The origin of hematopoietic cell type diversity

Hoang, Trang

doi:10.1038/sj.onc.1207937

Cited by 42 publications

(29 citation statements)

References 112 publications

(101 reference statements)

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“…In this way, stem cells in the model keep on either proliferating or differentiating, depending on the number ratio of the cell types. If the ratio of stem cell is too large (small), the ratio of differentiation (proliferation) increases, so that the number distribution of two cell types remains within a certain range, implying (macroscopic) robustness of the number ratio of cells of different types (see [20] for a demonstration of such regulation of cell number and [21] for possible relationship with the present theory. Also see [22] for a bifurcation analysis on the stabilization of a new cell type by cell-cell interaction.…”

Section: (D) Regulation Between Proliferation and Differentiation Leamentioning

confidence: 90%

Characterization of stem cells and cancer cells on the basis of gene expression profile stability, plasticity, and robustness

Kaneko

2011

BioEssays

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Here I present and discuss a model that, among other things, appears able to describe the dynamics of cancer cell origin from the perspective of stable and unstable gene expression profiles. In identifying such aberrant gene expression profiles as lying outside the normal stable states attracted through development and normal cell differentiation, the hypothesis explains why cancer cells accumulate mutations, to which they are not robust, and why these mutations create a new stable state far from the normal gene expression profile space. Such cells are in strong contrast with normal cell types that appeared as an attractor state in the gene expression dynamical system under cell-cell interaction and achieved robustness to noise through evolution, which in turn also conferred robustness to mutation. In complex gene regulation networks, other aberrant cellular states lacking such high robustness are expected to remain, which would correspond to cancer cells.

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Section: (D) Regulation Between Proliferation and Differentiation Leamentioning

confidence: 90%

Characterization of stem cells and cancer cells on the basis of gene expression profile stability, plasticity, and robustness

Kaneko

2011

BioEssays

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“…This is in agreement with our data, since we also predicted the possible role of VEGF, PDGF and STAT molecules in oncogenesis. It is also interesting that these molecules play a role in the diversity of the hematopoetic population and possibly in the leukemic populations (124). These observations bring mutations to mind.…”

Section: Modelling Jak-stat/mapk and Tgf-β Signaling Pathwaysmentioning

confidence: 99%

Pathway simulations in common oncogenic drivers of leukemic and rhabdomyosarcoma cells: A systems biology approach

et al. 2012

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Abstract. A part of current research has intensively been focused on the proliferation and metabolic processes governing biological systems. Since the advent of high throughput methodologies such as microarrays, the load of genomic data has increased geometrically and along with that the need for computational methods to interpret these data. In the present study, we investigated in vitro the common proliferation and metabolic processes, associated with common oncogenic pathways, as far as gene expression is concerned, between the T-cell acute lymphoblastic leukemia (CCRF-CEM) and the rhabdomyosarcoma (TE-671) cell lines. We present a computational approach, using cDNA microarrays, in order to identify commonalities between diverse biological systems. Our analysis predicted that JAK1, STAT1, PIAS2 and CDK4 are the driving forces in the two cell lines. This type of analysis may lead to the understanding of the common mechanisms that transform physiological cells to malignant, and may reveal a new holistic approach to understanding the dynamics of tumor onset as well as the mechanistics behind oncogenic drivers. IntroductionIt is a fact that tumors can be as diverse as the patients carrying them. Due to these differences, tumors are extremely difficult to cure, as the effects of treatments differ depending on the patient. Previously, Nicolis showed that stem cells are found in different tumor types, suggesting that they can be the etiology of tumor maintenance and growth (1). However, there is evidence that even normal, already differentiated cells can be transformed into tumorigenic ones (1). Perilongo et al also reported a case of a child manifesting five different tumor types simultaneously (2). It may be possible that stem cells originating from the same organism possess similar mutations or alterations, thus giving rise to five different tumor types. Therefore, there is a need for the investigation of common pathways between different tumor types. The discovery of similar or opposite gene expression profiles could lead us to the understanding of a common tumor origin, if such exists.A number of studies have investigated the detection of cancer germ line genes (CGGs) both in pediatric sarcomas (3) and pediatric brain tumors (4). The discovery of global antigens for tumor vaccines could become salvatory for childhood malignancies (3). Other studies have reported the common appearance of antigens in Ewing's sarcoma/primitive neuroectodermal tumor (EWS/PNET) with lymphoblastic lymphoma (5). Rhabdomyosarcoma (RMS) belongs to the PNET family of tumors, which utilize embryonic genes for their progression (6). Acute lymphoblastic leukemia (ALL), which originates from the lymphoblast, also uses embryonic mechanisms for its differentiation and progression.Another point which requires attention is the regulation of genes through transcription factors (TFs). Knowledge of gene regulatory networks is considered to be of crucial importance for understanding diseases such as cancer, and may lead to new therapeutic approaches...

