Peter J. M. Valk mostly deals with Leukemia, Myeloid leukemia, Cancer research, Myeloid and Internal medicine. Peter J. M. Valk interconnects Haematopoiesis, Stem cell and Survival analysis in the investigation of issues within Leukemia. His work carried out in the field of Myeloid leukemia brings together such families of science as Hepatocyte growth factor, Tyrosine kinase, Molecular biology, MECOM and NPM1.
His work deals with themes such as Mutation, Transcription factor, CEBPA, Allele and Regulation of gene expression, which intersect with Cancer research. The concepts of his Myeloid study are interwoven with issues in Pathology and Gene expression profiling. His study in Internal medicine is interdisciplinary in nature, drawing from both Oncology and Chromosome 7.
His primary areas of study are Myeloid leukemia, Cancer research, Leukemia, Internal medicine and Myeloid. His biological study spans a wide range of topics, including Molecular biology, CEBPA, NPM1 and Gene expression profiling. His Cancer research research includes elements of DNA methylation, Mutation, Gene, Stem cell and Bone marrow.
His work investigates the relationship between Leukemia and topics such as Haematopoiesis that intersect with problems in Progenitor cell and microRNA. In the subject of general Internal medicine, his work in Hematology, Cytarabine and Transplantation is often linked to Hazard ratio, thereby combining diverse domains of study. His Myeloid research incorporates themes from Transcription factor and Cellular differentiation.
Myeloid leukemia, Cancer research, Internal medicine, Oncology and Bone marrow are his primary areas of study. His Myeloid leukemia research integrates issues from Transcriptome, Gene expression, RNA, Epigenetics and Immunotherapy. His research in Cancer research is mostly concerned with Myeloid.
Peter J. M. Valk has included themes like Genocopy, Gene silencing, MECOM and Chromosomal translocation in his Myeloid study. The various areas that Peter J. M. Valk examines in his Oncology study include Discontinuation, MEDLINE, Gene, Tyrosine-kinase inhibitor and Cohort. Peter J. M. Valk combines subjects such as Regulation of gene expression and CEBPA with his study of GATA2.
His primary scientific interests are in Myeloid leukemia, Internal medicine, Cancer research, Oncology and Leukemia. Peter J. M. Valk has researched Myeloid leukemia in several fields, including Genocopy, Gene expression, Gene and Computational biology. Peter J. M. Valk is involved in the study of Cancer research that focuses on Myeloid in particular.
The study incorporates disciplines such as Immune system and Immunotherapy in addition to Oncology. His Immune system research is multidisciplinary, incorporating elements of Interleukin-3 receptor, Cancer, Antibody and Bone marrow. His Leukemia research is multidisciplinary, relying on both Arsenic trioxide, Cell cycle checkpoint, Cell growth, Acute promyelocytic leukemia and PI3K/AKT/mTOR pathway.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Leukemic IDH1 and IDH2 mutations result in a hypermethylation phenotype, disrupt TET2 function, and impair hematopoietic differentiation.
Maria E. Figueroa;Omar Abdel-Wahab;Chao Lu;Patrick S. Ward.
Cancer Cell (2010)
Prognostically useful gene-expression profiles in acute myeloid leukemia.
Peter J.M. Valk;Roel G.W. Verhaak;M. Antoinette Beijen;Claudia A.J. Erpelinck.
The New England Journal of Medicine (2004)
DNA Methylation Signatures Identify Biologically Distinct Subtypes in Acute Myeloid Leukemia
Maria E. Figueroa;Sanne Lugthart;Yushan Li;Claudia Erpelinck-Verschueren.
Cancer Cell (2010)
Mutations in nucleophosmin (NPM1) in acute myeloid leukemia (AML): Association with other gene abnormalities and previously established gene expression signatures and their favorable prognostic significance
Roel G. W. Verhaak;Chantal S. Goudswaard;Wim van Putten;Maarten A. Bijl.
Double CEBPA mutations, but not single CEBPA mutations, define a subgroup of acute myeloid leukemia with a distinctive gene expression profile that is uniquely associated with a favorable outcome
Bas J. Wouters;Bob Löwenberg;Claudia A. J. Erpelinck-Verschueren;Wim L. J. van Putten.
A Single Oncogenic Enhancer Rearrangement Causes Concomitant EVI1 and GATA2 Deregulation in Leukemia
Stefan Gröschel;Stefan Gröschel;Mathijs A Sanders;Remco Hoogenboezem;Elzo de Wit.
A 17-gene stemness score for rapid determination of risk in acute leukaemia
Stanley W. K. Ng;Amanda Mitchell;James A. Kennedy;James A. Kennedy;James A. Kennedy;Weihsu C. Chen.
Molecular Minimal Residual Disease in Acute Myeloid Leukemia
Mojca Jongen-Lavrencic;Tim Grob;Diana Hanekamp;François G Kavelaars.
The New England Journal of Medicine (2018)
MicroRNA expression profiling in relation to the genetic heterogeneity of acute myeloid leukemia.
Mojca Jongen-Lavrencic;Su Ming Sun;Menno K. Dijkstra;Peter J. M. Valk.
High Prognostic Impact of Flow Cytometric Minimal Residual Disease Detection in Acute Myeloid Leukemia: Data From the HOVON/SAKK AML 42A Study
Monique Terwijn;Wim L J van Putten;Angèle Kelder;Vincent H J van der Velden.
Journal of Clinical Oncology (2013)
If you think any of the details on this page are incorrect, let us know.
We appreciate your kind effort to assist us to improve this page, it would be helpful providing us with as much detail as possible in the text box below: