Molecular genetic changes in epithelial, stromal and mixed neoplasms of the endometrium
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Cited by (60)
A potpourri of pathogenetic pathways in endometrial carcinoma with a focus on Lynch Syndrome
2019, Annals of Diagnostic PathologyCitation Excerpt :A study undertaken by Broaddus et al [33] illustrated that in their cohort, all NEECs associated with LS harboured MSH2 mutations and that less NEECs were identified in LS patients than compared to the general population [33]. Microsatellites are one to five base pair sequences on DNA that are repeated a number of times and it is these short-tandem repeats that are prone to alterations in mismatch repair [16,29,30]. A repeat of CA is the most commonly occurring microsatellite identified in humans [16].
Clinicopathological analysis of mixed endometrial carcinomas: clinical relevance of different neoplastic components
2017, Human PathologyCitation Excerpt :Furthermore, although the 2014 WHO criteria defined that even the presence of 5% of each component is considered sufficient for categorizing tumors as mixed endometrial tumors, several authors suggested a different percentage of histotype components [1]. This distinction reflects the association of these components, with distinctive pathways leading to a different clinical behavior and histologic features [13-16]. In fact, although classical endometrial type I carcinomas are estrogen related and characterized by alteration of PTEN, K-Ras mutations, microsatellite instability, and late evidence of p53 mutations [25-27]; on the other hand, endometrial type II carcinomas are mostly unrelated to estrogen and with early p53 mutations [8,9].
Molecular events in endometrial carcinosarcomas and the role of high mobility group AT-hook 2 in endometrial carcinogenesis
2013, Human PathologyCitation Excerpt :Although ECSs are more aggressive than other endometrial carcinomas, the underlying molecular alterations remain poorly understood. Mutations in and loss of heterozygosity for TP53 (tumor protein p53) occur frequently in these endometrial tumors [4] together with p16 overexpression [1]. Moreover, mutations in several oncogenes have been described in some cases, such as in PIK3CA (phosphoinositide-3- kinase, catalytic, alpha polypeptide) and KRAS [5].
Searching for molecular targets in sarcoma
2012, Biochemical PharmacologyComparison of outcomes in early-stage uterine clear cell carcinoma and serous carcinoma
2019, BrachytherapyCitation Excerpt :While greater than 90% of patients with serous carcinoma harbor TP53 mutations, typically accompanied by loss of heterozygosity and nuclear protein overexpression (17), only 30–40% of patients with clear cell carcinoma harbor p53 mutations (18). Furthermore, the frequency of microsatellite instability (15%) and PTEN (30%) mutations in clear cell carcinoma is higher than that in serous carcinoma (5% and 10%, respectively) (19, 20). Moreover, DeLair et al. (21) recently evaluated the genetic heterogeneity of clear cell carcinomas and showed that it can be classified into the previously demonstrated four molecular subtypes for endometrioid and serous carcinomas.
Clear cell carcinoma of the female genital tract (not everything is as clear as it seems)
2012, Advances in Anatomic Pathology