Relationship between the Expression of CHK2 and p53 in Tumor Tissue and the Course of Papillary Thyroid Cancer in Patients with CHEK2 Germline Mutations.

Autor: Gąsior-Perczak, Danuta, Kowalik, Artur, Kopczyński, Janusz, Macek, Paweł, Niemyska, Kornelia, Walczyk, Agnieszka, Gruszczyński, Krzysztof, Siołek, Monika, Dróżdż, Tomasz, Kosowski, Marcin, Pałyga, Iwona, Przybycień, Piotr, Wabik, Olga, Góźdź, Stanisław, Kowalska, Aldona
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Zdroj: Cancers; Feb2024, Vol. 16 Issue 4, p815, 22p
Abstrakt: Simple Summary: CHK2 has functions in DNA damage repair. Germline CHEK2 mutations impair these functions, increasing the risk of PTC. The aim of this study was to determine whether CHK2 and p53 expression in patients with a germline CHEK2 mutation in tumor tissue can serve as a prognostic marker for papillary thyroid cancer (PTC), and whether copy number aberrations in CHEK2 and TP53 correlate with the course of PTC. This study included 156 patients with PTC who had been selected from a group of 1547 people previously tested for the presence of CHEK2 mutations in their peripheral blood. Higher CHK2 expression was associated with poorer treatment responses and disease outcomes in PTC patients. Higher CHK2 expression and positive p53 together with a TP53 deletion could have potential as a prognostic marker of unfavorable disease outcomes in patients with germline truncating mutations in CHEK2. The aim of this study was to determine whether the expression of CHK2 and p53 in tumor tissue in carriers of germline CHEK2 mutations can serve as a prognostic marker for PTC, and whether CHEK2 and TP53 copy numbers correlates with the course of PTC disease. This study included 156 PTC patients previously tested for the presence of CHEK2. Clinicopathological features, treatment response, disease outcome, and germline mutation status of the CHEK2 gene were assessed with respect to CHK2 and p53 expression, and CHEK2 and TP53 gene copy statuses. In patients with and without a germline mutation in CHEK2 and with higher CHK2 expression, the chances of an excellent treatment response and no evidence of disease were lower than in patients without or with lower CHK2 expression. TP53 deletion was associated with angioinvasion. In patients with a truncating mutation, the chance of a CHEK2 deletion was higher than in patients with WT CHEK2 alone or those with WT CHEK2 and with the missense I157T mutation. Higher CHK2 expression was associated with poorer treatment responses and disease outcomes. Higher CHK2 expression and positive p53 together with a TP53 deletion could be a prognostic marker of unfavorable disease outcomes in patients with germline truncating mutations in CHEK2. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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