431 results on '"Oshima, Hiroko"'
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2. Dual inhibition of SUMOylation and MEK conquers MYC-expressing KRAS-mutant cancers by accumulating DNA damage
3. Nano-scale physical properties characteristic to metastatic intestinal cancer cells identified by high-speed scanning ion conductance microscope
4. Toll-like Receptor 9 Promotes Initiation of Gastric Tumorigenesis by Augmenting Inflammation and Cellular Proliferation
5. Orchestration of myeloid-derived suppressor cells in the tumor microenvironment by ubiquitous cellular protein TCTP released by tumor cells
6. FOXO3 is a latent tumor suppressor for FOXO3-positive and cytoplasmic-type gastric cancer cells
7. Neutral selection and clonal expansion during the development of colon cancer metastasis.
8. Tumor-microvessel on-a-chip reveals sequential intravasation cascade of cancer cell clusters
9. Spatiotemporal observation reveals metastatic tumor-driven vascular remodeling as a potential route to polyclonal colonization
10. Identification of uromodulin deposition in the stroma of perinephric fibromyxoid nephrogenic adenoma by mass spectrometry
11. Supplementary Table S2 from Gain-of-Function p53 Mutation Acts as a Genetic Switch for TGFβ Signaling–Induced Epithelial-to-Mesenchymal Transition in Intestinal Tumors
12. Data from Gain-of-Function p53 Mutation Acts as a Genetic Switch for TGFβ Signaling–Induced Epithelial-to-Mesenchymal Transition in Intestinal Tumors
13. Supplementary Video S1A from Gain-of-Function p53 Mutation Acts as a Genetic Switch for TGFβ Signaling–Induced Epithelial-to-Mesenchymal Transition in Intestinal Tumors
14. Supplementary Figures S1-S8 from Gain-of-Function p53 Mutation Acts as a Genetic Switch for TGFβ Signaling–Induced Epithelial-to-Mesenchymal Transition in Intestinal Tumors
15. Supplementary Information from Gain-of-Function p53 Mutation Acts as a Genetic Switch for TGFβ Signaling–Induced Epithelial-to-Mesenchymal Transition in Intestinal Tumors
16. CRISPR-Cas9–mediated gene knockout in intestinal tumor organoids provides functional validation for colorectal cancer driver genes
17. Malignant subclone drives metastasis of genetically and phenotypically heterogenous cell clusters through fibrotic niche generation
18. The role of inflammation in gastric tumorigenesis
19. Contributors
20. Interleukin 1 Up-regulates MicroRNA 135b to Promote Inflammation-Associated Gastric Carcinogenesis in Mice
21. Gain-of-function p53 mutation acts as a genetic switch for TGF-β signaling-induced epithelial-to-mesenchymal transition in intestinal tumors
22. The inflammatory microenvironment that promotes gastrointestinal cancer development and invasion
23. Artists' groups in Japan and the UK and their impact on the creative individual
24. NF-κB-induced NOX1 activation promotes gastric tumorigenesis through the expansion of SOX2-positive epithelial cells
25. ROCK-I Regulates Closure of the Eyelids and Ventral Body Wall by Inducing Assembly of Actomyosin Bundles
26. The Role of Chronic Inflammation in the Promotion of Gastric Tumourigenesis
27. The Role of Inflammatory Responses in Mouse Gastric Tumorigenesis
28. Loss of wild-type p53 promotes mutant p53-driven metastasis through acquisition of survival and tumor-initiating properties
29. PGE2-Associated Inflammation and Gastrointestinal Tumorigenesis
30. Genetic and nongenetic mechanisms for colorectal cancer evolution
31. Supplementary Table S1 from Myeloid Differentiation Factor 88 Signaling in Bone Marrow–Derived Cells Promotes Gastric Tumorigenesis by Generation of Inflammatory Microenvironment
32. Data from Ink4a/Arf-Dependent Loss of Parietal Cells Induced by Oxidative Stress Promotes CD44-Dependent Gastric Tumorigenesis
33. Supplementary Methods and Figure legend from Ink4a/Arf-Dependent Loss of Parietal Cells Induced by Oxidative Stress Promotes CD44-Dependent Gastric Tumorigenesis
34. Data from Stemness Is Enhanced in Gastric Cancer by a SET/PP2A/E2F1 Axis
35. Supplementary Information from Myeloid Differentiation Factor 88 Signaling in Bone Marrow–Derived Cells Promotes Gastric Tumorigenesis by Generation of Inflammatory Microenvironment
36. Supplemental Figure S1 from Ink4a/Arf-Dependent Loss of Parietal Cells Induced by Oxidative Stress Promotes CD44-Dependent Gastric Tumorigenesis
37. Supplementary Figure 1 from Myeloid Differentiation Factor 88 Signaling in Bone Marrow–Derived Cells Promotes Gastric Tumorigenesis by Generation of Inflammatory Microenvironment
38. Supplementary Figure 5 from Myeloid Differentiation Factor 88 Signaling in Bone Marrow–Derived Cells Promotes Gastric Tumorigenesis by Generation of Inflammatory Microenvironment
39. Supplementary information from Stemness Is Enhanced in Gastric Cancer by a SET/PP2A/E2F1 Axis
40. Figure S5 from Combined Mutation of Apc, Kras, and Tgfbr2 Effectively Drives Metastasis of Intestinal Cancer
41. Table S2 from Combined Mutation of Apc, Kras, and Tgfbr2 Effectively Drives Metastasis of Intestinal Cancer
42. Data from Inflammasome Adaptor ASC Suppresses Apoptosis of Gastric Cancer Cells by an IL18-Mediated Inflammation-Independent Mechanism
43. Data from Combined Mutation of Apc, Kras, and Tgfbr2 Effectively Drives Metastasis of Intestinal Cancer
44. Supplementary Data from Inflammasome Adaptor ASC Suppresses Apoptosis of Gastric Cancer Cells by an IL18-Mediated Inflammation-Independent Mechanism
45. Supplementary Figure 1 from Induction of Prostaglandin E2 Pathway Promotes Gastric Hamartoma Development with Suppression of Bone Morphogenetic Protein Signaling
46. Data from Induction of Prostaglandin E2 Pathway Promotes Gastric Hamartoma Development with Suppression of Bone Morphogenetic Protein Signaling
47. Supplementary Figure S3 from Suppressing TGFβ Signaling in Regenerating Epithelia in an Inflammatory Microenvironment Is Sufficient to Cause Invasive Intestinal Cancer
48. Supplementary Figure 4 from Induction of Prostaglandin E2 Pathway Promotes Gastric Hamartoma Development with Suppression of Bone Morphogenetic Protein Signaling
49. Data from Suppressing TGFβ Signaling in Regenerating Epithelia in an Inflammatory Microenvironment Is Sufficient to Cause Invasive Intestinal Cancer
50. Supplementary Figure Legends from Suppressing TGFβ Signaling in Regenerating Epithelia in an Inflammatory Microenvironment Is Sufficient to Cause Invasive Intestinal Cancer
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