分子標的薬の併用による胃癌・間質相互作用の抑制

広島大学(Hiroshima University)博士(医学)Doctor of Philosophy in Medical Sciencedoctora

Pathology Images of Scanners and Mobilephones (PLISM) - Original Whole Slide Images Dataset

The Pathology Images of Scanners and Mobilephones (PLISM) dataset was created for the evaluation of AI models’ robustness to domain shifts. PLISM is the first group-wised pathological image dataset that encompasses diverse tissue types stained under 13 H&E conditions, with multiple imaging media, including smartphones (7 scanners and 6 smartphones).The PLISM-orginal subset consists of 91 original WSIs before image registration. Color and texture in digital pathology images are affected by H&E stain conditions (e.g. Harris or Carrazi) and digitalization devices (e.g. slide scanners or smartphones), which cause inter-institutional domain shifts.The extension of each WSI file is .svs, .ndpi, or .tiff.See the other subsets of the PLISM dataset in the Collection at https://doi.org/10.25452/figshare.plus.c.6773925</p

Combining Molecular Targeted Drugs to Inhibit Both Cancer Cells and Activated Stromal Cells in Gastric Cancer

Recent studies have revealed that PDGF plays a role in promoting progressive tumor growth in several cancers, including gastric cancer. Cancer-associated fibroblasts, pericytes, and lymphatic endothelial cells in stroma express high levels of PDGF receptor (PDGF-R); cancer cells and vascular endothelial cells do not. Mammalian target of rapamycin (mTOR) is a serine/threonine kinase that increases the production of proteins that stimulate key cellular processes such as cell growth and proliferation, cell metabolism, and angiogenesis. In the present study, we examined the effects of PDGF-R tyrosine kinase inhibitor (nilotinib) and mTOR inhibitor (everolimus) on tumor stroma in an orthotopic nude mice model of human gastric cancer. Expression of PDGF-B and PDGF-Rβ mRNAs was associated with stromal volume. Treatment with nilotinib did not suppress tumor growth but significantly decreased stromal reactivity, lymphatic invasion, lymphatic vessel area, and pericyte coverage of tumor microvessels. In contrast, treatment with everolimus decreased tumor growth and microvessel density but not stromal reactivity. Nilotinib and everolimus in combination reduced both the growth rate and stromal reaction. Target molecule-based inhibition of cancer-stromal cell interaction appears promising as an effective antitumor therapy