The RUNX transcription factors are frequently dysregulated in human cancers, suggesting their potential as attractive targets for drug treatment. However, all three transcription factors have been described as both tumor suppressors and oncogenes, indicating the need to determine their molecular mechanisms of action. Although RUNX3 has long been considered a tumor suppressor in human cancers, several recent studies have shown that RUNX3 is upregulated during the development or progression of various malignant tumors, suggesting it may act as a “conditional” oncogene. Resolving this paradox and understanding how a single gene can exhibit both oncogenic and tumor-suppressive properties is essential for successful drug targeting of RUNX. This review describes the evidence for the activities of RUNX3 in human cancer and proposes an explanation for the duality of RUNX3 involving the status of p53. In this model, p53 deficiency causes RUNX3 to become oncogenic, leading to aberrant upregulation of MYC.

今回われわれは，切除困難な舌小細胞癌頸部リンパ節転移に対し，セツキシマブ＋FP併用療法施行後，局所切除が可能となった1例を経験したので報告する。 患者は74歳男性。右側舌と右顎下部の腫瘤形成を主訴に当科を受診した。画像検査で内頸動脈を広範囲に取り巻く右ルビエールリンパ節転移があり，切除困難例と判断し，セツキシマブ＋FP併用療法を施行した。 全身療法施行後，左側根治的頸部郭清術変法，下顎区域切除を含む腫瘍切除術に加え，咽頭後リンパ節郭清を施行した。術後はS-1併用放射線療法を施行したが，術後9ヶ月で頸部および肺に腫瘤性病変がみられたため，頸部腫瘤の切除術を施行し，小細胞癌の確定診断を得た。姑息的化学療法を施行するも奏効せず，術後1年7ヶ月に永眠となった。