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1. The KRAS-G12D mutation induces metabolic vulnerability in B-cell acute lymphoblastic leukemia

2. Positive correlation between transcriptomic stemness and PI3K/AKT/mTOR signaling scores in breast cancer, and a counterintuitive relationship with PIK3CA genotype

3. Metabolic pathway alterations in microvascular endothelial cells in response to hypoxia.

4. MERIT40 Is an Akt Substrate that Promotes Resolution of DNA Damage Induced by Chemotherapy

5. JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States

6. PI3K drives the de novo synthesis of coenzyme A from vitamin B5

8. Supplementary Data from PTEN-Deficient Tumors Depend on AKT2 for Maintenance and Survival

9. Data from The Adherens Junction Protein Afadin Is an AKT Substrate that Regulates Breast Cancer Cell Migration

10. Supplementary Figures 1 - 8 from The Adherens Junction Protein Afadin Is an AKT Substrate that Regulates Breast Cancer Cell Migration

12. Data from The INPP4B Tumor Suppressor Modulates EGFR Trafficking and Promotes Triple-Negative Breast Cancer

14. Supplementary Methods, Figures S1 - S7 from PtdIns(3,4,5)P3-Dependent Activation of the mTORC2 Kinase Complex

18. Supplementary Table S3 from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States

20. Data from Aspirin Suppresses Growth in PI3K-Mutant Breast Cancer by Activating AMPK and Inhibiting mTORC1 Signaling

21. Data from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States

22. Supplementary Figures from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States

24. Data from A Secreted Form of ADAM9 Promotes Carcinoma Invasion through Tumor-Stromal Interactions

25. Supplementary Figure 1 from RhoB Differentially Controls Akt Function in Tumor Cells and Stromal Endothelial Cells during Breast Tumorigenesis

26. Supplementary Methods and Materials from RhoB Differentially Controls Akt Function in Tumor Cells and Stromal Endothelial Cells during Breast Tumorigenesis

27. Supplementary Figure 3 from RhoB Differentially Controls Akt Function in Tumor Cells and Stromal Endothelial Cells during Breast Tumorigenesis

28. Supplementary Figure 2 from RhoB Differentially Controls Akt Function in Tumor Cells and Stromal Endothelial Cells during Breast Tumorigenesis

29. Supplementary Information, Methods, Table 1, Figures 1-7 from 3-Phosphoinositide–Dependent Kinase 1 Potentiates Upstream Lesions on the Phosphatidylinositol 3-Kinase Pathway in Breast Carcinoma

31. Supplementary Figure 4 from RhoB Differentially Controls Akt Function in Tumor Cells and Stromal Endothelial Cells during Breast Tumorigenesis

32. Data from Targeting Akt3 Signaling in Triple-Negative Breast Cancer

33. Supplementary Figure 5 from RhoB Differentially Controls Akt Function in Tumor Cells and Stromal Endothelial Cells during Breast Tumorigenesis

34. Supplementary Figure 6 from RhoB Differentially Controls Akt Function in Tumor Cells and Stromal Endothelial Cells during Breast Tumorigenesis

36. Data from 3-Phosphoinositide–Dependent Kinase 1 Potentiates Upstream Lesions on the Phosphatidylinositol 3-Kinase Pathway in Breast Carcinoma

37. FGFR-inhibitor-mediated dismissal of SWI/SNF complexes from YAP-dependent enhancers induces adaptive therapeutic resistance

38. Multi-omic profiling of breast cancer cells uncovers stress MAPK-associated sensitivity to AKT degradation

40. Can improved use of biomarkers alter the fate of PI3K pathway inhibitors in the clinic?

41. WWP1 inactivation enhances efficacy of PI3K inhibitors while suppressing their toxicities in breast cancer models

43. Lactate Lights up PI3K Inhibitor Resistance in Breast Cancer

44. FGFR inhibitor mediated dismissal of SWI/SNF complexes from YAP-dependent enhancers induces adaptive therapeutic resistance

45. PI3K drives the de novo synthesis of coenzyme A from vitamin B5

46. The KRAS-G12D mutation induces metabolic vulnerability in B-cell acute lymphoblastic leukemia

47. Inhibition of the polyamine synthesis enzyme ornithine decarboxylase sensitizes triple-negative breast cancer cells to cytotoxic chemotherapy

48. Discovery of an AKT Degrader with Prolonged Inhibition of Downstream Signaling

49. Double trouble for cancer gene

50. Abstract 1400: SWI/SNF chromatin remodeling complex regulation of YAP-dependent enhancers drives therapeutic resistance in triple-negative breast cancer

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