The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Transformation from committed progenitor to leukaemia stem cell initiated by MLL–AF9
Abstract
Leukaemias and other cancers possess a rare population of cells capable of the limitless self-renewal necessary for cancer initiation and maintenance. Eradication of these cancer stem cells is probably a critical part of any successful anti-cancer therapy, and may explain why conventional cancer therapies are often effective in reducing tumour burden, but are only rarely curative. Given that both normal and cancer stem cells are capable of self-renewal, the extent to which cancer stem cells resemble normal tissue stem cells is a critical issue if targeted therapies are to be developed. However, it remains unclear whether cancer stem cells must be phenotypically similar to normal tissue stem cells or whether they can retain the identity of committed progenitors. Here we show that leukaemia stem cells (LSC) can maintain the global identity of the progenitor from which they arose while activating a limited stem-cell- or self-renewal-associated programme. We isolated LSC from leukaemias initiated in committed granulocyte macrophage progenitors through introduction of the MLL-AF9 fusion protein encoded by the t(9;11)(p22;q23). The LSC were capable of transferring leukaemia to secondary recipient mice when only four cells were transferred, and possessed an immunophenotype and global gene expression profile very similar to that of normal granulocyte macrophage progenitors. However, a subset of genes highly expressed in normal haematopoietic stem cells was re-activated in LSC. LSC ca…
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“PU.1 halpoinsufficiency causes subtle changes in hematopoietic differentiation, but is not sufficient to induce leukemia3, 9, 11, 13, 14.”
From Minimal PU.1 reduction induces a preleukemic state and promotes development of acute myeloid leukemia (2015) · cites this paper as [11]
In the citing paper
“Although loss or near-complete loss of the hematopoietic transcription factor PU.1 induces acute myeloid leukemia (AML) in mice”
From Minimal PU.1 reduction induces a preleukemic state and promotes development of acute myeloid leukemia (2015) · cites this paper as [11]
Citations
Cites
Subramanian, A., Tamayo, P., Mootha, V. K., Mukherjee, S., Ebert, B. L., Gillette, M. A., Paulovich, A., Pomeroy, S. L., Golub, T. R., Lander, E. S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506580102 · Cited by 53,625
Self-citationA cell initiating human acute myeloid leukaemia after transplantation into SCID mice
Lapidot, T., Sirard, C., Vormoor, J., Murdoch, B., Hoang, T., Caceres-Cortes, J., Minden, M., Paterson, B., Caligiuri, M. A., & Dick, J. E. (1994) · Nature · doi:10.1038/367645a0 · Cited by 4,783
A clonogenic common myeloid progenitor that gives rise to all myeloid lineages
Akashi, K., Traver, D., Miyamoto, T., & Weissman, I. L. (2000) · Nature · doi:10.1038/35004599 · Cited by 2,617
Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CML
Jamieson, C. H. M., Ailles, L. E., Dylla, S. J., Muijtjens, M., Jones, C., Zehnder, J. L., Gotlib, J., Li, K., Manz, M. G., Keating, A., et al. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa040258 · Cited by 1,485
Flagged first, then by citations
Research works printed but not linked: 26
- Reya, T., Morrison, S. J., Clarke, M. F. & Weissman, I. L. Stem cells, cancer, and cancer stem cells. Nature 414, 105–111 (2001) · DOI · Paper page
- Warner, J. K., Wang, J. C., Hope, K. J., Jin, L. & Dick, J. E. Concepts of human leukemic development. Oncogene 23, 7164–7177 (2004) · DOI
- Al-Hajj, M. & Clarke, M. F. Self-renewal and solid tumor stem cells. Oncogene 23, 7274–7282 (2004) · DOI
- Bonnet, D. & Dick, J. E. Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. Nature Med. 3, 730–737 (1997) · DOI
- Singh, S. K. et al. Identification of human brain tumour initiating cells. Nature 432, 396–401 (2004) · DOI
- Huntly, B. J. et al. MOZ-TIF2, but not BCR-ABL, confers properties of leukemic stem cells to committed murine hematopoietic progenitors. Cancer Cell 6, 587–596 (2004) · DOI · Paper page
- Cozzio, A. et al. Similar MLL-associated leukemias arising from self-renewing stem cells and short-lived myeloid progenitors. Genes Dev. 17, 3029–3035 (2003) · DOI
- So, C. W. et al. MLL-GAS7 transforms multipotent hematopoietic progenitors and induces mixed lineage leukemias in mice. Cancer Cell 3, 161–171 (2003) · DOI
- Lavau, C., Szilvassy, S. J., Slany, R. & Cleary, M. L. Immortalization and leukemic transformation of a myelomonocytic precursor by retrovirally transduced HRX-ENL. EMBO J. 16, 4226–4237 (1997) · DOI
- Corral, J. et al. An MLL–AF9 fusion gene made by homologous recombination causes acute leukemia in chimeric mice: a method to create fusion oncogenes. Cell 85, 853–861 (1996) · DOI
- Wang, J. et al. Conditional MLL-CBP targets GMP and models therapy-related myeloproliferative disease. EMBO J. 24, 368–381 (2005) · DOI
- Drynan, L. F. et al. Mll fusions generated by Cre-loxP-mediated de novo translocations can induce lineage reassignment in tumorigenesis. EMBO J. 24, 3136–3146 (2005) · DOI
- Ramalho-Santos, M., Yoon, S., Matsuzaki, Y., Mulligan, R. C. & Melton, D. A. “Stemness”: transcriptional profiling of embryonic and adult stem cells. Science 298, 597–600 (2002) · DOI
- Zeisig, B. B. et al. Hoxa9 and Meis1 are key targets for MLL-ENL-mediated cellular immortalization. Mol. Cell. Biol. 24, 617–628 (2004) · DOI
- Kumar, A. R. et al. Hoxa9 influences the phenotype but not the incidence of Mll-AF9 fusion gene leukemia. Blood 103, 1823–1828 (2004) · DOI
- Ayton, P. M. & Cleary, M. L. Transformation of myeloid progenitors by MLL oncoproteins is dependent on Hoxa7 and Hoxa9. Genes Dev. 17, 2298–2307 (2003) · DOI
- Armstrong, S. A. et al. MLL translocations specify a distinct gene expression profile that distinguishes a unique leukemia. Nature Genet. 30, 41–47 (2002) · DOI
