WT mice. The calculation seems to be wrong. The range of
percentage of mucosal surface with tumor is 1-40 and 1-5, in WT and
PBS-treated TLR4 KO mice, respectively. However, the incidence of these two
groups is not 100 %. Thus, the lower range of these two groups should be 0.
#2. Figure 3 B and C. The authors should describe the dose of prostaglandin E2
used in these experiments. In Fig. 3C, 15-d-PGJ2 levels should be compared
with untreated group.
#3. Figure 6A. The used dose of prostaglandin E2 should be described.
Level of interest: An article of limited interest
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Please review this paper.
user
Reviewer's report
Title:The role of prostaglandin E2 (PGE2) in toll-like receptor 4 (TLR4)-mediated
colitis-associated neoplasia
Version: 1Date:26 February 2010
Reviewer: Naofumi Mukaida
Reviewer's report:
Major comment
There are numerous reports, which indicate the indispensable roles of
COX-2-mediated prostaglandin E2 in colon carcinogenesis. The authors
demonstrated that COX-2 is present downstream TLR-4. Thus, the data in the
present paper seems to be confirmatory. The authors also tried to elucidate the
molecular mechanisms underlying prostaglandin E2-induced acceleration of
colon carcinogenesis. Low dose of prostaglandin increased the amount of
amphiregulin and phosphorylated EGF receptor without enhancing cell
proliferation. Thus, it is unlikely that amphiregulin and EGF receptor system can
be involved in prostaglandin E2-induced acceleration of colon carcinogenesis.
Thus, the authors are encouraged to provide mechanistic insights on the effects
of prostaglandin E2.
Specific comments
#1. Table 1. Tumor incidence in WT mice was calculated as 92.3 %, although the
authors used only 7 WT mice. The calculation seems to be wrong. The range of
percentage of mucosal surface with tumor is 1-40 and 1-5, in WT and
PBS-treated TLR4 KO mice, respectively. However, the incidence of these two
groups is not 100 %. Thus, the lower range of these two groups should be 0.
#2. Figure 3 B and C. The authors should describe the dose of prostaglandin E2
used in these experiments. In Fig. 3C, 15-d-PGJ2 levels should be compared
with untreated group.
#3. Figure 6A. The used dose of prostaglandin E2 should be described.
Level of interest: An article of limited interest
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
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