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Exact(5)

Immunohistochemical evaluation showed that loss of immunoreactivity to the antibody against the carboxyl terminus of the APC protein, presumably resulting from APC gene mutations, was more frequent in syndromic than in sporadic cases (40% versus 6.7%, P < 0.001).

The dates estimated for the duplications appear large as accumulation of silent mutations was more pronounced in this lineage.

A theoretical analysis demonstrated that this repeated presence of mutations was more probably due to their generation multiple times than to recombination [ 26].

An analysis of HCC development during the patient follow-up period revealed that the presence of G1613A and/or C1653T mutations was more prevalent in patients who developed HCC long afterward, as compared to the patients who never developed HCC.

To assess negative selection in the exome, we checked whether (i) there was a lower mutation frequency in the exome relative to the whole-genome, and whether (ii) the frequency of somatic mutations was more prominently decreased in the exome.

Similar(55)

Mutator mutations are more likely to occur early, and to occur when more oncogenic mutations are required to create a tumor.

In MDSs, U2AF1 mutations are more frequent in ASXL1-mutated than in ASXL1-wildtype cases [ 38, 42].

The present study revealed that PIK3CA mutations were more common in MSI and BRAF mutated tumours.

SDHB and SDHD mutations are more common, whereas SDHA and SDHC mutations are rare.

Somatic mutations are more common, and might account for malignant transformation of sporadic tumors.

In addition, smaller tumors (<4 cm) with PBRM1 mutations are more likely to exhibit stage II pathologic features.

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