MLL translocations, histone modifications and leukaemia stem-cell development

By Andrei Krivtsov, Scott A. Armstrong. Nature Reviews. Cancer, 2007

1,258 citations recorded by the source corpus.

Subfields: Hematology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/c8a4240cf451079bacc994c31e9b81b1a9cae4db

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Citations in the corpus

A temporarily distinct subpopulation of slow-cycling melanoma cells is required for continuous tumor growth (2010, background): “In cancer, it is known that demethylation of H3K4 supports transformation from hematopoietic precursors to leukemia stem cells via regulation of the developmental Hox gene family (Krivtsov and Armstrong, 2007).”
Cancer epigenetics reaches mainstream oncology (2011, background): “In the case of the MLL gene, which encodes the most thoroughly studied H3K4 HMT, its partial tandem duplication ( MLL-PTD ) and more than 50 gene fusions account for 80% of infant leukemias and 5–10% of adult AML and lymphocyte leukemia”
IDH mutation impairs histone demethylation and results in a block to cell differentiation (2012, background): “In addition to the data presented here, evidence is mounting for a direct role of histone methylation in stem cell maintenance, differentiation and tumorigenesi”
MLL-rearranged Leukemia is Dependent on Aberrant H3K79 Methylation by DOT1L (2011, positive): “, 2002), that is absent in the oncogenic fusion protein (Ayton and Cleary, 2001; Krivtsov and Armstrong, 2007).”
The role of mutations in epigenetic regulators in myeloid malignancies (2012, background): “TET1 was first identified and cloned as an MLL fusion partner in t(10,11)(q22;q23) AML patients (36).”
Cancer epigenetics: from mechanism to therapy. (2012, background): “Whereas the oncogenic effects exerted by the MLL fusions have been extensively studied and reviewed (Krivtsov and Armstrong , 2007), an emerging area of interest is the dichotomous role of EZH2 in human malignancies.”
Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia (2011, background): “ppt"/> Recurrent chromosomal translocations involving the mixed lineage leukaemia (MLL) gene initiate aggressive forms of leukaemia, which are often refractory to conventional therapie”
Covalent histone modifications: miswritten, misinterpreted, and miserased in human cancers (2010, background): “The MLL (also known as ALL-1 and KMT2A ) gene was initially identified through its involvement in recurrent translocations of chromosomal band 11q23 in human myeloid and lymphoid leukaemia”
Cancer Genetics and Epigenetics: Two Sides of the Same Coin? (2012, background): “The mismatch-repair gene MLH1 plays an important role in genomic stability, and the loss of function of this gene by promoter hypermethylation causes microsatellite instability, which is a key factor in several cancers, including colorectal and endometrial cancers (Krivtsov and Armstrong, 2007).”
Control of Embryonic Stem Cell State (2011, background): “Mutations that affect the functions or levels of TrxG and PcG chromatin regulators have been implicated in a variety of cancers (Bracken and Helin, 2009; Krivtsov and Armstrong, 2007).”
Stem cell-related "self-renewal" signature and high epidermal growth factor receptor expression associated with resistance to concomitant chemoradiotherapy in glioblastoma. (2008, background): “In leukemia, expression of translocation-related fusion proteins led to MLL-mediated chromatin remodeling associated with reexpression of HOX genes.(9,34,35) In glioblastoma, however, such fusion proteins have not been described, and no indications from the present data set link MLL expression with ”
Enhanced expression of EHMT2 is involved in the proliferation of cancer cells through negative regulation of SIAH1. (2011, background): “We previously reported that the histone methyltransferase SMYD3 stimulates cell proliferation through its methyltransferase activity and plays a crucial role in human carcinogenesis [7,8], and several groups also showed that deregulation of histone methyltransferases could be involved in human carci”
Analysis of the Coding Genome of Diffuse Large B-Cell Lymphoma (2011, background): “A role for MLL genes in malignant transformation is supported by the involvement of MLL in the pathogenesis of acute leukemi”
Hematopoiesis: a human perspective. (2012, background): “MLL translocates to over 50 partner genes and is found in over 50% of infant leukemias, which present as ALL, AML, or in some cases mixed-lineage diseases, with invariably poor prognosis (Krivtsov and Armstrong, 2007).”