In addition, they play a critical role in tumor formation, specifically in the etiology of human adamantinomatous craniopharyngioma, a clinically relevant tumor that is associated with mutations in CTNNB1 (gene encoding β-catenin).
In this review, we outline six major areas of advances: (i) changes in terminology from 'adenoma' to 'pituitary neuroendocrine tumour'; (ii) reclassification of hormone-negative tumours based on transcription factor expression that defines lineage; (iii) updates in new pathogenetic mechanisms, including those that underlie rare lesions such as X-LAG and pituitary blastoma; (iv) clarification of hypophysitis due to immunotherapy, xanthomatous hypophysitis due to rupture of a Rathke's cleft cyst and IgG4 disease as the cause of inflammatory pseudotumour; (v) the consolidation of pituicytoma variants, including spindle cell oncocytoma and granular cell tumour based on thyroid transcription factor-1 (TTF-1) reactivity; and (vi) the pathogenetic mechanisms that distinguish papillary from adamantinomatous craniopharyngioma.
In this study, we have investigated the influence of the quaternary structure of 2-trans-enoyl-ACP (CoA) reductase or InhA, from Mycobacterium tuberculosis, to its flexibility.
In this study, we have investigated the influence of the quaternary structure of 2-trans-enoyl-ACP (CoA) reductase or InhA, from Mycobacterium tuberculosis, to its flexibility.
Indeed, removal of zinc(II) ion from ISCU causes a moderate but significant increase in activity compared to SDA alone, and FXN can activate both zinc-depleted and zinc-bound forms of ISCU complexed to SDA.
Indeed, removal of zinc(II) ion from ISCU causes a moderate but significant increase in activity compared to SDA alone, and FXN can activate both zinc-depleted and zinc-bound forms of ISCU complexed to SDA.
Mutations in the CTNNB1 gene are primary drivers of adamantinomatous craniopharyngioma (ACP) and lead to the accumulation of β-catenin protein in a subset of the nuclei within the neoplastic epithelium of these tumors.
Mutations or polymorphisms in pituitary transcription factors are unlikely to contribute to the adamantinomatous craniopharyngioma pathogenesis, differently of CTNNB1 mutations.
Nuclear β-catenin, a hallmark of active canonical Wnt signaling, can be histologically detected in a subset of cells and cell clusters in up to 94% of adamantinomatous craniopharyngioma (ACP) samples.