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Related Concept Videos

The Ras Gene02:38

The Ras Gene

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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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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Novel Histologic Features in Ameloblastoma With RASQ61R Mutation.

Ivan J Stojanov1, Anna M Trzcinska2,3, Mohammed Qaisi4,5

  • 1Department of Pathology and Laboratory Medicine, Cleveland Clinic.

The American Journal of Surgical Pathology
|February 19, 2025
PubMed
Summary
This summary is machine-generated.

Ameloblastoma can exhibit unusual histological features and lack typical differentiation markers. Molecular testing, particularly for RAS mutations, is crucial for diagnosing these challenging ameloblastoma cases.

Keywords:
BRAFHRASMAPKNRASameloblastic carcinomaameloblastomaodontogenic tumor

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Area of Science:

  • Oral Pathology
  • Molecular Oncology
  • Head and Neck Neoplasms

Background:

  • Ameloblastoma typically shows ameloblastic differentiation and MAPK pathway alterations, including BRAFV600E and RAS mutations.
  • These molecular profiles are consistent across known histological variants, even those with subtle differentiation.

Purpose of the Study:

  • To describe four cases of maxillary ameloblastoma with atypical histological features not aligning with established variants.
  • To highlight the importance of molecular diagnostics in identifying ameloblastoma when histological evidence is ambiguous.

Main Methods:

  • Histopathological examination of four maxillary ameloblastoma cases with unusual features.
  • Molecular analysis, including mutation-specific immunohistochemistry for RAS Q61R mutations.

Main Results:

  • Three intraosseous tumors showed spindled to basaloid cells with varied growth patterns and NRASQ61R mutations, despite minimal or absent ameloblastic differentiation.
  • A fourth peripheral case with squamoid morphology harbored HRASQ61R mutation, with positive staining supporting surface origin.

Conclusions:

  • Ameloblastoma can present with non-traditional histology, sometimes lacking overt ameloblastic differentiation, broadening the differential diagnosis.
  • Accurate diagnosis of these atypical ameloblastomas requires a high index of suspicion and confirmation via molecular testing or mutation-specific immunohistochemistry.