- So, C. W., Karsunky, H., Wong, P., Weissman, I. L. & Cleary, M. L. Leukemic transformation of hematopoietic progenitors by MLL-GAS7 in the absence of Hoxa7 or Hoxa9. Blood 103, 3192–3199 (2004) · DOI
- Kiel, M. J., Yilmaz, O. H., Iwashita, T., Terhorst, C. & Morrison, S. J. SLAM family receptors distinguish hematopoietic stem and progenitor cells and reveal endothelial niches for stem cells. Cell 121, 1109–1121 (2005) · DOI · Paper page
- Ross, M. E. et al. Gene expression profiling of pediatric acute myelogenous leukemia. Blood 104, 3679–3687 (2004) · DOI
- Kolligs, F. T. et al. ITF-2, a downstream target of the Wnt/TCF pathway, is activated in human cancers with beta-catenin defects and promotes neoplastic transformation. Cancer Cell 1, 145–155 (2002) · DOI
- Abramovich, C. & Humphries, R. K. Hox regulation of normal and leukemic hematopoietic stem cells. Curr. Opin. Hematol. 12, 210–216 (2005) · DOI
- Milne, T. A. et al. MLL associates specifically with a subset of transcriptionally active target genes. Proc. Natl Acad. Sci. USA 102, 14765–14770 (2005) · DOI
- Guenther, M. G. et al. Global and Hox-specific roles for the MLL1 methyltransferase. Proc. Natl Acad. Sci. USA 102, 8603–8608 (2005) · DOI
- Du, Y., Spence, S. E., Jenkins, N. A. & Copeland, N. G. Cooperating cancer-gene identification through oncogenic-retrovirus-induced insertional mutagenesis. Blood 106, 2498–2505 (2005) · DOI
- Ernst, P., Mabon, M., Davidson, A. J., Zon, L. I. & Korsmeyer, S. J. An Mll-dependent Hox programme drives hematopoietic progenitor expansion. Curr. Biol. 14, 2063–2069 (2004) · DOI
Cited by
Sorted by citations
Items 101–200 of 1,002
The Origins of Medulloblastoma Subtypes
Gilbertson, R. J., & Ellison, D. W. (2008) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev.pathmechdis.3.121806.151518 · Cited by 302
Genomic and functional analysis of leukemic transformation of myeloproliferative neoplasms
Rampal, R., Ahn, J., Abdel-Wahab, O., Nahas, M., Wang, K., Lipson, D., Otto, G. A., Yelensky, R., Hricik, T., McKenney, A. S., et al. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1407792111 · Cited by 301
“4B), as is consistent with the progressive increase in self-renewal in vivo observed in other murine models of AML (26).”
BackgroundSelf-citationCancer Epigenetics, Tumor Immunity, and Immunotherapy
Cao, J. P., & Yan, Q. (2020) · Trends in cancer · doi:10.1016/j.trecan.2020.02.003 · Cited by 355
“Key examples include translocation of KMT2A (MLL1) driving acute leukemia [51,52], and KMT6A (EZH2) gain-of-function mutations driving non-Hodgkin’s lymphoma [53].”
BackgroundProtein arginine-methyltransferase-dependent oncogenesis
Cheung, N., Chan, L.-C., Thompson, A., Cleary, M., & So, C. (2007) · Nature Cell Biology · doi:10.1038/ncb1642 · Cited by 298
“, in which they resurrect the self-renewal transcriptional programmes in the leukaemic stem cell”
BackgroundMeis1 is an essential and rate-limiting regulator of MLL leukemia stem cell potentialPreprint
Wong, P., 岩崎, 正., Somervaille, T. C. P., So, C. W. E., & Cleary, M. L. (2007) · Genes & Development · doi:10.1101/gad.1602107 · Cited by 274
“This paradigm, however, may not apply to all myeloid leukemias, as suggested by recent studies using a mouse model of AML induced by the MLL-AF9 oncogene (Krivtsov et al. 2006; Somervaille and Cleary 2006), which is typically associated with FAB-M4 or M5 subtypes of human AML (Swansbury 1998).”
Epigenetics and Cancer Stem Cells: Unleashing, Hijacking, and Restricting Cellular Plasticity
Wainwright, E. N., & Scaffidi, P. (2017) · Trends in cancer · doi:10.1016/j.trecan.2017.04.004 · Cited by 348
Inhibition of Endosteal Vascular Niche Remodeling Rescues Hematopoietic Stem Cell Loss in AML
Duarte, D., Hawkins, E. D., Akinduro, O., Ang, H. Y.-K., Filippo, K. D., Kong, I. Y., Haltalli, M. L. R., Ruivo, N., Straszkowski, L., Vervoort, S. J., et al. (2017) · Cell stem cell · doi:10.1016/j.stem.2017.11.006 · Cited by 328
“Intravital Microscopy Enables the Study of AML Cells, Healthy Hematopoietic Cells, and the BM Microenvironment Simultaneously To study the effects of AML growth on BM vasculature and HSCs as disease propagates through the tissue, we used the well-established MLL-AF9-driven murine model of AML, which recapitulates phen…”
MethodInfluentialBasal epithelial stem cells are efficient targets for prostate cancer initiation
Lawson, D. A., Yang, Z., Memarzadeh, S., Li, X., Huang, J.-T., & Witte, O. (2010) · Proceedings of the National Academy of Sciences of the United States of America · doi:10.1073/pnas.0913873107 · Cited by 291
“(3) used this approach to demonstrate that BCR-ABL can induce myeloid disease in mice when introduced into HSC but not more committed progenitors, while other fusion oncogenes can initiate disease from both stem cells and progenitors (4, 5).”
MethodZuber, J., Rappaport, A. R., Luo, W., Wang, E., Chen, C., Vaseva, A. V., Shi, J.-W., Weissmueller, S., Fellmann, C., Taylor, M. J., et al. (2011) · Genes & Development · doi:10.1101/gad.17269211 · Cited by 289
“…to the up-regulation of a selfrenewal-associated transcriptional subprogram in ‘‘leukemia stem cells’’ (LSCs) that is similar to embryonic stem cells (Krivtsov et al. 2006; Somervaille et al. 2009) and overlaps with a transcriptional program controlled by the Myc oncoprotein (Kim et al. 2010).”
BackgroundAberrant chromatin at genes encoding stem cell regulators in human mixed-lineage leukemiaPreprint
Guenther, M. G., Lawton, L. N., Rozovskaia, T., Frampton, G. M., Levine, S. S., Volkert, T. L., Croce, C. M., Nakamura, T., Canaani, E., & Young, R. A. (2008) · Genes & Development · doi:10.1101/gad.1741408 · Cited by 271
“Other targets, including the RUNX2 transcription factor and JMJD1C histone demethylase, were previously shown to be up-regulated in MLL-AF9-induced leukemic stem cells (Krivtsov et al. 2006), but were not known to be direct targets of MLL fusion proteins.”
