Rat model of the human “Triton” tumor: direct genetic evidence for the myogenic differentiation capacity of schwannoma cells using the mutant neu gene as a cell lineage marker

1991 ◽  
Vol 48 (1) ◽  
pp. 33-42 ◽  
Author(s):  
Alexander Yu. Nikitin ◽  
Klaus Lennartz ◽  
Kazymir M. Pozharisski ◽  
Manfred F. Rajewsky
Keyword(s):  
Rat Model ◽  
Myogenic Differentiation ◽  
Cell Lineage ◽  
Genetic Evidence ◽  
Differentiation Capacity ◽  
A Cell ◽  
Lineage Marker ◽  
Direct Genetic Evidence

scholarly journals Limitations of Green Fluorescent Protein as a Cell Lineage Marker

Stem Cells ◽  
2007 ◽  
Vol 25 (10) ◽  
pp. 2593-2600 ◽  
Author(s):  
E. Scott Swenson ◽  
Joanna G. Price ◽  
Timothy Brazelton ◽  
Diane S. Krause
Keyword(s):  
Green Fluorescent Protein ◽  
Fluorescent Protein ◽  
Cell Lineage ◽  
A Cell ◽  
Lineage Marker ◽  
Green Fluorescent

scholarly journals Aspects of the biology of regeneration and repair in the human gastrointestinal tract

1998 ◽  
Vol 353 (1370) ◽  
pp. 925-933 ◽  
Author(s):  
Nicholas A. Wright
Keyword(s):  
Stem Cells ◽  
Gastric Gland ◽  
Cell Lineage ◽  
Mucosal Ulceration ◽  
Cell Lineages ◽  
Trefoil Peptides ◽  
Pyloric Mucosa ◽  
A Cell ◽  
Epidermal Growth ◽  
Altered Gene

The main pathways of epithelial differentiation in the intestine, Paneth, mucous, endocrine and columnar cell lineages are well recognized. However, in abnormal circumstances, for example in mucosal ulceration, a cell lineage with features distinct from these emerges, which has often been dismissed in the past as ‘pyloric’ metaplasia, because of its morphological resemblance to the pyloric mucosa in the stomach. However, we can conclude that this cell lineage has a defined phenotype unique in gastrointestinal epithelia, has a histogenesis that resembles that of Brunner's glands, but acquires a proliferative organization similar to that of the gastric gland. It expresses several peptides of particular interest, including epidermal growth factor, the trefoil peptides TFF1, TFF2, TFF3, lysozyme and PSTI. The presence of this lineage also appears to cause altered gene expression in adjacent indigenous cell lineages. We propose that this cell lineage is induced in gastrointestinal stem cells as a result of chronic mucosal ulceration, and plays an important part in ulcer healing; it should therefore be added to the repertoire of gastrointestinal stem cells.

scholarly journals Redefining interferon-producing killer dendritic cells as a novel intermediate in NK-cell differentiation

Blood ◽  
2012 ◽  
Vol 119 (19) ◽  
pp. 4349-4357 ◽  
Author(s):  
Fanny Guimont-Desrochers ◽  
Geneviève Boucher ◽  
Zhongjun Dong ◽  
Martine Dupuis ◽  
André Veillette ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Nk Cells ◽  
Adoptive Transfer ◽  
Nk Cell ◽  
Cell Lineage ◽  
Current View ◽  
Antitumoral Activity ◽  
Nk Cell Differentiation ◽  
A Cell

Abstract The cell lineage origin of IFN-producing killer dendritic cells (IKDCs), which exhibit prominent antitumoral activity, has been subject to debate. Although IKDCs were first described as a cell type exhibiting both plasmacytoid DC and natural killer (NK) cell properties, the current view reflects that IKDCs merely represent activated NK cells expressing B220, which were thus renamed B220+ NK cells. Herein, we further investigate the lineage relation of B220+ NK cells with regard to other NK-cell subsets. We surprisingly find that, after adoptive transfer, B220− NK cells did not acquire B220 expression, even in the presence of potent activating stimuli. These findings strongly argue against the concept that B220+ NK cells are activated NK cells. Moreover, we unequivocally show that B220+ NK cells are highly proliferative and differentiate into mature NK cells after in vivo adoptive transfer. Additional phenotypic, functional, and transcriptional characterizations further define B220+ NK cells as immediate precursors to mature NK cells. The characterization of these novel attributes to B220+ NK cells will guide the identification of their ortholog in humans, contributing to the design of potent cancer immunotherapies.

scholarly journals Expression of bcl-2 in bladder neoplasms is a cell lineage associated and p53-independent event.

