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2. In vivo vulnerabilities to GPX4 and HDAC inhibitors in drug-persistent versus drug-resistant BRAFV600E lung adenocarcinoma

3. Antimetabolic cooperativity with the clinically approved l-asparaginase and tyrosine kinase inhibitors to eradicate CML stem cells

4. CRISPR Base Editing to Create Potential Charcot–Marie–Tooth Disease Models with High Editing Efficiency: Human Induced Pluripotent Stem Cell Harboring SH3TC2 Variants.

8. ANTIMETABOLIC COOPERATIVITY WITH THE CLINICALLY-APPROVED L-ASPARAGINASE AND TYROSINE KINASE INHIBITORS TO ERADICATE CML STEM CELLS

11. A genome-scale CRISPR knock-out screen in chronic myeloid leukemia identifies novel drug resistance mechanisms along with intrinsic apoptosis and MAPK signaling

12. Inhibition of DDR1 enhances in vivo chemosensitivity in KRAS-mutant lung adenocarcinoma

13. In vivovulnerabilities to GPX4 and HDAC inhibitors in drug-persistent versus drug-resistant BRAFV600Elung adenocarcinoma

15. The Expression of Myeloproliferative Neoplasm-Associated Calreticulin Variants Depends on the Functionality of ER-Associated Degradation

16. CRISPR-Cas9 genome editing induces megabase-scale chromosomal truncations

17. Dasatinib-Loaded Erythrocytes Trigger Apoptosis in Untreated Chronic Myelogenous Leukemic Cells

19. Killer immunoglobulin‐like receptor genotypes and chronic myeloid leukemia outcomes after imatinib cessation for treatment‐free remission.

20. Loss of mutL homolog-1 (MLH1) expression promotes acquisition of oncogenic and inhibitor-resistant point mutations in tyrosine kinases.

25. Evidence that Resistance to Nilotinib May Be Due to BCR-ABL, Pgp, or Src Kinase Overexpression

26. Heat Shock Protein 70 over Expression Is Associated to Imatinib Resistance in Chronic Myelogenous Leukemia.

40. Identification and characterisation of genetic polymorphisms associated to imatinib sensitivity in chronic myeloid leukemia

41. A genome-scale CRISPR knock-out screen in chronic myeloid leukemia identifies novel drug resistance mechanisms along with intrinsic apoptosis and MAPK signaling.

42. Dasatinib-Loaded Erythrocytes Trigger Apoptosis in Untreated Chronic Myelogenous Leukemic Cells: A Cellular Reservoir Participating in Dasatinib Efficiency.

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