231 results on '"Klarenbeek, Sjoerd"'
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2. Natural deletion of mouse carboxylesterases Ces1c/d/e impacts drug metabolism and metabolic syndrome development
3. LGR6-dependent conditional inactivation of E-cadherin and p53 leads to invasive skin and mammary carcinomas in mice
4. Truncated FGFR2 is a clinically actionable oncogene in multiple cancers
5. RNF31 inhibition sensitizes tumors to bystander killing by innate and adaptive immune cells
6. Publisher Correction: Truncated FGFR2 is a clinically actionable oncogene in multiple cancers
7. Exogenous ERα Expression in the Mammary Epithelium Decreases Over Time and Does Not Contribute to p53-Deficient Mammary Tumor Formation in Mice
8. MYC is a clinically significant driver of mTOR inhibitor resistance in breast cancer
9. Multiple low dose therapy as an effective strategy to treat EGFR inhibitor-resistant NSCLC tumours
10. Neoadjuvant immune checkpoint blockade triggers persistent and systemic Treg activation which blunts therapeutic efficacy against metastatic spread of breast tumors
11. Abstract 3488: Truncated FGFR2 - a clinically actionable oncogene in multiple cancers
12. Supplementary data from Transcriptomics and Transposon Mutagenesis Identify Multiple Mechanisms of Resistance to the FGFR Inhibitor AZD4547
13. Supplementary Table 1 from Truncated ASPP2 Drives Initiation and Progression of Invasive Lobular Carcinoma via Distinct Mechanisms
14. Data from Truncated ASPP2 Drives Initiation and Progression of Invasive Lobular Carcinoma via Distinct Mechanisms
15. Supplementary Figures S1-5 from Transcriptomics and Transposon Mutagenesis Identify Multiple Mechanisms of Resistance to the FGFR Inhibitor AZD4547
16. Data from A BRCA1 Coiled-Coil Domain Variant Disrupting PALB2 Interaction Promotes the Development of Mammary Tumors and Confers a Targetable Defect in Homologous Recombination Repair
17. Supplementary Table 2 from Truncated ASPP2 Drives Initiation and Progression of Invasive Lobular Carcinoma via Distinct Mechanisms
18. Supplementary Figures from Truncated ASPP2 Drives Initiation and Progression of Invasive Lobular Carcinoma via Distinct Mechanisms
19. Supplementary Data from A BRCA1 Coiled-Coil Domain Variant Disrupting PALB2 Interaction Promotes the Development of Mammary Tumors and Confers a Targetable Defect in Homologous Recombination Repair
20. Data from Transcriptomics and Transposon Mutagenesis Identify Multiple Mechanisms of Resistance to the FGFR Inhibitor AZD4547
21. Supplementary Figure 2 from Loss of p120-Catenin Induces Metastatic Progression of Breast Cancer by Inducing Anoikis Resistance and Augmenting Growth Factor Receptor Signaling
22. Supplementary Figure Legend from A Preclinical Mouse Model of Invasive Lobular Breast Cancer Metastasis
23. Supplementary Methods from A Preclinical Mouse Model of Invasive Lobular Breast Cancer Metastasis
24. Supplementary Figure 3 from Loss of p120-Catenin Induces Metastatic Progression of Breast Cancer by Inducing Anoikis Resistance and Augmenting Growth Factor Receptor Signaling
25. Supplementary Table 1 from A Preclinical Mouse Model of Invasive Lobular Breast Cancer Metastasis
26. Supplementary Figure Legends from Loss of p120-Catenin Induces Metastatic Progression of Breast Cancer by Inducing Anoikis Resistance and Augmenting Growth Factor Receptor Signaling
27. Supplementary Figure 1 from A Preclinical Mouse Model of Invasive Lobular Breast Cancer Metastasis
28. Data from A Preclinical Mouse Model of Invasive Lobular Breast Cancer Metastasis
29. Supplementary Figure 5 from Loss of p120-Catenin Induces Metastatic Progression of Breast Cancer by Inducing Anoikis Resistance and Augmenting Growth Factor Receptor Signaling
30. Supplementary Figure 6 from Loss of p120-Catenin Induces Metastatic Progression of Breast Cancer by Inducing Anoikis Resistance and Augmenting Growth Factor Receptor Signaling
31. Supplementary Figure 1 from Loss of p120-Catenin Induces Metastatic Progression of Breast Cancer by Inducing Anoikis Resistance and Augmenting Growth Factor Receptor Signaling
32. Supplementary Figure 2 from A Preclinical Mouse Model of Invasive Lobular Breast Cancer Metastasis
33. Supplementary Figure 4 from Loss of p120-Catenin Induces Metastatic Progression of Breast Cancer by Inducing Anoikis Resistance and Augmenting Growth Factor Receptor Signaling
34. Supplementary Table 3 from Loss of p120-Catenin Induces Metastatic Progression of Breast Cancer by Inducing Anoikis Resistance and Augmenting Growth Factor Receptor Signaling
35. Supplementary Table 4 from Loss of p120-Catenin Induces Metastatic Progression of Breast Cancer by Inducing Anoikis Resistance and Augmenting Growth Factor Receptor Signaling
36. Supplementary Table 1 from Loss of p120-Catenin Induces Metastatic Progression of Breast Cancer by Inducing Anoikis Resistance and Augmenting Growth Factor Receptor Signaling
37. Supplementary Table 2 from Loss of p120-Catenin Induces Metastatic Progression of Breast Cancer by Inducing Anoikis Resistance and Augmenting Growth Factor Receptor Signaling
38. Supplementary Figure 3 from A Preclinical Mouse Model of Invasive Lobular Breast Cancer Metastasis
39. Supplementary Materials and Methods from Loss of p120-Catenin Induces Metastatic Progression of Breast Cancer by Inducing Anoikis Resistance and Augmenting Growth Factor Receptor Signaling
40. Supplementary Figure 4 from A Preclinical Mouse Model of Invasive Lobular Breast Cancer Metastasis
41. MYC is a clinically significant driver of mTOR inhibitor resistance in breast cancer
42. MYC is a clinically significant driver of mTOR inhibitor resistance in breast cancer
43. Natural deletion of mouse carboxylesterases Ces1c/d/e impacts drug metabolism and metabolic syndrome development
44. LGR6-dependent conditional inactivation of E-cadherin and p53 leads to invasive skin and mammary carcinomas in mice
45. Conserved crosstalk between histone deacetylation and H3K79 methylation generates DOT1L‐dose dependency in HDAC1‐deficient thymic lymphoma
46. p120-Catenin Is Critical for the Development of Invasive Lobular Carcinoma in Mice
47. Publisher Correction:Truncated FGFR2 is a clinically actionable oncogene in multiple cancers (Nature, (2022), 608, 7923, (609-617), 10.1038/s41586-022-05066-5)
48. Carboxylesterase 1 family knockout alters drug disposition and lipid metabolism
49. CD26-negative and CD26-positive tissue-resident fibroblasts contribute to functionally distinct CAF subpopulations in breast cancer
50. XenofilteR: computational deconvolution of mouse and human reads in tumor xenograft sequence data
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