BackgroundThe prognostic and functional role of microRNAs in acute myeloid leukemia
Marcucci, G., Mrózek, K., Radmacher, M. D., Garzon, R., & Bloomfield, C. D. (2010) · Blood · doi:10.1182/blood-2010-09-191312 · Cited by 274
“MEF2C mRNA levels are up-regulated in highly proliferative leukemic granulocyte– monocyte progenitors and that MEF2C ectopic expression enhanced their proliferation.(100) Thus, miR-223 acts normally as a negative regulator of granulocytic proliferation (Table 2) as part of an autoregulatory negative feedback loop also…”
BackgroundPei, S., Pollyea, D. A., Gustafson, A. L., Stevens, B. M., Minhajuddin, M., Fu, R., Riemondy, K. A., Gillen, A. E., Sheridan, R. M., Kim, J., et al. (2020) · Cancer Discovery · doi:10.1158/2159-8290.cd-19-0710 · Cited by 565
“This is notable because unlike most other previously reported LSC signatures, MLL-specific LSCs have a myeloid phenotype (39,40).”
ResultAKT/FOXO Signaling Enforces Reversible Differentiation Blockade in Myeloid Leukemias
Sykes, S. M., Lane, S., Bullinger, L., Kalaitzidis, D., Yusuf, R. Z., Sáez, B., Ferraro, F., Mercier, F., Singh, H., Brumme, K. M., et al. (2011) · Cell · doi:10.1016/j.cell.2011.07.032 · Cited by 261
“Because specific modifications of AKT confer distinct clinical outcomes of human AML (Gallay et al., 2009; Park et al., 2010; Tamburini et al., 2007), we examined Akt status in a murine model of MLL-AF9-induced myeloid leukemia that closely phenocopies human AML (Krivtsov et al., 2006).”
Self-citationDOT1L, the H3K79 methyltransferase, is required for MLL-AF9–mediated leukemogenesis
Nguyen, A. T., Taranova, O., He, J., & Zhang, Y. (2011) · Blood · doi:10.1182/blood-2011-02-334359 · Cited by 280
Metastatic osteosarcoma induced by inactivation of Rb and p53 in the osteoblast lineage
Berman, S. D., Calo, E., Landman, A. S., Danielian, P. S., Miller, E. S., West, J. C., Fonhoue, B. D., Caron, A. M., Bronson, R. T., Bouxsein, M., et al. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0805462105 · Cited by 271
“For example, it has been shown that acute myeloid leukemia can arise from a committed progenitor cell (23).”
BackgroundCore circadian clock genes regulate leukemia stem cells in AML
Puram, R. V., Kowalczyk, M. S., de Boer, C. G., Schneider, R. K., Miller, P. G., McConkey, M., Tothova, Z., Tejero, H., Heckl, D., Järås, M., et al. (2016) · Cell · doi:10.1016/j.cell.2016.03.015 · Cited by 274
“GMPswere isolated fromthebonemarrow of Actin-dsRed mice, asdescribed previously (Krivtsov et al., 2006).”
Inhibitory receptors bind ANGPTLs and support blood stem cells and leukaemia development
Zheng, J., Umikawa, M., Cui, C., Li, J., Chen, X., Zhang, C., Huynh, H., Kang, X., Silvany, R. E., Wan, X., et al. (2012) · Nature · doi:10.1038/nature11095 · Cited by 277
“The manufacturers and catalogue numbers for other antibodies are as follows: anti-LILRB1, Biolegend (33707); anti-LILRB2, eBioscience (125149); anti-LILRB3, eBioscience (12-5159); anti-LILRB4, eBiosciene (12-5139); anti-LILRB5, R&D Systems (AF3065); anti-PIRB–PE, R&D Systems (FAB2754P); anti-human LAIR1–PE, BD Pharmin…”
BackgroundCancer heterogeneity—a multifaceted view
Melo, F. D. S. E., Vermeulen, L., Fessler, E., & Medema, J. P. (2013) · EMBO Reports · doi:10.1038/embor.2013.92 · Cited by 287
Kerenyi, M. A., Shao, Z., Hsu, Y., Guo, G., Luc, S., O’Brien, K., Fujiwara, Y., Peng, C., Nguyen, M., & Orkin, S. H. (2013) · eLife · doi:10.7554/elife.00633 · Cited by 267
“To pursue the potential significance of this observation, we performed gene set enrichment analysis (GSEA; Subramanian et al., 2005 ) using a gene signature derived from HSPCs (LSK signature; Figure 5—source data 1 ; Krivtsov et al., 2006 ).”
Methodβ-Catenin Mediates the Establishment and Drug Resistance of MLL Leukemic Stem Cells
Yeung, J., Esposito, M. T., Gandillet, A., Zeisig, B. B., Griessinger, E., Bonnet, D. A., & So, C. W. E. (2010) · Cancer Cell · doi:10.1016/j.ccr.2010.10.032 · Cited by 275
Glycogen synthase kinase 3β missplicing contributes to leukemia stem cell generation
Abrahamsson, A., Geron, I., Gotlib, J., Dao, K.-H. T., Barroga, C., Newton, I., Giles, F., Durocher, J., Creusot, R. S., Karimi, M., et al. (2009) · Proceedings of the National Academy of Sciences of the United States of America · doi:10.1073/pnas.0900189106 · Cited by 264
Kikushige, Y., Miyamoto, T., Yuda, J., Jabbarzadeh‐Tabrizi, S., Shima, T., Takayanagi, S., Niiro, H., Yurino, A., Miyawaki, K., Takenaka, K., et al. (2015) · Cell stem cell · doi:10.1016/j.stem.2015.07.011 · Cited by 288
“In mouse AML models, LSCs can arise from HSCs as well as from GMPs after introduction of AML-related chimeric fusion genes (Cozzio et al., 2003; Huntly et al., 2004; Krivtsov et al., 2006).”
BackgroundInfluentialRecent advances in cancer stem cells
Cho, R. W., & Clarke, M. F. (2008) · Current Opinion in Genetics & Development · doi:10.1016/j.gde.2008.01.017 · Cited by 237
“Just as normal mouse hematopoiesis and transgenic leukemia mouse models have helped in the understanding of leukemogenesis [26,30,41,42], it is hoped that the understanding of breast tumor biology can be furthered by the study of normal mouse breast development and transgenic models of breast cancer such as the MMTVWn…”
BackgroundDrug resistance: Still a daunting challenge to the successful treatment of AML
Shaffer, B. C., Gillet, J., Patel, C. M., Baer, M. R., Bates, S. E., & Gottesman, M. M. (2012) · Drug Resistance Updates · doi:10.1016/j.drup.2012.02.001 · Cited by 265
“For example, it was demonstrated that LSCs can be generated from committed progenitors retrovirally transduced with either MLL-ENL, MOZ-TIF2 or MLL-AF9 oncogenes, leading to the reacquisition of self-renewal properties and the initiation of AML (Cozzio et al., 2003; Huntly et al., 2004; Krivtsov et al., 2006).”
