Reviewer's report
Title:The pro-apoptotic K-Ras 4A proto-oncoprotein does not affect
tumorigenesis in the ApcMin/+ mouse small intestine
Version: 1Date:3 January 2008
Reviewer: Sylvie Robine
Reviewer's report:
The ratio of Kras 4A/ Kras 4B splicing variants is frequently altered in intestinal
tumours. The authors want to study the effect of K-Ras 4A splicing variant
deficiency in intestinal tumorigenesis without affecting the transcription of the
K-Ras 4B splicing variant.
To this purpose, they use mice deficient for the K-Ras 4A splicing variant in an
APC Min/+ background. The APC Min/+ mice develop spontaneously a high
number of intestinal tumours.
They expect to accelerate tumorigenesis in absence of the K-Ras 4A splicing
variant. But, in fact, they show that in absence of K-Ras 4A, there is no effect on
tumorigenesis driven by the mutation of APC, as shown by unaffected mouse
survival and unmodified tumour number and size.
One comment: The authors show that in WT intestinal epithelium and in APC
Min/+ normal intestinal epithelium, the K-Ras4A/ K-Ras4B ratio is about 50% and
is comparable between WT and APC Min/+ mice. It would be interesting to show
what is the K-Ras 4A/ 4B ratio in tumours arising spontaneously in the APC
Min/+ mice. Evaluation of proliferation and apoptosis as well as tumour grading
could be performed in order to better characterize the tumours in both genetic
backgrounds.
What next?: Accept after minor essential revisions
Level of interest: An article whose findings are important to those with closely
related research interests
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
'I declare that I have no competing interests'
Reviewer's report
Title:The pro-apoptotic K-Ras 4A proto-oncoprotein does not affect
tumorigenesis in the ApcMin/+ mouse small intestine
Version: 1Date:3 January 2008
Reviewer: Sylvie Robine
Reviewer's report:
The ratio of Kras 4A/ Kras 4B splicing variants is frequently altered in intestinal
tumours. The authors want to study the effect of K-Ras 4A splicing variant
deficiency in intestinal tumorigenesis without affecting the transcription of the
K-Ras 4B splicing variant.
To this purpose, they use mice deficient for the K-Ras 4A splicing variant in an
APC Min/+ background. The APC Min/+ mice develop spontaneously a high
number of intestinal tumours.
They expect to accelerate tumorigenesis in absence of the K-Ras 4A splicing
variant. But, in fact, they show that in absence of K-Ras 4A, there is no effect on
tumorigenesis driven by the mutation of APC, as shown by unaffected mouse
survival and unmodified tumour number and size.
One comment: The authors show that in WT intestinal epithelium and in APC
Min/+ normal intestinal epithelium, the K-Ras4A/ K-Ras4B ratio is about 50% and
is comparable between WT and APC Min/+ mice. It would be interesting to show
what is the K-Ras 4A/ 4B ratio in tumours arising spontaneously in the APC
Min/+ mice. Evaluation of proliferation and apoptosis as well as tumour grading
could be performed in order to better characterize the tumours in both genetic
backgrounds.
What next?: Accept after minor essential revisions
Level of interest: An article whose findings are important to those with closely
related research interests
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
'I declare that I have no competing interests'
Please review this paper.
user
Reviewer's report
Title:The pro-apoptotic K-Ras 4A proto-oncoprotein does not affect
tumorigenesis in the ApcMin/+ mouse small intestine
Version: 1Date:3 January 2008
Reviewer: Sylvie Robine
Reviewer's report:
The ratio of Kras 4A/ Kras 4B splicing variants is frequently altered in intestinal
tumours. The authors want to study the effect of K-Ras 4A splicing variant
deficiency in intestinal tumorigenesis without affecting the transcription of the
K-Ras 4B splicing variant.
To this purpose, they use mice deficient for the K-Ras 4A splicing variant in an
APC Min/+ background. The APC Min/+ mice develop spontaneously a high
number of intestinal tumours.
They expect to accelerate tumorigenesis in absence of the K-Ras 4A splicing
variant. But, in fact, they show that in absence of K-Ras 4A, there is no effect on
tumorigenesis driven by the mutation of APC, as shown by unaffected mouse
survival and unmodified tumour number and size.
One comment: The authors show that in WT intestinal epithelium and in APC
Min/+ normal intestinal epithelium, the K-Ras4A/ K-Ras4B ratio is about 50% and
is comparable between WT and APC Min/+ mice. It would be interesting to show
what is the K-Ras 4A/ 4B ratio in tumours arising spontaneously in the APC
Min/+ mice. Evaluation of proliferation and apoptosis as well as tumour grading
could be performed in order to better characterize the tumours in both genetic
backgrounds.
What next?: Accept after minor essential revisions
Level of interest: An article whose findings are important to those with closely
related research interests
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
'I declare that I have no competing interests'
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