Christoph Bartenhagen

Abstract Alternative lengthening of telomeres (ALT) is a specialized telomere extension mechanism associated with 5–10% of all cancers1. Although ALT has been linked to epigenetic dysregulation and genome instability, specific genomic and epigenetic rearrangements generated after ALT activation have not been identified.

Keywords ferroptosis cancer metabolism selenium selenocysteine metabolism cell death neuroblastoma Introduction Ferroptosis is a non-apoptotic form of cell death characterized by the iron-dependent accumulation of phospholipid hydroperoxides, ultimately leading to membrane rupture and cell death.1 Due to its association with various pathological conditions, including cancer, neurodegeneration, and tissue damage,2 the mechanisms regulating ferroptosis have garnered increasing interest.

ORIGINAL REPORTS Introduction Neuroendocrine neoplasms of the lung are classified into typical carcinoid, atypical carcinoid (AC), large-cell neuroendocrine carcinoma (LCNEC), and small cell lung cancer (SCLC) on the basis of histologic criteria.1,2 Pulmonary carcinoids account for 1%-2% of all lung tumors.