BackgroundKirstetter, P., Schuster, M. B., Bereshchenko, O., Moore, S., Dvinge, H., Kurz, E., Theilgaard-Mönch, K., Månsson, R., Pedersen, T. Å., Pabst, T., et al. (2008) · Cancer Cell · doi:10.1016/j.ccr.2008.02.008 · Cited by 251
Drosophila melanogaster: A Model Organism to Study Cancer
Mirzoyan, Z., Sollazzo, M., Allocca, M., Valenza, A., Grifoni, D., & Bellosta, P. (2019) · Frontiers in Genetics · doi:10.3389/fgene.2019.00051 · Cited by 348
“The progression from normal progenitors to stem-like cancer cells was first explored in leukemia, although nowadays we know that several solid tumors such as brain, breast, lung and colon cancer originate from cells with stem features (Krivtsov et al., 2006).”
BackgroundMLL-AF9-Induced Leukemogenesis Requires Coexpression of the Wild-Type Mll Allele
Thiel, A. T., Blessington, P., Zou, T., Feather, D., Wu, X., Yan, J., Zhang, H., Liu, Z., Ernst, P., Koretzky, G. A., et al. (2010) · Cancer Cell · doi:10.1016/j.ccr.2009.12.034 · Cited by 249
“…and expression of 50 Hoxa genes, including Hoxa9 (Jude et al., 2007; McMahon et al., 2007), yet these Hox genes are upregulated in an MA9-transformed leukemia stem cell (LSC)–enriched population (Krivtsov et al., 2006), raising the possibility that WT MLL is involved in MA9-induced leukemogenesis.”
BackgroundInfluentialPC3 human prostate carcinoma cell holoclones contain self-renewing tumor-initiating cells.
Li, H.-W., Chen, X., Calhoun-Davis, T., Claypool, K., & Tang, D. G. (2008) · Cancer Research · doi:10.1158/0008-5472.can-07-5878 · Cited by 247
“In support of the first tenet, both chronic myelogenous leukemia (11) and acute myelogenous leukemia ( 12 ) seem to have arisen from the committed progenitor cells that have acquired self-renewing capabilities.”
BackgroundSaito, Y., Chapple, R. H., Lin, A. J., Kitano, A., & Nakada, D. (2015) · Cell stem cell · doi:10.1016/j.stem.2015.08.019 · Cited by 279
“Consistent with the previous report (Krivtsov et al., 2006), we confirmed that clonogenic cells reside in the L-GMP”
MethodResultInfluentialMapping cellular hierarchy by single cell analysis of the cell surface repertoire
Guo, G., Luc, S., Marco, E., Lin, T.-W., Peng, C., Kerényi, M., Beyaz, S., Kim, W., Xu, J., Das, P., et al. (2013) · Cell Stem Cell · doi:10.1016/j.stem.2013.07.017 · Cited by 245
“Single-Cell Analysis of the AML Cellular Hierarchy Having obtained a comprehensive data set in the wild-type hematopoietic system, we next applied the single-cell expression approach to characterization of LSCs in MLL-AF9-driven AML, a clinically relevant model of hematopoietic malignancy (Krivtsov et al., 2006; Neff…”
InfluentialCell type-specific DNA methylation patterns in the human breast
Bloushtain-Qimron, N., Yao, J., Snyder, E. L., Shipitsin, M., Campbell, L. L., Mani, S. A., Hu, M., Chen, H., Ustyansky, V., Antosiewicz, J., et al. (2008) · Proceedings of the National Academy of Sciences of the United States of America · doi:10.1073/pnas.0805206105 · Cited by 243
Targeting Chromatin Regulators Inhibits Leukemogenic Gene Expression in NPM1 Mutant Leukemia
Kühn, M. W. M., Song, E., Feng, Z., Sinha, A., Chen, C.-W. D., Deshpande, A. J., Cusan, M., Farnoud, N. R., Mupo, A., Grove, C. S., et al. (2016) · Cancer Discovery · doi:10.1158/2159-8290.cd-16-0237 · Cited by 281
“MLL1-rearranged leukemias exhibit aberrant HOXA-cluster expression as a consequence of chromatin binding of the MLL1fusion complex(18), which in turn requires the association with at least two other proteins, menin and LEDGF.”
BackgroundSelf-citationCancer stem cells: A contentious hypothesis now moving forward
O'Connor, M., Xiang, D., Shigdar, S. L., MacDonald, J. P., Li, Y., Wang, T., Pu, C., Wang, Z., Qiao, L., & Duan, W. (2013) · Cancer Letters · doi:10.1016/j.canlet.2013.11.012 · Cited by 233
“Despite the attractiveness of the CSC concept, it has been countered by other evidence implicating progenitor cells as reacquiring self-renewal capacity through genetic mutations and epigenetic modifications [22–24].”
BackgroundMalignant Transformation Initiated by Mll-AF9: Gene Dosage and Critical Target Cells
Chen, W., Kumar, A. R., Hudson, W. A., Li, Q., Wu, B., Staggs, R. A., Lund, E. A., Sam, T. N., & Kersey, J. H. (2008) · Cancer Cell · doi:10.1016/j.ccr.2008.03.005 · Cited by 216
“Similarly, retrovirally transduced MLL-AF9 transformed GMP cells and produced leukemia (Krivtsov et al., 2006).”
InfluentialShih, A. H., Jiang, Y., Meydan, C., Shank, K., Pandey, S., Barreyro, L., Antony-Debre, I., Viale, A., Socci, N., Sun, Y., et al. (2015) · Cancer Cell · doi:10.1016/j.ccell.2015.03.009 · Cited by 236
“In the murine context, transplantation studies using MLL-fusion leukemia models have shown that GMPs can serve as LSCs, with acquisition of self-renewal by committed progenitors (Heuser et al., 2011; Krivtsov et al., 2006).”
BackgroundCells of origin in osteosarcoma: Mesenchymal stem cells or osteoblast committed cells?
Mutsaers, A. J., & Walkley, C. R. (2014) · Bone · doi:10.1016/j.bone.2014.02.003 · Cited by 233
“as cells of origin in leukemia and will be an equally powerful approach to understanding sarcoma [72–74].”
BackgroundIs Tumor Growth Sustained by Rare Cancer Stem Cells or Dominant Clones?
