scholarly journals Molecular alterations and expression of succinate dehydrogenase complex in wild-type KIT/PDGFRA/BRAF gastrointestinal stromal tumors

2012 ◽  
Vol 21 (5) ◽  
pp. 503-510 ◽  
Author(s):  
Ricardo Celestino ◽  
Jorge Lima ◽  
Alexandra Faustino ◽  
João Vinagre ◽  
Valdemar Máximo ◽  
...  
2013 ◽  
Vol 9 (1) ◽  
pp. 121-126 ◽  
Author(s):  
Margherita Nannini ◽  
Annalisa Astolfi ◽  
Paola Paterini ◽  
Milena Urbini ◽  
Donatella Santini ◽  
...  

2019 ◽  
Vol 12 ◽  
pp. 251686571984253 ◽  
Author(s):  
Gloria Ravegnini ◽  
Riccardo Ricci

Various molecular triggers define heterogeneous subsets of gastrointestinal stromal tumors (GISTs), differing in clinical behavior and drug sensitivity. KIT/PDGFRA-wild-type GISTs, including those succinate dehydrogenase (SDH)-deficient, are overall unresponsive to the tyrosine kinase inhibitors commonly used, fostering the development of specific alternative therapeutic strategies. Epigenetic inactivation of O6-methylguanine-DNA methyltransferase (MGMT) through promoter methylation leads to effectiveness of alkylating agents in several human cancers. SDH-deficient GISTs typically feature widespread DNA methylation. However, the actual occurrence of MGMT methylation in these tumors, potentially predisposing them to respond to alkylating drugs, has not been investigated so far. Here we discuss the recent findings concerning the occurrence of MGMT methylation in different GIST subgroups, including SDH-deficient ones, as a premise for a possible reappraisal of alkylating agents specifically targeting these small, otherwise overall chemorefractory, GIST subgroups.


2013 ◽  
Vol 22 (1) ◽  
pp. 32-39 ◽  
Author(s):  
Maria A Pantaleo ◽  
◽  
Annalisa Astolfi ◽  
Milena Urbini ◽  
Margherita Nannini ◽  
...  

2010 ◽  
Vol 28 (15_suppl) ◽  
pp. 10008-10008 ◽  
Author(s):  
K. A. Janeway ◽  
S. Kim ◽  
M. Lodish ◽  
V. Nose ◽  
P. Dahia ◽  
...  

2021 ◽  
Vol 24 (1) ◽  
pp. 67-72
Author(s):  
H Ozkayalar ◽  
MC Ergoren ◽  
G Tuncel ◽  
S Kurt ◽  
E Cevik ◽  
...  

Abstract Being one of the leading causes of cancer deaths worldwide and their resistance to conventional treatment methods, made gastrointestinal stromal tumors (GISTs) one of the hot topics in medical research areas in the past decade. To investigate molecular alterations underlying the tumor is of great importance to be able to develop new, targeted treatment options. In this study, GIST samples obtained from 40 Turkish patients were analyzed for actionable epidermal growth factor receptor (EGFR) mutations that are related to treatment regimes in non small cell lung cancer (NSCLC) to understand whether EGFR expression is altered in GISTs. Established alterations in EGFR can make the use of tyrosine kinase inhibitors possible, which are currently used in cancer therapy, especially in NSCLC. Our results indicated that EGFR mutations are rare in GISTs. Further research is needed to sequence whole coding regions of the gene to investigate new actionable mutations in EGFR in an increased sample size.


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