TSC2 mutations were seen in both high and low grade tumors and none of the TSC2 mutated cases showed concomitant TSC1 mutations.
BRCA1 findings for all tumors are presented as Figure 2. Based on these results, ovarian cancers were divided into six groups: (1) BRCA1 mutations, (2) BRCA1 epigenetic loss, (3) equivocal for BRCA1 loss, (4) high grade serous/undifferentiated cancers without BRCA1 loss, (5) BRCA2 mutations, and (6) clear cell, endometrioid, and low grade serous cancers.
Inactivating mutation was associated with low tumour stage (P = 0.001) and low grade (P = 0.0002).
In serous lesions KRAS mutation seems to be a typical feature of borderline tumors and low grade carcinoma.
In a study that examined a larger proportion of Ta tumours (65.5% Ta, 11.5% Ta, 23% T2), a significant association of mutation with low grade and stage was found [ 24], though overall frequency was lower (13%).
This is particularly important given that the survival of patients with malignant NETs appears to be different based on the driver mutation(s) present in the tumour and low-grade or intermediate-grade tumours can have a relatively indolent growth.
Although no statistically significant associations were found, p53 mutations reflected histological progression in Barrett's patients with p53 mutations found in 30% of metaplasia patients (P=0.4) and low-grade dysplasia patients (P=0.33) and 45% of high-grade dysplasia patients (P=0.15).
The presence of KRAS alterations in both high-grade and low-grade tumors suggests that the KRAS mutation occurs earlier in the course of tumorigenesis.
ER-positive tumors versus ER-negative tumors, and low-grade tumors versus high-grade tumors, also have mutually exclusive mutations – making transition to ER-negative tumors and to high-grade tumors, respectively, during late tumor progression less likely [ 25].
Meningiomas and low-grade gliomas also occur.