Adams, J. M., & Strasser, A. (2008) · Cancer Research · doi:10.1158/0008-5472.can-07-6334 · Cited by 210
“Similarly, in another MLL-AF9 model, up to 50% of granulocyte-macrophage progenitors could initiate leukemia (18).”
Characterization of a subpopulation of colon cancer cells with stem cell‐like properties
Chu, P., Clanton, D. J., Snipas, T., Lee, J., Mitchell, E., Nguyen, M., Hare, E., & Peach, R. (2008) · International Journal of Cancer · doi:10.1002/ijc.24061 · Cited by 209
“suggests that leukemic stem cells can arise from stem cells or progenitor cells that have reacquired stem cell properties, such as self-renewal capacity.(16,18,19) This is consistent with the hypothesis that colon progenitors can regain stem cell functions, and suggests”
BMP and Wnt specify hematopoietic fate by activation of the Cdx-Hox pathway.
Lengerke, C., Schmitt, S., Bowman, T., Jang, I., Maouche-Chretien, L., McKinney-Freeman, S., Davidson, A., Hammerschmidt, M., Rentzsch, F., Green, J. B. A., et al. (2008) · Cell Stem Cell · doi:10.1016/j.stem.2007.10.022 · Cited by 225
Cancer stem cells and human malignant melanoma
Schatton, T., & Frank, M. H. (2008) · Pigment Cell & Melanoma Research · doi:10.1111/j.1755-148x.2007.00427.x · Cited by 219
“However, recent results obtained in the hematopoietic system indicate that CSC can also arise through oncogenic transformation of lineagerestricted progenitor or differentiated cell types (Jamieson et al., 2004; Krivtsov et al., 2006).”
Evolution of acute myelogenous leukemia stem cell properties after treatment and progression
Ho, T., LaMere, M. W., Stevens, B. M., Ashton, J. M., Myers, J. R., O’Dwyer, K. M., Liesveld, J. L., Mendler, J. H., Guzmán, M. L., Morrissette, J. D., et al. (2016) · Blood · doi:10.1182/blood-2016-02-695312 · Cited by 241
“Studies in CML blast crisis andmurinemodels for AML demonstrate that LSC population phenotypes are in part dependent on the stage of differentiation from which the fully transformed leukemia arises, as well as the oncogenic event or events; thus non-self-renewing normal hematopoietic elements may be transformed into s…”
BackgroundWill, B., Zhou, L., Vogler, T. O., Ben-Neriah, S., Schinke, C., Tamari, R., Yu, Y., Bhagat, T. D., Bhattacharyya, S., Barreyro, L., et al. (2012) · Blood · doi:10.1182/blood-2011-12-399683 · Cited by 240
Stavropoulou, V., Kaspar, S., Brault, L., Sanders, M. A., Juge, S., Morettini, S., Tzankov, A., Iacovino, M., Lau, I., Milne, T. A., et al. (2016) · Cancer Cell · doi:10.1016/j.ccell.2016.05.011 · Cited by 234
“Several of these genes have previously been linked to EMT or invasion in solid cancers but never associated with AML (Bindels et al., 2012; Chen et al., 2008; Krivtsov et al., 2006).”
BackgroundChen, C.-W. D., Koche, R. P., Sinha, A. U., Deshpande, A. J., Zhu, N., Eng, R., Doench, J. G., Xu, H., Chu, S. H., Qi, J., et al. (2015) · Nature Medicine · doi:10.1038/nm.3832 · Cited by 235
Self-citationEpigenetic alterations involved in cancer stem cell reprogramming
Muñoz, P., Iliou, M. S., & Esteller, M. (2012) · Molecular Oncology · doi:10.1016/j.molonc.2012.10.006 · Cited by 205
The peripheral nervous system supports blood cell homing and survival in the Drosophila larva
Makhijani, K., Alexander, B., Tanaka, T., Rulifson, E. J., & Brückner, K. (2011) · Development · doi:10.1242/dev.067322 · Cited by 219
“, 2010), and neoplasias such as leukemias can develop from differentiated cells that re-gain the ability to expand (Krivtsov et al., 2006; Guibal et al., 2009).”
BackgroundA novel tumour-suppressor function for the Notch pathway in myeloid leukaemia
Klinakis, A., Lobry, C., Abdel-Wahab, O. I., Oh, P., Haeno, H., Buonamici, S., de Walle, I. V., Cathelin, S., Trimarchi, T., Araldi, E., et al. (2011) · Nature · doi:10.1038/nature09999 · Cited by 400
Adult Lineage-Restricted CNS Progenitors Specify Distinct Glioblastoma Subtypes
Llaguno, S. R. A., Wang, Z., Sun, D., Chen, J., Xu, J., Kim, E., Hatanpaa, K. J., Raisanen, J. M., Burns, D. K., Johnson, J. E. B., et al. (2015) · Cancer Cell · doi:10.1016/j.ccell.2015.09.007 · Cited by 231
“…as a major nal subclassification of GBM and identification of subtype ancer Cell 28, 429–440, October 12, 2015 ª2015 Elsevier Inc. 429 (legend on next page) 430 Cancer Cell 28, 429–440, October 12, 2015 ª2015 Elsevier Inc. from stem cells, myeloid, and lymphoid progenitors (Krivtsov et al., 2006).”
Liu, G., Bollig-Fischer, A., Kreike, B., van de Vijver, M., Abrams, J., Ethier, S., & Yang, Z.-Q. (2009) · Oncogene · doi:10.1038/onc.2009.297 · Cited by 208
“This results in increased self-renewal potential and transforms these cells into cancer stem cells capable of initiating, maintaining and propagating the leukemia(Krivtsov et al., 2006).”
