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51. Supplementary Figure 2 from Molecular Mechanisms Involved in the Synergistic Interaction of the EZH2 Inhibitor 3-Deazaneplanocin A with Gemcitabine in Pancreatic Cancer Cells

52. Supplementary Figure 1 from Molecular Mechanisms Involved in the Synergistic Interaction of the EZH2 Inhibitor 3-Deazaneplanocin A with Gemcitabine in Pancreatic Cancer Cells

53. Supplementary Figure Legend from Molecular Mechanisms Involved in the Synergistic Interaction of the EZH2 Inhibitor 3-Deazaneplanocin A with Gemcitabine in Pancreatic Cancer Cells

55. Data from Lysosomal Sequestration of Sunitinib: A Novel Mechanism of Drug Resistance

57. Supplementary Data from Tumor Drug Concentration and Phosphoproteomic Profiles After Two Weeks of Treatment With Sunitinib in Patients with Newly Diagnosed Glioblastoma

58. Supplementary Figures 1-3 from Lysosomal Sequestration of Sunitinib: A Novel Mechanism of Drug Resistance

59. Supplementary Data from Trifluorothymidine Resistance Is Associated with Decreased Thymidine Kinase and Equilibrative Nucleoside Transporter Expression or Increased Secretory Phospholipase A2

60. Supplementary Figure 1 from Crizotinib Inhibits Metabolic Inactivation of Gemcitabine in c-Met–driven Pancreatic Carcinoma

61. Data from Crizotinib Inhibits Metabolic Inactivation of Gemcitabine in c-Met–driven Pancreatic Carcinoma

62. Supplementary Methods from MicroRNA-21 in Pancreatic Cancer: Correlation with Clinical Outcome and Pharmacologic Aspects Underlying Its Role in the Modulation of Gemcitabine Activity

63. Supplementary Figure 3 from Crizotinib Inhibits Metabolic Inactivation of Gemcitabine in c-Met–driven Pancreatic Carcinoma

64. Supplementary Figure 8 from Crizotinib Inhibits Metabolic Inactivation of Gemcitabine in c-Met–driven Pancreatic Carcinoma

65. Supplementary Figure 6 from Crizotinib Inhibits Metabolic Inactivation of Gemcitabine in c-Met–driven Pancreatic Carcinoma

66. Supplementary Figure 4 from Crizotinib Inhibits Metabolic Inactivation of Gemcitabine in c-Met–driven Pancreatic Carcinoma

67. Supplementary Figure 7 from Crizotinib Inhibits Metabolic Inactivation of Gemcitabine in c-Met–driven Pancreatic Carcinoma

68. Supplementary Figures 1-5 from MicroRNA-21 in Pancreatic Cancer: Correlation with Clinical Outcome and Pharmacologic Aspects Underlying Its Role in the Modulation of Gemcitabine Activity

69. Supplementary Methods from Crizotinib Inhibits Metabolic Inactivation of Gemcitabine in c-Met–driven Pancreatic Carcinoma

70. Data from MicroRNA-21 in Pancreatic Cancer: Correlation with Clinical Outcome and Pharmacologic Aspects Underlying Its Role in the Modulation of Gemcitabine Activity

71. Supplementary Video from MicroRNA-21 in Pancreatic Cancer: Correlation with Clinical Outcome and Pharmacologic Aspects Underlying Its Role in the Modulation of Gemcitabine Activity

72. Supplementary Figure Legend from Crizotinib Inhibits Metabolic Inactivation of Gemcitabine in c-Met–driven Pancreatic Carcinoma

73. Supplementary Figure 5 from Crizotinib Inhibits Metabolic Inactivation of Gemcitabine in c-Met–driven Pancreatic Carcinoma

74. Supplementary Video 1 from Crizotinib Inhibits Metabolic Inactivation of Gemcitabine in c-Met–driven Pancreatic Carcinoma

75. Supplementary Figure 2 from Crizotinib Inhibits Metabolic Inactivation of Gemcitabine in c-Met–driven Pancreatic Carcinoma

86. Destabilizers of the thymidylate synthase homodimer accelerate its proteasomal degradation and inhibit cancer growth

90. Obituary to Lynette Fairbanks, PhD.

92. Novel insights in folate receptors and transporters: implications for disease and treatment of immune diseases and cancer

93. Author response: Destabilizers of the thymidylate synthase homodimer accelerate its proteasomal degradation and inhibit cancer growth

99. Thymidine Phosphorylase in Angiogenesis and Drug Resistance : Homology with platelet-derived endothelial cell growth factor

100. The Role of Deoxycytidine Kinase in Gemcitabine Cytotoxicity

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