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1. A cyclic dipeptide for salinity stress alleviation and the trophic flexibility of endophyte provide insights into saltmarsh plant-microbe interactions

2. Tumor Evolution of Glioma-Intrinsic Gene Expression Subtypes Associates with Immunological Changes in the Microenvironment

3. A cyclic dipeptide for salinity stress alleviation and the trophic flexibility of an endophyte reveal niches in salt marsh plant-microbe interactions

4. An enolase inhibitor for the targeted treatment of ENO1-deleted cancers

5. Homozygous MTAP deletion in primary human glioblastoma is not associated with elevation of methylthioadenosine

7. An inhibitor of oxidative phosphorylation exploits cancer vulnerability

8. Mutations in the SWI/SNF complex induce a targetable dependence on oxidative phosphorylation in lung cancer

10. Anaplerotic nutrient stress drives synergy of angiogenesis inhibitors with therapeutics targeting tumor metabolism

12. Abstract 3097: Prodrugs of a 1-hydroxy-2-oxopiperidin-3-yl phosphonate enolase inhibitor for the treatment of ENO1-deleted cancers

13. Supplementary Figures S1-S4 from A Novel B7-H6–Targeted IgG-Like T Cell–Engaging Antibody for the Treatment of Gastrointestinal Tumors

14. Comparative Pharmacology of a Bis-Pivaloyloxymethyl Phosphonate Prodrug Inhibitor of Enolase after Oral and Parenteral Administration

15. Author Correction: An enolase inhibitor for the targeted treatment of ENO1-deleted cancers

17. Prodrugs of a 1-Hydroxy-2-oxopiperidin-3-yl Phosphonate Enolase Inhibitor for the Treatment of ENO1-Deleted Cancers

18. A Novel B7-H6–Targeted IgG-Like T Cell–Engaging Antibody for the Treatment of Gastrointestinal Tumors

22. Additional file 1 of Impaired anaplerosis is a major contributor to glycolysis inhibitor toxicity in glioma

23. Correspondence to "Oral immunotherapy in alpha‐gal red meat allergy: Could specific IgE be a potential biomarker in monitoring management?".

25. Author Correction: An enolase inhibitor for the targeted treatment of ENO1-deleted cancers

26. Impaired Anaplerosis Is a Major Contributor to Glycolysis Inhibitor Toxicity in Glioma

29. Enhancer Reprogramming Confers Dependence on Glycolysis and IGF Signaling in KMT2D Mutant Melanoma

30. KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer

31. Methylthioadenosine is Not Dramatically Elevated inMTAP-Homozygous Deleted Primary Glioblastomas

32. Enhancer Reprogramming Confers Dependence on Glycolysis and IGF signaling in KMT2D Mutant Melanoma

34. Author Correction: Mutations in the SWI/SNF complex induce a targetable dependence on oxidative phosphorylation in lung cancer

35. Abstract 2831: Collateral lethality: A new target for personalized oncology

36. Eradication of ENO1-deleted Glioblastoma through Collateral Lethality

37. Tumor Evolution of Glioma-Intrinsic Gene Expression Subtypes Associates with Immunological Changes in the Microenvironment

38. TMIC-22. DECIPHERING GLIOMA INTRINSIC TRANSCRIPTIONAL SUBTYPES IDENTIFIES TUMOR EVOLUTION ASSOCIATES WITH CHANGES IN IMMUNE-MICROENVIRONMENT

39. Abstract A39: Pomhex, a cell-permeable high potency enolase inhibitor with utility for collateral lethality treatment of cancer

41. TMIC-14. TUMOR EVOLUTION OF GLIOMA INTRINSIC GENE EXPRESSION SUBTYPE ASSOCIATES WITH IMMUNOLOGICAL CHANGES IN THE MICROENVIRONMENT

42. SF2312 is a natural phosphonate inhibitor of enolase

46. Tumor evolution of glioma intrinsic gene expression subtype associates with immunological changes in the microenvironment

47. Abstract C183: Pomhex: a cell-permeable high potency Enolase inhibitor with in vivo anti-neoplastic activity

48. MTR-19A MACROPHAGE-/MICROGLIAL-RICH TUMOR MICROENVIRONMENT MIMICS PRONEURAL TO MESENCHYMAL TRANSITION IN GLIOBLASTOMA

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