BackgroundInfluentialSpindle orientation, asymmetric division and tumour suppression in Drosophila stem cells
González, C. (2007) · Nature Reviews Genetics · doi:10.1038/nrg2103 · Cited by 196
DNA-damage-induced differentiation of leukaemic cells as an anti-cancer barrier
Santos, M. A., Faryabi, R. B., Ergen, A. V., Day, A., Malhowski, A. J., Canela, A., Onozawa, M., Lee, J., Callén, E., Gutierrez‐Martinez, P., et al. (2014) · Nature · doi:10.1038/nature13483 · Cited by 200
Self-citationGetting to the stem of chronic myeloid leukaemia
Savona, M. R., & Talpaz, M. (2008) · Nature reviews. Cancer · doi:10.1038/nrc2368 · Cited by 193
Cell of origin determines clinically relevant subtypes of MLL-rearranged AML
Krivtsov, A. V., Figueroa, M. E., Sinha, A. U., Stubbs, M. C., Feng, Z., Valk, P. J. M., Delwel, R., Döhner, K., Bullinger, L., Kung, A. L., et al. (2013) · Leukemia · doi:10.1038/leu.2012.363 · Cited by 203
Self-citationHe, J., Nguyen, A. T., & Zhang, Y. (2011) · Blood · doi:10.1182/blood-2010-10-312736 · Cited by 215
Barreyro, L., Will, B., Bartholdy, B., Zhou, L., Todorova, T. I., Stanley, R. F., Ben-Neriah, S., Montagna, C., Parekh, S., Pellagatti, A., et al. (2012) · Blood · doi:10.1182/blood-2012-01-404699 · Cited by 201
Ezh2 augments leukemogenicity by reinforcing differentiation blockage in acute myeloid leukemia
Tanaka, S., Miyagi, S., Sashida, G., Chiba, T., Yuan, J., Mochizuki‐Kashio, M., Suzuki, Y., Sugano, S., Nakaseko, C., Yokote, K., et al. (2012) · Blood · doi:10.1182/blood-2011-11-394932 · Cited by 195
Goff, D. J., Recart, A. C., Sadarangani, A., Chun, H.-J. E., Barrett, C. L., Krajewska, M., Leu, H. S., Low-Marchelli, J. M., Ma, W., Shih, A. Y., et al. (2013) · Cell stem cell · doi:10.1016/j.stem.2012.12.011 · Cited by 206
“Confocal fluorescence microscopic and immunohistochemical (IHC) analysis revealed dormant pHis-H3 Ki-67low human CD45+CD34+CD38+ cells adjacent to the marrow endosteal region (Figures 2D, 2E, S3A, and S3B), as previously reported in AML LSC xenograft models (Saito et al., 2010).”
InfluentialMechanisms of Disease: Cancer stem cells--targeting the evil twin
Trumpp, A., & Wiestler, O. D. (2008) · Nature Clinical Practice Oncology · doi:10.1038/ncponc1110 · Cited by 199
“While malignant development or transformation from HSCs or progenitor cells is likely to be the initiating event in leukemias and selected bone marrow-derived neoplasms”
BackgroundSATB1 Defines the Developmental Context for Gene Silencing by Xist in Lymphoma and Embryonic Cells
Agrelo, R., Souabni, A., Novatchkova, M., Haslinger, C., Leeb, M., Komnenovic, V., Kishimoto, H., Gresh, L., Kohwi-Shigematsu, T., Kenner, L., et al. (2009) · Developmental Cell · doi:10.1016/j.devcel.2009.03.006 · Cited by 197
“Progenitor-derived leukemia stem cells have also been observed to maintain progenitor identity and reactivate a self-renewal-associated program (Krivtsov et al., 2006).”
BackgroundResistance of mature T cells to oncogene transformation.
Newrzela, S., Cornils, K., Li, Z.-X., Baum, C., Brugman, M., Hartmann, M., Meyer, J., Hartmann, S., Hansmann, M., Fehse, B., et al. (2008) · Blood · doi:10.1182/blood-2007-12-128751 · Cited by 196
van Rhenen, A., Moshaver, B., Kelder, A., Feller, N., Nieuwint, A. W. M., Zweegman, S., Ossenkoppele, G. J., & Schuurhuis, G. J. (2007) · Leukemia · doi:10.1038/sj.leu.2404754 · Cited by 193
Forte, D., García-Fernández, M., Sánchez‐Aguilera, A., Stavropoulou, V., Fielding, C., Martín-Pérez, D., López, J. A., Costa, A. S. H., Tronci, L., Nikitopoulou, E., et al. (2020) · Cell Metabolism · doi:10.1016/j.cmet.2020.09.001 · Cited by 217
Menin inhibitor MI-3454 induces remission in MLL1-rearranged and NPM1-mutated models of leukemia
Kłossowski, S., Miao, H. Z., Kempińska, K., Wu, T., Purohit, T., Kim, E., Linhares, B. M., Chen, D., Jih, G. T., Perkey, E., et al. (2019) · Journal of Clinical Investigation · doi:10.1172/jci129126 · Cited by 253
“MLL1 translocations lead to fusion of the N-terminal fragment of MLL1 with one of over 60 protein partners (11-13), resulting in the expression of MLL fusion proteins that enhance proliferation and block hematopoietic differentiation, ultimately driving the development of leukemia (14).”
Self-citationIdentification of genes with abnormal expression changes in acute myeloid leukemia
Stirewalt, D. L., Meshinchi, S., Kopecky, K. J., Fan, W., Pogosova‐Agadjanyan, E. L., Engel, J. H., Cronk, M. R., Dorcy, K. S., McQuary, A. R., Hockenbery, D., et al. (2008) · Genes, Chromosomes and Cancer · doi:10.1002/gcc.20500 · Cited by 191
“In addition, certain genetic abnormalities have been found to convert committed normal hematopoietic cells into repopulating transformed blasts that behave like malignant stem cells (Huntly et al., 2004; Krivtsov et al., 2006).”
BackgroundCancer cell plasticity: Impact on tumor progression and therapy response
da Silva-Diz, V., Lorenzo-Sanz, L., Bernat‐Peguera, A., Lopez-Cerda, M., & Muñoz, P. (2018) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2018.08.009 · Cited by 217
“However, some reports have indicated that CSCs could also originate from more committed progenitors by dedifferentiation or reprogramming processes [13-16].”
BackgroundThe challenge of targeting cancer stem cells to halt metastasis
Agliano, A., Calvo, A., & Box, C. (2017) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2017.03.003 · Cited by 201
Reprogramming Cellular Identity for Regenerative Medicine
Cherry, A. B. C., & Daley, G. Q. (2012) · Cell · doi:10.1016/j.cell.2012.02.031 · Cited by 193
Structure of the MLL CXXC domain–DNA complex and its functional role in MLL-AF9 leukemia
Cierpicki, T., Risner, L. E., Grembecka, J. E., Lukasik, S. M., Popovic, R., Omonkowska, M., Shultis, D., Zeleznik‐Le, N. J., & Bushweller, J. H. (2009) · Nature Structural & Molecular Biology · doi:10.1038/nsmb.1714 · Cited by 179
“All mice expressing the C1188A mutant developed AML within 46 d ( n = 8), as expected for MLL-AF9–infected mic”
Myeloid progenitor cluster formation drives emergency and leukaemic myelopoiesis
Hérault, A., Binnewies, M., Leong, S., Calero‐Nieto, F. J., Zhang, S. Y., Kang, Y.-A., Wang, X., Pietras, E. M., Chu, S. H., Barry-Holson, K. Q., et al. (2017) · Nature · doi:10.1038/nature21693 · Cited by 215
Self-citationCancer Stem Cells in Breast: Current Opinion and Future Challenges
Charafe‐Jauffret, E., Monville, F., Ginestier, C., Dontu, G., Birnbaum, D., & Wicha, M. S. (2008) · Pathobiology · doi:10.1159/000123845 · Cited by 178
“Recent work provided support for this idea, based on the features of gene fusions found in human acute myeloid leukemia. A fusion protein called MLL-AF9 was genetically engineered in granulocyte-macrophage progenitor cells and transplanted into mice where it generated leukemia similar to acute myeloid leukemia. Isolat…”
BackgroundMagee, J. A., Ikenoue, T., Nakada, D., Lee, J., Guan, K., & Morrison, S. J. (2012) · Cell stem cell · doi:10.1016/j.stem.2012.05.026 · Cited by 188
“These self-renewal mechanisms are co-opted by leukemia cells irrespective of whether they arise from HSCs or from restricted progenitors (Krivtsov et al., 2006).”
