Comparative immunohistochemical expression of β-catenin, EGFR, ErbB2, and p63 in adamantinomatous and papillary craniopharyngiomas

Abstract

Nuclear accumulation of β-catenin is a diagnostic hallmark of the ACP and is very helpful in the differential diagnosis between both ACP and PCP in the setting of small biopsies. Moreover, the restricted nuclear β-catenin accumulation in the cohesive cell clusters within the whorl-like areas supports that aberrant β-catenin expression may play a role in the morphogenesis of ACP.

Molecular pathology of adamantinomatous craniopharyngioma: review and opportunities for practice

“…In the limited molecular studies to date, increased expression of proliferation markers and TP53 have been observed in malignantly transformed specimens as well as in some rapidly recurring tumors. 25,41 While TP53 expression appears to be rare in nontransformed ACP, its related family member TP63 is widely expressed, particularly the deltaNp63 isoform 11,14,37 translating the therapeutic Opportunities and Challenges Ahead…”

Potential evolution of neurosurgical treatment paradigms for craniopharyngioma based on genomic and transcriptomic characteristics

“…9,11,12,24,28,38 As a result of this mechanism, nuclear accumulation of b-catenin is a histological hallmark of CTNNB1 mutation. 10,12,16,26,41 In the case of craniopharyngiomas, mutation of CTNNB1 has been described in 69%-100% 9,20,28 of ACP specimens, while it is not routinely observed in PCP or other parasellar tumors. 9,28 In the most detailed study to date, CTNNB1 mutation was identified in 95% of ACP specimens, using massively parallel sequencing and targeted genotyping.…”

“…10,32 This protein plays a critical role in development, cellular proliferation, differentiation, and cell migration. 10,11,16,41 A destruction complex restrains b-catenin within the cytosol and facilitates its ubiquitination and proteasomal degradation. 31 The Wnt protein family includes approximately 20 different proteins that bind to the Frizzled (Fz) family of receptors.…”

“…When Wnt proteins bind the Fz receptors, the Wnt pathway is activated, 31 leading to an intracellular signaling cascade that ultimately prevents formation of the b-catenin destruction complex. 9,11,16,22,31 Without the destruction complex, b-catenin protein accumulates and ultimately translocates to the nucleus, where it facilitates transcription of b-catenin target genes and stimulates cellular proliferation and other Wnt regulated cellular processes. 8,9,11,16,22,31 Increased migratory capacity and invasiveness have been observed in neoplastic cells with elevated b-catenin levels and activated target genes.…”

“…9,11,16,22,31 Without the destruction complex, b-catenin protein accumulates and ultimately translocates to the nucleus, where it facilitates transcription of b-catenin target genes and stimulates cellular proliferation and other Wnt regulated cellular processes. 8,9,11,16,22,31 Increased migratory capacity and invasiveness have been observed in neoplastic cells with elevated b-catenin levels and activated target genes. 22 In ACP, b-catenin accumulation can be found within cell clusters localized at invasive protrusions of tumor into normal brain 22 ( Fig.…”