1997 ◽  
Vol 50 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Q L Lu ◽  
M Laniado ◽  
P D Abel ◽  
G W Stamp ◽  
E N Lalani
Keyword(s):  
Bladder Neoplasms ◽  
Cell Lineage ◽  
Independent Event ◽  
A Cell

scholarly journals Epigenetic mechanisms mediating cell state transitions in chondrocytes

2020 ◽  
Author(s):  
Manuela Wuelling ◽  
Christoph Neu ◽  
Andrea M. Thiesen ◽  
Simo Kitanovski ◽  
Yingying Cao ◽  
...  
Keyword(s):  
Metabolic Pathways ◽  
Cell Lineage ◽  
Cell Types ◽  
State Transitions ◽  
Epigenetic Mechanisms ◽  
Cell Type ◽  
Transition Analysis ◽  
Lineage Differentiation ◽  
A Cell ◽  
Cell Type Specific

AbstractEpigenetic modifications play critical roles in regulating cell lineage differentiation, but the epigenetic mechanisms guiding specific differentiation steps within a cell lineage have rarely been investigated. To decipher such mechanisms, we used the defined transition from proliferating (PC) into hypertrophic chondrocytes (HC) during endochondral ossification as a model. We established a map of activating and repressive histone modifications for each cell type. ChromHMM state transition analysis and Pareto-based integration of differential levels of mRNA and epigenetic marks revealed that differentiation associated gene repression is initiated by the addition of H3K27me3 to promoters still carrying substantial levels of activating marks. Moreover, the integrative analysis identified genes specifically expressed in cells undergoing the transition into hypertrophy.Investigation of enhancer profiles detected surprising differences in enhancer number, location, and transcription factor binding sites between the two closely related cell types. Furthermore, cell type-specific upregulation of gene expression was associated with a shift from low to high H3K27ac decoration. Pathway analysis identified PC-specific enhancers associated with chondrogenic genes, while HC-specific enhancers mainly control metabolic pathways linking epigenetic signature to biological functions.

scholarly journals HNF1A recruits UTX to activate a differentiation program that suppresses pancreatic cancer

2019 ◽  
Author(s):  
Mark Kalisz ◽  
Edgar Bernardo ◽  
Anthony Beucher ◽  
Miguel Angel Maestro ◽  
Natalia del Pozo ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Epithelial Mesenchymal Transition ◽  
Pancreatic Acinar Cells ◽  
Ductal Adenocarcinoma ◽  
Molecular Phenotype ◽  
Mesenchymal Transition ◽  
A Cell ◽  
Pancreatic Exocrine ◽  
Direct Genetic Evidence

AbstractDefects in transcriptional regulators of pancreatic exocrine differentiation have been implicated in pancreatic tumorigenesis, but the molecular mechanisms are poorly understood. The locus encoding the transcription factor HNF1A harbors susceptibility variants for pancreatic ductal adenocarcinoma (PDAC), while KDM6A, encoding the histone demethylase UTX, carries somatic mutations in PDAC. Here, we show that pancreas-specific Hnf1a null mutations phenocopy Utx deficient mutations, and both synergize with KrasG12D to cause PDAC with sarcomatoid features. We combine genetic, epigenomic and biochemical studies to show that HNF1A recruits UTX to genomic binding sites in pancreatic acinar cells. This remodels the acinar enhancer landscape, activates a differentiation program, and indirectly suppresses oncogenic and epithelial-mesenchymal transition genes. Finally, we identify a subset of non-classical PDAC samples that exhibit the HNF1A/UTX-deficient molecular phenotype. These findings provide direct genetic evidence that HNF1A-deficiency promotes PDAC. They also connect the tumor suppressive role of UTX deficiency with a cell-specific molecular mechanism that underlies PDAC subtype definition.

A single cell approach to problems of cell lineage and commitment during embryogenesis of Drosophila melanogaster

Development ◽  
1987 ◽  
Vol 100 (1) ◽  
pp. 1-12 ◽  
Author(s):  
G.M. Technau
Keyword(s):  
Drosophila Melanogaster ◽  
Single Cell ◽  
Cell Lineage ◽  
Cellular Level ◽  
Central Importance ◽  
Cell Level ◽  
Combined Application ◽  
A Cell ◽  
Pole Cells ◽  
Drosophila Embryos

The mechanisms leading to the commitment of a cell to a particular fate or to restrictions in its developmental potencies represent a problem of central importance in developmental biology. Both at the genetic and at the molecular level, studies addressing this topic using the fruitfly Drosophila melanogaster have advanced substantially, whereas, at the cellular level, experimental techniques have been most successfully applied to organisms composed of relatively large and accessible cells. The combined application of the different approaches to one system should improve our understanding of the process of commitment as a whole. Recently, a method has been devised to study cell lineage in Drosophila embryos at the single cell level. This method has been used to analyse the lineages, as well as the state of commitment of single cell progenitors from various ectodermal, mesodermal and endodermal anlagen and of the pole cells. The results obtained from a clonal analysis of wild-type larval structures are discussed in this review.

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