Identification and targeting of cancer stem cells
Schatton, T., Frank, N. Y., & Frank, M. H. (2009) · BioEssays · doi:10.1002/bies.200900058 · Cited by 182
Stem cells in prostate cancer initiation and progression.
Lawson, D. A., & Witte, O. (2007) · Journal of Clinical Investigation · doi:10.1172/jci32810 · Cited by 183
MEF2 transcription factors: developmental regulators and emerging cancer genes
Pon, J. R., & Marra, M. A. (2015) · Oncotarget · doi:10.18632/oncotarget.6223 · Cited by 207
“Myeloid leukemias initiated through MLL-AF9 displayed increased Mef2c expression and required elevated MEF2C levels to maintain a high capacity for colony formation [128].”
BackgroundLi, Z.-J., Huang, H., Li, Y.-Y., Jiang, X., Chen, P., Arnovitz, S., Radmacher, M., Maharry, K., Elkahloun, A., Yang, X., et al. (2012) · Blood · doi:10.1182/blood-2011-10-386235 · Cited by 182
“M4 8 (24) 11 (21) 8 (23) 23 (26) 18 (30) 58 (21)”
InfluentialNonstochastic Reprogramming from a Privileged Somatic Cell State
Guo, S., Zi, X., Schulz, V., Cheng, J., Zhong, M., Koochaki, S., Megyola, C. M., Pan, X., Heydari, K., Weissman, S. M., et al. (2014) · Cell · doi:10.1016/j.cell.2014.01.020 · Cited by 174
“…(Aasen et al., 2008; Li et al., 2010; Samavarchi-Tehrani et al., 2010), do not endogenously express any of the Yamanaka factors (Kim et al., 2008; Krivtsov et al., 2006; Wakao et al., 2011), are more differentiated than stem cells (Eminli et al., 2009; Stadtfeld and Hochedlinger, 2010), and do…”
Methodp53 loss promotes acute myeloid leukemia by enabling aberrant self-renewalPreprint
Zhao, Z., Zuber, J. A., Díaz-Flores, E., Lintault, L., Kogan, S. C., Shannon, K., & Lowe, S. W. (2010) · Genes & Development · doi:10.1101/gad.1940710 · Cited by 175
“How this occurs has been a topic of much debate, although fusion proteins involving the mixedlineage leukemia (MLL) gene and lesions enhancing Wnt/ b-catenin signaling can confer this capability (Cozzio et al. 2003; Jamieson et al. 2004; Krivtsov et al. 2006).”
BackgroundKsiążkiewicz, M., Markiewicz, A., & Zaczek, A. J. (2012) · Pathobiology · doi:10.1159/000337106 · Cited by 192
Hofmann, I., Stover, E. H., Cullen, D. E., Mao, J., Morgan, K. J., Lee, B. H., Kharas, M. G., Miller, P. G., Cornejo, M., Okabe, R. O., et al. (2009) · Cell stem cell · doi:10.1016/j.stem.2009.03.016 · Cited by 181
“For example, activated kinases like BCR-ABL that do not have the potential for activating self-renewal programs in stem cells may be more reliant on these pathways than alleles such as MLL fusion genes that can confer properties of leukemia stem cells to committed progenitors (Cozzio et al., 2003; Huntly et al., 2004;…”
InfluentialSelf-citationKang, X., Kim, J., Deng, M., John, S., Chen, H., Wu, G., Phan, H., & Zhang, C. C. (2015) · Cell Cycle · doi:10.1080/15384101.2015.1121324 · Cited by 207
Normal stem cells and cancer stem cells: similar and different
Shackleton, M. J. (2010) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2010.04.002 · Cited by 168
AF10 Regulates Progressive H3K79 Methylation and HOX Gene Expression in Diverse AML Subtypes
Deshpande, A., Deshpande, A., Sinha, A., Chen, L., Chang, J., Cihan, A., Fazio, M., Chen, C., Zhu, N., Koche, R., et al. (2014) · Cancer Cell · doi:10.1016/j.ccell.2014.10.009 · Cited by 172
“…HOX cluster are critical for hematopoietic stem cell (HSC) self-renewal, and the expression of a particular subset of the HOXA gene cluster, specifically the Hoxa7–10 genes, is sharply downregulated when murine HSCs differentiate to granulocyte macrophage progenitors (GMPs) (Krivtsov et al., 2006).”
BackgroundInfluentialSelf-citationNotch pathway activation targets AML-initiating cell homeostasis and differentiation
Lobry, C., Ntziachristos, P., Ndiaye‐Lobry, D., Oh, P., Cimmino, L., Zhu, N., Araldi, E., Hu, W., Freund, J. E., Abdel-Wahab, O. I., et al. (2013) · The Journal of Experimental Medicine · doi:10.1084/jem.20121484 · Cited by 169
“Notch signaling is silenced in an MLL-AF9–driven mouse AML model To study in vivo the role of Notch signaling in AML, we used the MLL-AF9–driven AML animal model that shares several common features with MLL translocation-driven human AML (Krivtsov et al., 2006).”
