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3. A case of T-cell acute lymphoblastic leukemia in retroviral gene therapy for ADA-SCID

4. CD32 captures committed haemogenic endothelial cells during human embryonic development

7. miR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease

9. Longitudinal single-cell profiling of chemotherapy response in acute myeloid leukemia

10. Circulating hematopoietic stem/progenitor cell subsets contribute to human hematopoietic homeostasis

11. Removal of innate immune barriers allows efficient transduction of quiescent human hematopoietic stem cells

12. StreamFlow: cross-breeding cloud with HPC

14. In vivo macrophage engineering reshapes the tumor microenvironment leading to eradication of liver metastases

16. GenHap: A Novel Computational Method Based on Genetic Algorithms for Haplotype Assembly

17. Interferon‐inducible phospholipids govern IFITM3‐dependent endosomal antiviral immunity

18. NeoHiC: A Web Application for the Analysis of Hi-C Data

20. Combining Bayesian Approaches and Evolutionary Techniques for the Inference of Breast Cancer Networks

21. AAV vectors trigger DNA damage responses and STING-dependent inflammation in human CNS cells

22. Supplementary Table 10 from Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

23. FIGURE 1 from Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

24. Supplementary Figure S4 from Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

25. FIGURE 3 from Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

26. FIGURE 5 from Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

27. Supplementary Table 9 from Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

28. FIGURE 2 from Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

29. Supplementary Table 7 from Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

30. Supplementary Table 3 from Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

31. Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

32. Supplementary Table 8 from Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

33. Supplementary Table 5 from Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

34. Supplementary Table 2 from Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

35. Supplementary Table 4 from Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

36. FIGURE 4 from Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

37. Data from Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

38. Supplementary Table 6 from Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment

39. Hepatic and adipose tissue transcriptome analysis highlights a commonly deregulated autophagic pathway in severe MASLD

41. Exonic knockout and knockin gene editing in hematopoietic stem and progenitor cells rescues RAG1 immunodeficiency

42. Comparing Deep and Machine Learning Approaches in Bioinformatics: A miRNA-Target Prediction Case Study

43. High Performance Computing for Haplotyping: Models and Platforms

44. TIM-3, LAG-3, or 2B4 gene disruptions increase the anti-tumor response of engineered T cells

45. Exonic knockout and knockin gene editing in hematopoietic stem and progenitor cells rescues RAG1 immunodeficiency

46. Oncogene-induced senescence in hematopoietic progenitors features myeloid restricted hematopoiesis, chronic inflammation and histiocytosis

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