scholarly journals Linking genomic reorganization to tumor initiation via the giant cell cycle

Oncogenesis ◽  
2016 ◽  
Vol 5 (12) ◽  
pp. e281-e281 ◽  
Author(s):  
N Niu ◽  
J Zhang ◽  
N Zhang ◽  
I Mercado-Uribe ◽  
F Tao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Giant Cell ◽  
Tumor Initiation ◽  
Genomic Reorganization

In situ cell cycle analysis in giant cell tumor of bone reveals patients with elevated risk of reduced progression-free survival

Bone ◽  
2019 ◽  
Vol 127 ◽  
pp. 188-198 ◽  
Author(s):  
Mate E. Maros ◽  
Sven Schnaidt ◽  
Peter Balla ◽  
Zoltan Kelemen ◽  
Zoltan Sapi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Giant Cell Tumor ◽  
Giant Cell ◽  
Progression Free Survival ◽  
Elevated Risk ◽  
Cell Tumor ◽  
Cell Cycle Analysis ◽  
Free Survival

Oncogenic KRAS signaling and YAP1/β-catenin: Similar cell cycle control in tumor initiation

2016 ◽  
Vol 58 ◽  
pp. 79-85 ◽  
Author(s):  
Ruth Nussinov ◽  
Chung-Jung Tsai ◽  
Hyunbum Jang ◽  
Tamás Korcsmáros ◽  
Peter Csermely
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Control ◽  
Tumor Initiation ◽  
Similar Cell

scholarly journals Monocyte progenitors give rise to multinucleated giant cells

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Anne Kathrin Lösslein ◽  
Florens Lohrmann ◽  
Lisa Scheuermann ◽  
Kourosh Gharun ◽  
Jana Neuber ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Immune Response ◽  
Giant Cell ◽  
Cell Transformation ◽  
Cholesterol Metabolism ◽  
Giant Cells ◽  
Multinucleated Giant Cells ◽  
Toll Like Receptor ◽  
High Cholesterol ◽  
Mycobacterial Infections

AbstractThe immune response to mycobacteria is characterized by granuloma formation, which features multinucleated giant cells as a unique macrophage type. We previously found that multinucleated giant cells result from Toll-like receptor-induced DNA damage and cell autonomous cell cycle modifications. However, the giant cell progenitor identity remained unclear. Here, we show that the giant cell-forming potential is a particular trait of monocyte progenitors. Common monocyte progenitors potently produce cytokines in response to mycobacteria and their immune-active molecules. In addition, common monocyte progenitors accumulate cholesterol and lipids, which are prerequisites for giant cell transformation. Inducible monocyte progenitors are so far undescribed circulating common monocyte progenitor descendants with high giant cell-forming potential. Monocyte progenitors are induced in mycobacterial infections and localize to granulomas. Accordingly, they exhibit important immunological functions in mycobacterial infections. Moreover, their signature trait of high cholesterol metabolism may be piggy-backed by mycobacteria to create a permissive niche.

scholarly journals Reprogramming the Cell Cycle for Endoreduplication in Rodent Trophoblast Cells

1998 ◽  
Vol 9 (4) ◽  
pp. 795-807 ◽  
Author(s):  
Alasdair MacAuley ◽  
James C. Cross ◽  
Zena Werb
Keyword(s):  
Cell Cycle ◽  
Cell Differentiation ◽  
Giant Cell ◽  
Mitotic Cycle ◽  
Mitotic Cell ◽  
Giant Cells ◽  
Cyclin B ◽  
Helix Loop Helix ◽  
Trophoblast Giant Cells ◽  
Cycle Regulation

Differentiation of trophoblast giant cells in the rodent placenta is accompanied by exit from the mitotic cell cycle and onset of endoreduplication. Commitment to giant cell differentiation is under developmental control, involving down-regulation of Id1and Id2, concomitant with up-regulation of the basic helix-loop-helix factor Hxt and acquisition of increased adhesiveness. Endoreduplication disrupts the alternation of DNA synthesis and mitosis that maintains euploid DNA content during proliferation. To determine how the mammalian endocycle is regulated, we examined the expression of the cyclins and cyclin-dependent kinases during the transition from replication to endoreduplication in the Rcho-1 rat choriocarcinoma cell line. We cultured these cells under conditions that gave relatively synchronous endoreduplication. This allowed us to study the events that occur during the transition from the mitotic cycle to the first endocycle. With giant cell differentiation, the cells switched cyclin D isoform expression from D3 to D1 and altered several checkpoint functions, acquiring a relative insensitivity to DNA-damaging agents and a coincident serum independence. The initiation of S phase during endocycles appeared to involve cycles of synthesis of cyclins E and A, and termination of S was associated with abrupt loss of cyclin A and E. Both cyclins were absent from gap phase cells, suggesting that their degradation may be necessary to allow reinitiation of the endocycle. The arrest of the mitotic cycle at the onset of endoreduplication was associated with a failure to assemble cyclin B/p34cdk1complexes during the first endocycle. In subsequent endocycles, cyclin B expression was suppressed. Together these data suggest several points at which cell cycle regulation could be targeted to shift cells from a mitotic to an endoreduplicative cycle.