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“…[1][2][3] In the mouse, the primitive or embryonic wave of hematopoiesis occurs around embryonic day 7.5 in the yolk-sac blood island, and produces primitive erythrocytes and macrophages. 4,5 This primitive wave of hematopoiesis lasts for a transient period of a few days and is subsequently replaced by the definitive program.…”

Section: Introductionmentioning

confidence: 99%

The zebrafish udu gene encodes a novel nuclear factor and is essential for primitive erythroid cell development

Liu

Osato

et al. 2007

Blood

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Hematopoiesis is a complex process which gives rise to all blood lineages in the course of an organism's lifespan. However, the underlying molecular mechanism governing this process is not fully understood. Here we report the isolation and detailed study of a newly identified zebrafish ugly duckling (Udu) mutant allele, Udu sq1 . We show that loss-of-function mutation in the udu gene disrupts primitive erythroid cell proliferation and differentiation in a cell-autonomous manner, resulting in red blood cell (RBC) hypoplasia. Positional cloning reveals that the Udu gene encodes a novel factor that contains 2 paired amphipathic ␣-helix-like IntroductionHematopoiesis in vertebrate occurs in 2 waves, primitive and definitive. [1][2][3] In the mouse, the primitive or embryonic wave of hematopoiesis occurs around embryonic day 7.5 in the yolk-sac blood island, and produces primitive erythrocytes and macrophages. 4,5 This primitive wave of hematopoiesis lasts for a transient period of a few days and is subsequently replaced by the definitive program. Murine definitive hematopoiesis is believed to originate from a distinctive region known as the aorta-gonad-mesonephros at embryonic days 7.5 to 8. 6,7 These definitive hematopoietic precursors, presumably the definitive hematopoietic stem cells, then migrate to the fetal liver, where they undergo rapid proliferation and differentiation, and finally colonize the bone marrow for adult hematopoiesis. In contrast to primitive hematopoiesis, the definitive hematopoietic program gives rise to all the mature blood cell types and remains active throughout the lifetime of the organism.In zebrafish, hematopoiesis also comprises both primitive and definitive programs and produces mature blood cell types similar to those found in mammals. 8,9 Zebrafish primitive erythropoiesis begins at the 4-somite stage as a pair of bilateral stripes in the posterior lateral mesoderm. 10 These stripes extend anteriorly and posteriorly, and then converge in the midline at the 20-somite stage to form the intermediate cell mass (ICM), where erythroid precursors further develop and enter the circulation by 24 to 26 hours after fertilization (hpf). 10,11 On the other hand, primitive myelopoiesis originates from the rostral blood island in the anterior lateral mesoderm at around the 10-somite stage and produces mainly macrophages and possibly some neutrophils. [12][13][14][15] Recent studies demonstrate that zebrafish definitive hematopoiesis initiates in the ventral wall of dorsal aorta between 26 and 48 hpf, 16,17 and then establishes the adult hematopoietic organ in the kidney by 5 days after fertilization (dpf). 11 The zebrafish mutant, ugly duckling (Udu tu24 ), was first isolated from the 1996 Tuebingen large-scale screen as a mutant defective in morphogenesis during gastrulation and tail formation. 18 In this article, we report the isolation and detailed study of a new udu allele, udu sq1 , as a mutant with a defect in blood cell development. Cell-cycle, cytologic, and transplantation analyses sho...

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The origin of hematopoietic cell type diversity

Cited by 42 publications

References 112 publications

Characterization of stem cells and cancer cells on the basis of gene expression profile stability, plasticity, and robustness

Characterization of stem cells and cancer cells on the basis of gene expression profile stability, plasticity, and robustness

Pathway simulations in common oncogenic drivers of leukemic and rhabdomyosarcoma cells: A systems biology approach

The zebrafish udu gene encodes a novel nuclear factor and is essential for primitive erythroid cell development

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