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The Ras Gene02:38

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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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Impact of Co-Mutations and Genetic Variations on Malignancy Risk in RAS-Positive Indeterminate Thyroid Nodules: an

Lawrence Q Wong1, Zubair W Baloch2

  • 1Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, 6 Founders Pavilion, 3400 Spruce Street, Philadelphia, PA, 19104, USA.

Endocrine Pathology
|March 5, 2026
PubMed
Summary

RAS mutations in thyroid nodules are common but their prognostic role is unclear. Co-occurring genetic alterations with RAS mutations significantly increase malignancy risk, unlike isolated RAS mutations, highlighting the need for comprehensive molecular profiling.

Keywords:
NRAS/HRAS/KRASRAS mutationFollicular-patterned lesionsIEFVPTCIndeterminate cytologyNIFTPNext-generation sequencingThyroid nodule

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Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • RAS proto-oncogenes (NRAS, HRAS, KRAS) mutations are frequently detected in thyroid nodules.
  • The prognostic significance of RAS mutations, especially in conjunction with other genetic alterations, remains incompletely understood.
  • Accurate risk stratification of thyroid nodules is crucial for appropriate patient management.

Purpose of the Study:

  • To investigate the clinical and pathological implications of isolated RAS mutations versus RAS mutations with co-occurring genetic alterations in thyroid nodules.
  • To determine the association between specific molecular profiles and the risk of malignancy.
  • To evaluate the impact of co-occurring mutations on tumor aggressiveness.

Main Methods:

  • Retrospective analysis of 354 thyroid nodules from 346 patients diagnosed between 2018 and 2023.
  • Comprehensive molecular profiling to identify RAS mutations and co-occurring genetic alterations (e.g., EIF1AX, TERT).
  • Correlation of molecular findings with clinical data, pathological diagnoses, and surgical follow-up outcomes.

Main Results:

  • Isolated RAS mutations were found in 41.0% of nodules, while 54.8% had RAS with additional alterations; NRAS was the most frequent RAS subtype.
  • Malignancy rate was 52.3% overall, with NRAS mutations in 64.6% of malignant cases.
  • Nodules with RAS mutations plus concomitant alterations showed a significantly higher malignancy risk (54.3% with one additional alteration, nearly 100% with three) compared to isolated RAS mutations (p=0.0026).
  • Isolated RAS mutations were more frequently associated with benign or indolent neoplasms, whereas co-occurring mutations indicated more aggressive phenotypes.

Conclusions:

  • Co-occurring genetic alterations with RAS mutations substantially increase thyroid nodule malignancy risk and are linked to aggressive tumor phenotypes.
  • Isolated RAS mutations are more often found in indolent neoplasms.
  • Comprehensive molecular profiling is essential for precise risk stratification and guiding the management of indeterminate thyroid nodules.