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ePoster Display

1755P - A comprehensive study of the role of EIF1AX mutations in anaplastic thyroid carcinomas. Relationship with established mutational events, tumor progression and dedifferentiation

Date

16 Sep 2021

Session

ePoster Display

Topics

Targeted Therapy;  Cancer Biology;  Translational Research

Tumour Site

Thyroid Cancer

Presenters

Sara Gil

Citation

Annals of Oncology (2021) 32 (suppl_5): S1205-S1210. 10.1016/annonc/annonc715

Authors

S. Gil1, N. Feas2, S. Minguela De Pablo2, J. Fra Rodríguez3, G. García-Rostán2

Author affiliations

  • 1 Pathobiology Of Cancer, Institute of Molecular Biology and Genetics IBGM, 47007 - Valladolid/ES
  • 2 Pathobiology Of Cancer, Institute of Molecular Biology and Genetics IBGM, 47003 - Valladolid/ES
  • 3 Oncology, Hospital Universitario Rio Hortega, 47003 - Valladolid/ES

Resources

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Abstract 1755P

Background

Anaplastic thyroid carcinomas (ATCs) are fast-growing carcinomas, with a dismal prognosis. Several studies have attempted to identify new biomarkers involved in its development and behavior. The role played by EIF1AX mutations has not been fully clarified. There are significant discrepancies related to their overall frequency and mutation location.

Methods

By genotyping 69 tumor areas from 36 patients we sought to determine the prevalence, clonal nature, and implication in tumor progression of EIF1AX mutations. Mutational analysis was performed by PCR and SSCP or direct sequencing. Mutations at TERTp, BRAF, NRAS, KRAS, HRAS, and PIK3CA were evaluated in parallel to assess the level of concurrence and degree of intratumoral heterogeneity (ITGH).

Results

EIF1AX mutations were found in 8 cases(22.2%). The c.338-1G>T mutation, previously associated with thyroid cancer, did not show. Half of the mutated cases resulted clonal. EIF1AX was mutated in 50% of the cases in which a better differentiated area was investigated (8/16) and in half of those cases, it was involved in progression. In 6 cases (75%) EIF1AX mutations coexisted with other mutational events [RAS+EIF1AX (50%), BRAF+EIF1AX (33%), PIK3CA+EIF1AX (50%),TERTp+EIF1AX (100%)]. In 28 cases at least one of the 7 genes analysed resulted mutated (77.8%) [TERTp(61%), BRAF (33.3%), KRAS (8.3%), NRAS(17%), PIK3CA(22.9%) and EIF1AX(22.2%)]. ITGH was seen in 20 cases (55.6%).

Conclusions

The prevalence of EIF1AX mutations is within the range previously reported in ATC [9-33%] and much higher than in better differentiated thyroid carcinomas. EIF1AX does not seem to have a hotspot mutation as other works have reported. In agreement with the high degree of genomic instability in ATCs, EIF1AX mutations appear frequently associated with mutations in other genes. Oncogenic EIF1AX activation should be taken into consideration when applying targeted therapies to ATC patients.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

University of Valladolid- IBGM.

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.

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