On 2014 May 01, Giovanni M. Dall’Olio commented:

Interesting article that explores the role of pseudogene formation by retrotranscription of mRNAs in somatic cells in cancer.

After reading the article, my impression is that pseudogene formation is not a major process driving cancer. In fact, the percentage of pseudogenes found in the cancer samples analyzed is relatively low, and only few of these cases seem to be relevant to the cancer process. However, it is very good to have an estimate of how much somatic retrotransposition is important in cancer, and to have a few examples of newly formed pseudogenes causing damage to the expression of cancer genes.

One detail that didn't convince me of the article is the result presented in Figure 3. I don't think there are enough points for the Wilcoxon test, except maybe only for the lung samples. Maybe a permutation test would be more robust, although the real problem is that there are too few data points.

A colleague of mine also noted, from Figure 1, that most of the pseudogenes observed seem to be patient-specific, rather than cancer-type specific. For example patient PD7354 (if we interpret the sample naming scheme right) seems to host half of pseudogene events observed. Can it be that this individual is somehow more prone to this process, e.g. that retrontransposon activity is higher in this individual?

It would also be useful to have an estimate of the overall mutation rate in somatic cells in the samples analyzed, to know if this correlates with pseudogene formation.

Congratulations again to the author for the work presented.

On 2014 May 01, Giovanni M. Dall’Olio commented:

Interesting article that explores the role of pseudogene formation by retrotranscription of mRNAs in somatic cells in cancer.

After reading the article, my impression is that pseudogene formation is not a major process driving cancer. In fact, the percentage of pseudogenes found in the cancer samples analyzed is relatively low, and only few of these cases seem to be relevant to the cancer process. However, it is very good to have an estimate of how much somatic retrotransposition is important in cancer, and to have a few examples of newly formed pseudogenes causing damage to the expression of cancer genes.

One detail that didn't convince me of the article is the result presented in Figure 3. I don't think there are enough points for the Wilcoxon test, except maybe only for the lung samples. Maybe a permutation test would be more robust, although the real problem is that there are too few data points.

A colleague of mine also noted, from Figure 1, that most of the pseudogenes observed seem to be patient-specific, rather than cancer-type specific. For example patient PD7354 (if we interpret the sample naming scheme right) seems to host half of pseudogene events observed. Can it be that this individual is somehow more prone to this process, e.g. that retrontransposon activity is higher in this individual?

It would also be useful to have an estimate of the overall mutation rate in somatic cells in the samples analyzed, to know if this correlates with pseudogene formation.

Congratulations again to the author for the work presented.