Giant cell formation: the way to cell death or cell survival?

2011 ◽  
Vol 6 (5) ◽  
pp. 675-684 ◽  
Author(s):  
Rostyslav Horbay ◽  
Rostyslav Stoika
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Giant Cell ◽  
Cell Formation ◽  
Giant Cells ◽  
Cancer Development ◽  
Mitotic Catastrophe ◽  
Giant Cell Formation ◽  
Cycle Disorders

AbstractThe study of giant cells in populations of different tumor cells and evaluation of their role in cancer development is an expanding field. The formation of giant cells has been shown to be followed by mitotic catastrophe, apoptosis, necrosis, and other types of cell elimination. Reports also demonstrate that giant cells can escape cell death and give rise to new cancer cells. However, it is not known if the programmed cell death is involved in this type of cell cycle disorders. Here we describe principal events that are observed during giant cell formation. We also consider the role of giant cells in cancer development, taking into account both published work and our own recent data in this field.

scholarly journals Cell Cycle Regulatory Protein Expression in Multinucleated Giant Cells of Giant Cell Tumor of Bone: do They Proliferate?

2021 ◽  
Vol 27 ◽  
Author(s):  
Mate E. Maros ◽  
Peter Balla ◽  
Tamas Micsik ◽  
Zoltan Sapi ◽  
Miklos Szendroi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Giant Cell Tumor ◽  
Giant Cell ◽  
Regulatory Protein ◽  
Giant Cells ◽  
Cell Tumor ◽  
G1 Phase ◽  
Cdk Inhibitors ◽  
Multinucleated Giant Cells ◽  
Early Replication

Cells of the monocyte macrophage lineage form multinucleated giant cells (GCs) by fusion, which may express some cell cycle markers. By using a comprehensive marker set, here we looked for potential replication activities in GCs, and investigated whether these have diagnostic or clinical relevance in giant cell tumor of bone (GCTB). GC rich regions of 10 primary and 10 first recurrence GCTB cases were tested using immunohistochemistry in tissue microarrays. The nuclear positivity rate of the general proliferation marker, replication licensing, G1/S-phase, S/G2/M-phase, mitosis promoter, and cyclin dependent kinase (CDK) inhibitor reactions was analyzed in GCs. Concerning Ki67, moderate SP6 reaction was seen in many GC nuclei, while B56 and Mib1 positivity was rare, but the latter could be linked to more aggressive (p = 0.012) phenotype. Regular MCM6 reaction, as opposed to uncommon MCM2, suggested an initial DNA unwinding. Early replication course in GCs was also supported by widely detecting CDK4 and cyclin E, for the first time, and confirming cyclin D1 upregulation. However, post-G1-phase markers CDK2, cyclin A, geminin, topoisomerase-2a, aurora kinase A, and phospho-histone H3 were rare or missing. These were likely silenced by upregulated CDK inhibitors p15INK4b, p16INK4a, p27KIP1, p53 through its effector p21WAF1 and possibly cyclin G1, consistent with the prevention of DNA replication. In conclusion, the upregulation of known and several novel cell cycle progression markers detected here clearly verify early replication activities in GCs, which are controlled by cell cycle arresting CDK inhibitors at G1 phase, and support the functional maturation of GCs in GCTB.

scholarly journals p63 regulates cell proliferation and cell cycle progression-associated genes in stromal cells of giant cell tumor of the bone

2012 ◽  
Vol 42 (2) ◽  
pp. 437-443 ◽  
Author(s):  
CAROL PO YING LAU ◽  
PATRICK KWOK SHING NG ◽  
MAN SHAN LI ◽  
STEPHEN KWOK WING TSUI ◽  
LIN HUANG ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Giant Cell Tumor ◽  
Giant Cell ◽  
Stromal Cells ◽  
Cell Cycle Progression ◽  
Cell Tumor ◽  
Cycle Progression
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