Tijmen van Dam

ORCID: 0000-0003-3461-1689
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • DNA Repair Mechanisms
  • Protein Degradation and Inhibitors
  • Cancer, Hypoxia, and Metabolism
  • Ubiquitin and proteasome pathways
  • Polyomavirus and related diseases
  • RNA and protein synthesis mechanisms
  • Acute Myeloid Leukemia Research
  • Immunodeficiency and Autoimmune Disorders
  • Cancer-related gene regulation
  • Chronic Myeloid Leukemia Treatments
  • Genetic factors in colorectal cancer

Amsterdam University Medical Centers
2019-2020

University of Amsterdam
2019-2020

The BCR-ABL1 fusion gene is the driver oncogene in chronic myeloid leukemia (CML) and Philadelphia-chromosome positive (Ph+) acute lymphoblastic (ALL). introduction of tyrosine kinase inhibitors (TKIs) targeting ABL (such as imatinib) has dramatically improved survival CML Ph+ ALL patients. However, primary acquired resistance to TKIs remains a clinical challenge. patients who achieve complete cytogenetic (CCR) or deep molecular response (MR) (≥4.5log reduction transcripts) represent...

10.1080/15384101.2019.1646068 article EN cc-by-nc-nd Cell Cycle 2019-07-26

ABSTRACT In B cells, the error-prone repair of activation-induced cytidine deaminase (AID)-induced lesions in immunoglobulin variable genes cause somatic hypermutation (SHM) antibody genes. Due to clonal selection germinal centers (GC) this active mutation process provides molecular basis for affinity maturation. AID deaminates cytosine (C) create uracil (U) DNA. Typically, short patch base excision (spBER) effectively restores genomic U lesions. We here demonstrate that GC cells actively...

10.1101/2020.01.30.926964 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2020-01-31
Coming Soon ...