BackgroundMethodSelf-citationSashida, G., Harada, H., Matsui, H., Oshima, M., Yui, M., Harada, Y., Tanaka, S., Mochizuki‐Kashio, M., Wang, C., Saraya, A., et al. (2014) · Nature Communications · doi:10.1038/ncomms5177 · Cited by 176
Requirement for CDK6 in MLL-rearranged acute myeloid leukemia
Placke, T., Faber, K., Nonami, A., Putwain, S. L., Salih, H. R., Heidel, F. H., Krämer, A., Root, D. E., Barbie, D. A., Krivtsov, A. V., et al. (2014) · Blood · doi:10.1182/blood-2014-02-558114 · Cited by 170
“A key functional feature of mixed-lineage leukemia (MLL) rearrangements is their ability to confer leukemia-initiating activity to hematopoietic stem and progenitor cells (HSPC).(5,6) MLL fusions are characterized by loss of the C-terminal H3K4 methyltransferase domain, and their leukemogenic activity is dependent on…”
Self-citationStoyanova, T., Cooper, A. R., Drake, J., Liu, X., Armstrong, A., Pienta, K., Zhang, H., Kohn, D., Huang, J.-T., Witte, O., et al. (2013) · Proceedings of the National Academy of Sciences of the United States of America · doi:10.1073/pnas.1320565110 · Cited by 170
Detection and analysis of mammary gland stem cells
Stingl, J. (2008) · The Journal of Pathology · doi:10.1002/path.2457 · Cited by 163
“Committed progenitors can also function as the cell of origin in human acute promyelocytic leukaemia and mouse acute myelogenous leukaemia [79,87,88].”
BackgroundToward modeling the bone marrow niche using scaffold-based 3D culture systems
Maggio, N. D., Piccinini, E., Jaworski, M., Trumpp, A., Wendt, D. J., & Martín, I. (2010) · Biomaterials · doi:10.1016/j.biomaterials.2010.09.041 · Cited by 166
Identification of Tumorsphere- and Tumor-Initiating Cells in HER2/Neu-Induced Mammary Tumors
Liu, J. C., Deng, T., Lehal, R., Kim, J., & Zacksenhaus, E. (2007) · Cancer Research · doi:10.1158/0008-5472.can-07-1486 · Cited by 163
“Similarly, MLL can be induced by oncogenic transformation of progenitor cells and activation of self-renewal genes (11).”
BackgroundMyeloproliferative neoplasm stem cells
Mead, A. J., & Mullally, A. (2017) · Blood · doi:10.1182/blood-2016-10-696005 · Cited by 187
Li, Z., Huang, H., Chen, P., He, M., Li, Y., Arnovitz, S., Jiang, X., He, C., Hyjek, E. M., Zhang, J., et al. (2012) · Nature Communications · doi:10.1038/ncomms1681 · Cited by 167
Self-citationSomatic stem cell heterogeneity: diversity in the blood, skin and intestinal stem cell compartments
Goodell, M. A., Nguyen, H., & Shroyer, N. F. (2015) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3980 · Cited by 182
Zhang, X., Weissman, S. M., & Newburger, P. E. (2014) · RNA Biology · doi:10.4161/rna.28828 · Cited by 172
“HOX genes also contribute to the pathogenesis of acute leukemia and the selfrenewal capacity of leukemia stem cells.(12,14,15) Within the four paralogous clusters of human HOX genes, lincRNAs constitute a newly recognized but probably more abundant intergenic transcription activity than the betterdefined microRNAs, su…”
BackgroundDifferential niche and Wnt requirements during acute myeloid leukemia progression.
Lane, S. W., Wang, Y., Celso, C. L., Ragu, C., Bullinger, L., Sykes, S. M., Ferraro, F., Shterental, S., Lin, C. P., Gilliland, D., et al. (2011) · Blood · doi:10.1182/blood-2011-03-345165 · Cited by 162
Self-citationThe non-coding RNA landscape of human hematopoiesis and leukemia
Schwarzer, A., Emmrich, S., Schmidt, F., Beck, D., Ng, M. S. W., Reimer, C., Adams, F. F., Grasedieck, S., Witte, D., Käbler, S., et al. (2017) · Nature Communications · doi:10.1038/s41467-017-00212-4 · Cited by 158
Cancer Stem Cells: Controversial or Just Misunderstood?
Jordan, C. (2009) · Cell Stem Cell · doi:10.1016/j.stem.2009.02.003 · Cited by 161
“The origin of such a cell need not necessarily be a normal stem cell, an observation that has become increasingly clear from experimental cancer models (Krivtsov et al., 2006).”
BackgroundConcise Review: Cancer/Testis Antigens, Stem Cells, and Cancer
Costa, F. F., Blanc, K. L., & Brodin, B. A. (2006) · Stem Cells · doi:10.1634/stemcells.2006-0469 · Cited by 147
Stretching the limits: from homeostasis to stem cell plasticity in wound healing and cancer
Ge, Y., & Fuchs, E. V. (2018) · Nature Reviews Genetics · doi:10.1038/nrg.2018.9 · Cited by 172
Brain tumor stem cells: The cancer stem cell hypothesis writ large
Dirks, P. B. (2010) · Molecular Oncology · doi:10.1016/j.molonc.2010.08.001 · Cited by 144
HBO1 is required for the maintenance of leukaemia stem cells
MacPherson, L., Anokye, J., Yeung, M. M., Lam, E. Y. N., Chan, Y.-C., Weng, C.-F., Yeh, P. S.-H., Knezevic, K., Butler, M. S., Hoegl, A., et al. (2019) · Nature · doi:10.1038/s41586-019-1835-6 · Cited by 172
Metadata
- Authors
- Krivtsov, A. V., Twomey, D., Feng, Z., Stubbs, M. C., Wang, Y., Faber, J., Levine, J. E., Wang, J., Hahn, W. C., Gilliland, D. G., Golub, T. R., & Armstrong, S. A.
- Affiliations
- Boston Children's Hospital (US)
- Broad Institute (US)
- Brigham and Women's Hospital (US)
- Corresponding author
- Armstrong, Scott A.
- ORCID
- Venue
- Nature
- Published
- 2006-07-16
- Volume
- 442
- Issue
- 7104
- Pages
- 818-822
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2109336877
- Cited by
- 1,513
- References
- 0
- Citations by year
- 2026: 37 · 2025: 45 · 2024: 66 · 2023: 70 · 2022: 60 · 2021: 65 · 2020: 66 · 2019: 73 · 2018: 70 · 2017: 75 · 2016: 85 · 2015: 83 · 2014: 77 · 2013: 79 · 2012: 92
- FWCI
- 59.70
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Damon Runyon Cancer Research Foundation
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- leukemia stem cells, committed progenitors, MLL-AF9 fusion, CFU-GM, self-renewal, cancer stem cells, hematopoietic stem cells, gene expression profiling, oncogenic transformation, targeted cancer therapy
- MeSH terms
- Animals, Cell Differentiation, Cell Division, Cell Line, Cell Transformation, Neoplastic, Granulocytes, Humans, Leukemia, Macrophages, Neoplasm Transplantation, Neoplastic Stem Cells, Leukemia, Myelomonocytic, Acute, Oncogene Proteins, Fusion, Survival Rate, Cell Lineage, Mice, Myeloid-Lymphoid Leukemia Protein
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
