43 results on '"Case, Marian"'
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2. Supplementary Table 4 from Mutation of Genes Affecting the RAS Pathway Is Common in Childhood Acute Lymphoblastic Leukemia
3. Supplementary Table 3 from Mutation of Genes Affecting the RAS Pathway Is Common in Childhood Acute Lymphoblastic Leukemia
4. Supplementary Table 1 from Mutation of Genes Affecting the RAS Pathway Is Common in Childhood Acute Lymphoblastic Leukemia
5. Supplementary Table 2 from Mutation of Genes Affecting the RAS Pathway Is Common in Childhood Acute Lymphoblastic Leukemia
6. Hyperactive CREB subpopulations increase during therapy in paediatric B lineage acute lymphoblastic leukaemia
7. Ras pathway mutations are prevalent in relapsed childhood acute lymphoblastic leukemia and confer sensitivity to MEK inhibition
8. Quantitative proteomic analysis reveals maturation as a mechanism underlying glucocorticoid resistance in B lineage ALL and re-sensitization by JNK inhibition
9. A comprehensive analysis of the CDKN2A gene in childhood acute lymphoblastic leukemia reveals genomic deletion, copy number neutral loss of heterozygosity, and association with specific cytogenetic subgroups
10. High-resolution analysis of allelic imbalance in neuroblastoma cell lines by single nucleotide polymorphism arrays
11. Label‐Free Leukemia Monitoring by Computer Vision
12. Glucocorticoids and selumetinib are highly synergistic in RAS pathway-mutated childhood acute lymphoblastic leukemia through upregulation of BIM
13. DHFR and MSH3 co-amplification in childhood acute lymphoblastic leukaemia, in vitro and in vivo
14. The V617F mutation in Jak2 is not found in childhood acute lymphoblastic leukaemia
15. THE UNIVERSALITY OF IMMUNO-PCR FOR ULTRASENSITIVE ANTIGEN DETECTION: OHh394
16. Exploring Pre-B Cell Receptor Signalling As a Therapeutic Target in Acute Lymphoblastic Leukaemia
17. Validation of MRD Quantification By Flow Cytometry for Pediatric BCP ALL Relapsed Patients Treated on the Intreall Protocol
18. Label-Free Analyses of Minimal Residual Disease in ALL Using Deep Learning and Imaging Flow Cytometry
19. RAS Pathway Mutations Are Highly Prevalent In Relapsed Childhood Acute Lymphoblastic Leukaemia, Are Frequently Relapse-Drivers and Confer Sensitivity To MEK Inhibition
20. Casitas B lymphoma mutations in childhood acute lymphoblastic leukemia
21. The complex genomic profile ofETV6-RUNX1positive acute lymphoblastic leukemia highlights a recurrent deletion ofTBL1XR1
22. The CD34+CD38LowCD19+ Candidate Leukemic Stem Cell Phenotype Revisited: Useful for Flow MRD Monitoring?
23. In Childhood ALL, Both Blasts with a CD20−/Low and a CD20High Immunophenotype Have the Ability to Transfer the Leukemia Onto Immune-Deficient NOD/Scid Y−/− Mice.
24. Mutation of Genes Affecting the RAS Pathway Is Common in Childhood Acute Lymphoblastic Leukemia
25. Inactivation of CDKN2A in Childhood Acute Lymphoblastic Leukemia (ALL) Occurs Principally by Deletion and Is Strongly Correlated with Cytogenetic Subgroups.
26. DHFR and MSH3 co-amplification in childhood acute lymphoblastic leukaemia, in vitro and in vivo
27. Comprehensive Analysis of p16INK4a in Childhood Acute Lymphoblastic Leukemia Reveals Homozygous Deletion, Haploinsufficiency and Acquired Isodisomy at the 9p Locus with Intact p16INK4a.
28. Assessment of Aneuploidy in Childhood Acute Lymphoblastic Leukaemia Using High Density Oligonucleotide Arrays.
29. Mutation in Genes Impacting on the RAS-RAF-MEK-ERK Pathway Are Found at High Incidence in Childhood Acute Lymphoblastic Leukemia at Both Diagnosis and at Relapse.
30. Loss of Heterozygosity in Childhood Acute Lymphoblastic Leukemia Detected by Genome-Wide Microarray Single Nucleotide Polymorphism Analysis
31. Enhanced ultrasensitive detection of structurally diverse antigens using a single immuno-PCR assay protocol
32. The universality of immuno-PCR for ultrasensitive antigen detection
33. Casitas B lymphoma mutations in childhood acute lymphoblastic leukemia.
34. The complex genomic profile of ETV6-RUNX1 positive acute lymphoblastic leukemia highlights a recurrent deletion of TBL1XR1.
35. A comprehensive analysis of the CDKN2Agene in childhood acute lymphoblastic leukemia reveals genomic deletion, copy number neutral loss of heterozygosity, and association with specific cytogenetic subgroups
36. The CD34+CD38LowCD19+Candidate Leukemic Stem Cell Phenotype Revisited: Useful for Flow MRD Monitoring?
37. In Childhood ALL, Both Blasts with a CD20−/Lowand a CD20HighImmunophenotype Have the Ability to Transfer the Leukemia Onto Immune-Deficient NOD/Scid Y−/−Mice.
38. Inactivation of CDKN2Ain Childhood Acute Lymphoblastic Leukemia (ALL) Occurs Principally by Deletion and Is Strongly Correlated with Cytogenetic Subgroups.
39. Comprehensive Analysis of p16INK4ain Childhood Acute Lymphoblastic Leukemia Reveals Homozygous Deletion, Haploinsufficiency and Acquired Isodisomy at the 9p Locus with Intact p16INK4a.
40. Hyperactive CREB subpopulations increase during therapy in pediatric B-lineage acute lymphoblastic leukemia.
41. Glucocorticoids and selumetinib are highly synergistic in RAS pathway-mutated childhood acute lymphoblastic leukemia through upregulation of BIM.
42. Flow minimal residual disease monitoring of candidate leukemic stem cells defined by the immunophenotype, CD34+CD38lowCD19+ in B-lineage childhood acute lymphoblastic leukemia.
43. Establishment and validation of a standard protocol for the detection of minimal residual disease in B lineage childhood acute lymphoblastic leukemia by flow cytometry in a multi-center setting.
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