ぼくは
若いのに
2015年
骨粗鬆症
やばかつた
骨密度
骨代謝マーカー
やばかつた
骨質も
研究医
だから
骨🦴の精査
したのみ
日本
若いと
骨密度
調べない
骨代謝マーカー
若いと
調べない
日本は
骨転移🦴☠️💀
し放題
なんかね
がん患者
再発
転移
骨転移🦴💀
なんか
よろこんでる
なぜだろう?
ぼくは
2015年から
骨質
コラーゲン
など
いろいろ
補強
してる
コラーゲン
骨転移予防🦴
研究医のみ
しつてる
2015年から
骨質補強
コラーゲンも
ビタミンDも
にぼしも
いろんな
コラーゲン
試したよ
ほんま
ほんまに
値段たかいと
あかんな
The periosteum is the layer of cells that covers nearly the entire surface of every bone. Upon infection, injury or malignancy the bone surface undergoes new growth—the periosteal reaction—but the mechanism and physiological role of this process remain unknown1,2. Here we show that the periosteal reaction protects against cancer invasion into the bone. Histological analyses of human lesions of head and neck squamous cell carcinomas (HNSCCs) show that periosteal thickening occurs in proximity to the tumour. We developed a genetically dissectible mouse model of HNSCC and demonstrate that inducible depletion of periosteal cells accelerates cancerous invasion of the bone. Single-cell RNA sequencing reveals that expression of the gene encoding the protease inhibitor TIMP1 is markedly increased in the periosteum at the pre-invasive stage. This increase is due to upregulation of HIF1α expression in the tumour microenvironment, and increased TIMP1 inactivates matrix-degrading proteases, promoting periosteal thickening to inhibit cancer invasion. Genetic deletion of Timp1 impairs periosteal expansion, exacerbating bone invasion and decreasing survival in tumour-bearing mice. Together, these data show that the periosteal reaction may act as a functional stromal barrier against tumour progression, representing a unique example of tissue immunity mediated by stromal cells.