King's College London - Leukaemia and Stem Cell Biology

Haemato-oncology

Leukaemia and Stem Cell Biology

Research focus

Leukaemia is a clonal disease initiated from a very small number of pre-leukaemic stem cells (pre-LSCs) carrying the initiating genetic events, which subsequently convert to full blown LSCs by acquiring further mutations necessary for the overt diseases such as acute myeloid leukaemia (AML). Emerging evidence indicates that pathways critical for regulation of normal stem cells are frequently hijacked or mutated in LSCs. My group is interested in understanding the molecular and cellular mechanisms underlying the oncogenic conversion of normal cells into AML stem cells.

Current projects

The origin of AML stem cells and their biology.
Transcriptional and epigenetic deregulation by leukaemia associated transcription factors.
Self-renewal pathways critical for normal and leukaemic stem cells.
Discovery of novel targets for epigenetic and stem cell therapies.

Please visit Professor. So’s website for further details.

Relevant publications

Yeung J, Esposito M, Gandillet A, Zeisig B, Griessinger E, Bonnet D, So CW. Β-catenin mediates the establishment and drug resistance of MLL keukemic stem cells. Cancer Cell vol. 18. 2010 December 14. (In press).
Kwok C, Zeisig BB, Dong S, So CW. The role of CBFbeta in AML1-ETO’s activity. Blood. 2010 Apr 15;115(15):3176-7. No abstract available. Erratum in: Blood. 2010 Sep 2;116(9):1627.
Mikesch JH, Gronemeyer H, *So CW. Discovery of novel transcriptional and epigenetic targets in APL by global ChIP analyses: emerging opportunity and challenge. Cancer Cell vol. 17 (2): 112-4, 2010
*So CW. An overview: from discovery of candidate mutations to disease modelling and transformation mechanisms of acute leukemia. Methods Mol Biol vol. 538: 1-5, 2009.
Kwok C, Zeisig BB, Qui J, Dong S, *So CW, Transforming activity of AML1-ETO is independent of CBFb and ETO interaction but requires formation of homo-oligomeric complexes. Proc Natl Acad Sci U S A, vol. 106 (8), 2853-8, 2009.
Zeisig BB, Chueng N, Yeung J, *So CW. Reconstructing the disease model and epigenetic networks for MLL-AF4 leukemia. Cancer Cell, vol. 14 (5), 345-7, 2008.
*So CW, *van der Reijden BA. C/EBPa, don’t forget your TIP60. Leukemia, vol. 22 (4): 676-7, 2008.
Cheung N, Chan LC, Thompson A, Cleary ML, *So CW. Protein arginine methyltransferase dependent oncogenesis. Nature Cell Biology, vol. 9 (10): 1208-15, 2007.
Wong P, Iwasaki M, Somervaille TC, So, CW, Cleary ML. Meis1 is an essential and rate-limiting regulator of MLL leukemia stem cell potential. Genes and Development, vol. 21 (21): 2762-74, 2007.
Zeisig BB, Kwok C, Zelent A, Shankaranarayanan P, Gronemeyer H, Dong S, *So CW. Recruitment of RXR by homo-tetrameric RARa fusion proteins is essential for transformation. Cancer Cell, vol. 12 (1): 36-51, 2007 (Journal Cover and accompanied with a preview article; Research Highlights by Nature Reviews Cancer).
Kwok C, Zeisig BB, Dong S, *So CW. Forced homo-oligomerization of RARa leads to transformation of primary hematopoietic cells. Cancer Cell vol. 9: 95-108, 2006 (accompanied with a preview article).
Greaves MF, So CW. Alert and sniffy-nosed about Mll-AF4. Blood vol. 108: 416-7, 2006.
*So CW, Cleary ML. Homodimerization: a versatile switch for oncogenesis. Blood, vol. 104: 919-922, 2004.
So CW, Lin M , Ayton PM , Chen EH , Cleary ML. Dimerization contributes to oncogenic activation of MLL chimeras in acute leukemias. Cancer Cell vol. 4, 99-110, 2003 (the featured article accompanied with a perspective).
So CW, Karsunky H, Cozzio A, Passegue E, Weissman IL, Cleary ML. MLL-GAS7 transforms multipotent hematopoietic progenitors and induces mixed lineage leukemias in mice. Cancer Cell vol. 3: 161-171, 2003 (A cover article).

* Corresponding author

Contact

Professor Eric So
Haemato-Oncology Section
Email: eric.so@kcl.ac.uk
Tel (Direct): (44) 020 7848 5888
Tel (PA): (44) 0207848 5890
Webpage:www.ericso.org