Self-Renewal, Pluripotency and Tumorigenesis in Pluripotent Stem Cells Revisited

Li, Yanzhen; Tanaka, Tetsuya

doi:10.5772/15196

Cited by 4 publications

(4 citation statements)

References 146 publications

(123 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This allogenic source can raise concern about immunologic rejection; moreover, tumorigenesis was reported in transplantations with embryonic stem cells. 24 Induced pluripotent stem cells are also a feasible source for cell therapy; however, their tumorigenesis was documented, 20,25 such as that shown with malignant germ cell-like tumors. 26 Therefore, adult stem cells such as ADSCs are safe sources for transplantation.…”

Section: Discussionmentioning

confidence: 99%

Untitled

Kadkhodaeian

Tiraihi²,

Ahmadieh³

et al. 2018

Exp Clin Transplant

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Untitled

Kadkhodaeian

Tiraihi²,

Ahmadieh³

et al. 2018

Exp Clin Transplant

View full text Add to dashboard Cite

show abstract

“…Mouse embryonic stem cells (mESCs) derived from the early 3.5day-old ICM can be maintained in culture. These cells are capable of retaining the naïve pluripotent state but can also transition to a primed pluripotent state, eventually differentiating into ESCs of lower potency [64][65][66][67][68][69][70]. It has become evident that blastocyst pluripotency gives rise to pluripotent ESCs, and following implantation, epiblast cells develop into somatic cells and primordial germ cells (PGCs), which are the precursors of sperm and oocytes.…”

Section: Naïve and Primed Pluripotencymentioning

confidence: 99%

Understanding cancer from an evolutionary perspective: high-risk reprogramming of genome-damaged stem cells

Niculescu

2024

Academia Medicine

View full text Add to dashboard Cite

Background: One of the most astounding discoveries of recent times is the recognition that cancer embodies a transition from a higher level of metazoan cell organization to a more foundational premetazoic state. This shift is steered by genes housed within the ancestral genome compartment, pervasive across all metazoan genomes, encompassing humans, and governed by a premetazoic ancestral gene regulatory network. This work aims to highlight the emerging field of evolutionary cancer cell biology (ECCB), which points to the deep homology between cancer and protist life cycles tracing back to the common ancestor of amoebozoans, metazoans, and fungi (AMF). The ECCB analysis reveals the essence of the non-gametogenic germline of the AMF ancestor, which serves as a blueprint for all metazoan germlines and stem cell lineages and controls the life cycle of cancer. Every germ and stem cell lineage of humans and metazoans traces its lineage back to this Urgermline, transmitting crucial processes such as asymmetric cell cycling, differentiation, stemness, and phenomena like germ-to-soma GST and soma-to-germ transition (aka epithelial-mesenchymal transition EMT and MET) to their subsequent evolutionary descendants. Oxygen-sensitive germline and stem cells suffer DNA doublestrand breaks due to stress and oxygen ranges reminiscent of ancestral hyperoxia, leading to cell senescence. Cells that can overcome senescence can proliferate as defective symmetric cell division, paving the way for malignancy and polyploid giant cancer cell cancers. Conclusions: Understanding cancer from its evolutionary origins may help break some of the logjams in cancer prevention and open up new therapeutic pathways.

show abstract

“…Mouse embryonic stem cells (mESCs) derived from early 3.5-day-old ICM could be maintained in culture. They were able to maintain the state of naïve pluripotency but can also transition to primed pluripotency and differentiation into ESCs of lower potency [48][49][50][51][52][53][54]. It has been clear that blastocyst pluripotency gives rise to pluripotent ESCs, and after implantation, epiblast cells (EPI cells) develop into somatic cells and primordial germ cells (PGCs), the precursors of sperm and oocyte.…”

Section: Naive and Primed Pluripotencymentioning

confidence: 99%

Understanding Cancer from an Evolutionary Perspective; DSCD Cells as Cell-of-Origin in Non-Mutational Sporadic Cancers

Niculescu

2023

Preprint

View full text Add to dashboard Cite

The life cycle of cancer follows the life cycle of the common ancestor of amoebozoans, metazoans, and fungi (AMF) and its systemic germline, which serves as a blueprint for all germlines capable of asymmetric cell division (ACD) and stem cell differentiation. Consequently, the oxygen sensitivity of the ancient non-gametogenic germline (Urgermline) was inherited by all germ and stem cell lines including the cancer germline. They all respond to Ugermline’s hyperoxia with loss of stemness and ACD ability and a dysregulated phenotype with irreparable DNA defects and defective symmetric cell divisions (DSCD). In protists, defective DSCD cells undergo an ancient MGRS repair program involving cell and nuclear fusion and hyperploid giant nuclei that restores the damaged genome to its former pre-DSCD state, with ACD potential and stemness. Human and metazoan DSCD use the same MGRS repair program inherited from the AMF ancestor. Ectopic DSCDs and DSCD-like phenotypes can survive in humans for many years in suitable niches. Under favorable environmental conditions, they also have access to the ancient MGRS repair mechanism including the ancient gene regulatory network (aGRN) and all other AMF genes. The aGRN takes control of cancer’s hybrid genome and represses human genes. It installs a G+S cancer life cycle of AMF imprinting that shapes the differentiation of naïve cancer stem cells (CSCs). CSCs are deeply homologous to the aGSCs of the AMF ancestor. Reprogramming of the DSCD genome by MGRS paves the way for oncogenesis. In this light, cancer is not a mutational or genetic disease, but a non-mutational genome-altering disease.

show abstract

Self-Renewal, Pluripotency and Tumorigenesis in Pluripotent Stem Cells Revisited

Cited by 4 publications

References 146 publications

Untitled

Untitled

Understanding cancer from an evolutionary perspective: high-risk reprogramming of genome-damaged stem cells

Understanding Cancer from an Evolutionary Perspective; DSCD Cells as Cell-of-Origin in Non-Mutational Sporadic Cancers

Contact Info

Product

Resources

About