Plasticity within stem cell hierarchies in mammalian epithelia

Tetteh, Paul W.; Farin, Henner F.; Clevers, Hans

doi:10.1016/j.tcb.2014.09.003

Cited by 150 publications

(153 citation statements)

References 85 publications

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“…This mechanism has enormous implications for control of normal cell growth and deregulated proliferation in cancer. In a stem cell context, R-point control is crucial for determining the balance between self-renewal, quiescence and differentiation of stem cell populations (Li and Clevers, 2010;Tetteh et al, 2015). For example, proliferative control of hematopoietic stem cells is a critical determinant that distinguishes normal and cancer-related hematopoietic function (Pietras et al, 2011).…”

Section: Progression Through the Cell Cycle As A Cell Fate Decisionmentioning

confidence: 99%

Cycling through developmental decisions: how cell cycle dynamics control pluripotency, differentiation and reprogramming

2016

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A strong connection exists between the cell cycle and mechanisms required for executing cell fate decisions in a wide-range of developmental contexts. Terminal differentiation is often associated with cell cycle exit, whereas cell fate switches are frequently linked to cell cycle transitions in dividing cells. These phenomena have been investigated in the context of reprogramming, differentiation and trans-differentiation but the underpinning molecular mechanisms remain unclear. Most progress to address the connection between cell fate and the cell cycle has been made in pluripotent stem cells, in which the transition through mitosis and G1 phase is crucial for establishing a window of opportunity for pluripotency exit and the initiation of differentiation. This Review will summarize recent developments in this area and place them in a broader context that has implications for a wide range of developmental scenarios.

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Section: Progression Through the Cell Cycle As A Cell Fate Decisionmentioning

confidence: 99%

Cycling through developmental decisions: how cell cycle dynamics control pluripotency, differentiation and reprogramming

2016

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“…Furthermore, progenitors expressing the same putative stem cell marker can exhibit heterogeneous fate choices (Graf and Stadtfeld, 2008), while stem cells with different expression profiles may behave similarly in the long term. Finally, recent studies in disparate tissues have also shown that cells normally committed to differentiation can, in the course of regeneration following the targeted ablation of endogenous stem cell populations, re-acquire the hallmark properties of tissue stem cells, including the potential for long-term self-renewal (Rompolas et al, 2012;van Es et al, 2012;Tata et al, 2013;Yanger et al, 2014;Tetteh et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Dynamic stem cell heterogeneity

2015

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Recent lineage-tracing studies based on inducible genetic labelling have emphasized a crucial role for stochasticity in the maintenance and regeneration of cycling adult tissues. These studies have revealed that stem cells are frequently lost through differentiation and that this is compensated for by the duplication of neighbours, leading to the consolidation of clonal diversity. Through the combination of long-term lineage-tracing assays with short-term in vivo live imaging, the cellular basis of this stochastic stem cell loss and replacement has begun to be resolved. With a focus on mammalian spermatogenesis, intestinal maintenance and the hair cycle, we review the role of dynamic heterogeneity in the regulation of adult stem cell populations.

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“…Both stem cells and progenitor cells can produce differentiated cells. However, only stem cells can self-renew and give rise to more stem cells [48][49][50][51][52]. This means that stem cells have the exclusive potential to produce an unlimited number of cells.…”

Section: Stem Cells Progenitor Cells Differentiated Cells Differenmentioning

confidence: 99%

“…Our life would also be at risk if our differentiated cells (e.g., neurons, cardiomyocytes) abandoned their normal functions to dedifferentiate and become other cells. In some situations, however, cell differentiation can be reversible [48][49][50][51][52]. Since most human cells have the same DNA (except some blood cells, gametes, etc), the shape and function of a cell largely depend on epigenetic modifications that determine which parts of the DNA are active or inactive.…”

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The Stem Cell Division Theory of Cancer

López‐Lázaro

2017

Preprint

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All cancer registries constantly show striking differences in cancer incidence by age and among tissues. For example, lung cancer is diagnosed hundreds of times more often at age 70 than at age 20, and this cancer in nonsmokers occurs thousands of times more frequently than heart cancer in smokers. An analysis of these differences using basic concepts in cell biology indicates that cancer is the end-result of the accumulation of cell divisions in stem cells. In other words, the main determinant of carcinogenesis is the number of cell divisions that the DNA of a stem cell has accumulated in any type of cell from the zygote. Cell division, process by which a cell copies and separates its cellular components to finally split into two cells, is necessary to produce the large number of cells required for living. However, cell division can lead to a variety of cancer-promoting errors, such as mutations occurring during DNA replication, chromosome aberrations arising during mitosis, errors in the distribution of cell-fate determinants between the daughter cells, and failures to restore physical interactions with other tissue components. Some of these errors are spontaneous, others are promoted by endogenous DNA damage occurring during quiescence, and others are influenced by pathological and environmental factors. The cell divisions required for carcinogenesis are primarily caused by multiple local and systemic physiological signals rather than by errors in the DNA of the cells. As carcinogenesis progresses, the accumulation of DNA errors promotes cell division and eventually triggers cell division under permissive extracellular environments. The accumulation of cell divisions in stem cells drives not only the accumulation of the DNA alterations required for carcinogenesis, but also the formation and growth of the abnormal cell populations that characterize the disease. This model of carcinogenesis provides a new framework for understanding the disease and has important implications for cancer prevention and therapy.

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Plasticity within stem cell hierarchies in mammalian epithelia

Cited by 150 publications

References 85 publications

Cycling through developmental decisions: how cell cycle dynamics control pluripotency, differentiation and reprogramming

Cycling through developmental decisions: how cell cycle dynamics control pluripotency, differentiation and reprogramming

Dynamic stem cell heterogeneity

The Stem Cell Division Theory of Cancer

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