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New Horizon

Anders M. Lindroth (NCC-GCSP)

  • 작성자

    Anders M. Lindroth (국립암센터 국제암대학원대학교)
  • 작성일자

    2024-12-13
  • 조회수

    48



Anders M. Lindroth

NCC-GCSP

lindroth@ncc.re.kr


[Introduce researchers & research content]

 

With a background in molecular genetics in various model organisms, Dr. Anders Lindroth arrived in South Korea in 2014 with the ambition of pursuing research in childhood cancer in a laboratory at the National Cancer Center (NCC) in Ilsan outside Seoul. His research interests revolve around fundamental aspects of cell and developmental biology, which is central to how cancer is initiated and progress to malignancy. After receiving a PhD in 2000, his research has been devoted to epigenetic modifications and regulations, first as a postdoc investigating DNA methylation in Dr. Steve Jacobsen’s lab at the University of California, Los Angeles (USA). In that collaboration, he identified a DNA methyltransferase, chromomethylase3 (CMT3), that participate in silencing a developmental gene with a specific phenotype that could be traced in a mutagenesis suppressor screen (1, 2). This subsequently led to an appointment as a research associate at Cornell University in Ithaca, New York, under Dr. Paul Soloway. Utilizing a sophisticated mouse model Dr. Soloway had developed, he described one of the first examples of epigenetic dichotomy between to gene silencing marks common in eukaryotic organisms, i.e. DNA methylation and H3K27me3 (3). A short stint as a teacher and researcher at his alma mater Uppsala University and Swedish University of Agricultural Sciences, finally led him to the German Cancer Research Center in Heidelberg, Germany. There he became involved in several projects of identifying and characterizing histone mutations in cancer, so called oncohistones (4, 5). This topic has remained a major interest, as he joined the faculty of NCC to run his own laboratory and pursue cancer epigenetic studies. There he has characterized epigenomic and RNA processing-related tumorigenic features of giant cell tumor of bone, and established oncohistone mouse models for drug and genetic knockout screens (6-9). Other areas of research are also under development in the Lindroth lab. The most important one is how metabolic pathways contribute to alterations of the epigenetic modifications, in particular DNA methylation. While this is a novel development in his lab, he remains focused on fundamental aspects of chromatin remodeling activity linked to gene expression. This is exemplified in his ambition to determine how epigenetic remodelers senses external stimuli, such as metabolic alterations, to regulate transcriptional activity and accommodate the need for tissue response and functionality governing tissue and whole body homeostasis. The Lindroth lab has currently one PhD student, two postdocs and one research assistant. If you are interested in joining the Lindroth lab as a graduate student or postdoc, please find the contact information below. 

 

[Research team] 

 

 

 

 

[Contact information]

 

National Cancer Center

GCSP, Cancer Biomedical Science

323 Ilsanro, Goyangsi, S. Korea

+82-31-920-2747 (office), 2487 (lab)

URL: tinyurl.com/NCC-GCSP-Lindroth

 

​[Representative publications] 

 

1. A. M. Lindroth et al., Requirement of CHROMOMETHYLASE3 for maintenance of CpXpG methylation. Science 292, 2077-2080 (2001).

2. J. P. Jackson, A. M. Lindroth, X. Cao, S. E. Jacobsen, Control of CpNpG DNA methylation by the KRYPTONITE histone H3 methyltransferase. Nature 416, 556-560 (2002).

3. A. M. Lindroth et al., Antagonism between DNA and H3K27 methylation at the imprinted Rasgrf1 locus. PLoS Genet 4, e1000145 (2008).

4. J. Schwartzentruber et al., Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma. Nature 482, 226-231 (2012).

5. D. Sturm et al., Hotspot mutations in H3F3A and IDH1 define distinct epigenetic and biological subgroups of glioblastoma. Cancer Cell 22, 425-437 (2012).

6. P. Lutsik et al., Globally altered epigenetic landscape and delayed osteogenic differentiation in H3.3-G34W-mutant giant cell tumor of bone. Nat Commun 11, 5414 (2020).

7. J. Lim et al., The histone variant H3.3 G34W substitution in giant cell tumor of the bone link chromatin and RNA processing. Sci Rep 7, 13459 (2017).

8. E. Lee, Y. J. Park, A. M. Lindroth, H3.3-G34W in giant cell tumor of bone functionally aligns with the exon choice repressor hnRNPA1L2. Cancer Gene Ther 31, 1177-1185 (2024).

9. A. M. Lindroth, Y. J. Park, V. Matia, M. Squatrito, The mechanistic GEMMs of oncogenic histones. Hum Mol Genet 29, R226-R235 (2020).