And is cancer a disease of cell differentiation in multicellular organisms or does it have deeper roots in the evolutionary history of life? Cancer stem cells were found in tumors of various tissues and organs as well as in established tumor cell lines. Like normal stem cells, CSCs are capable of self-renewal, quiescence, and cell differentiation.
They invade other tissues and cause secondary tumors, metastases and cancer recurrence. All these findings cancer genetic regulatory network previous cancer researchers to the assumption that CSCs arise from deficient human stem cells hSCs.
Some cancer researchers regarded cancer as a "stem cell cancer genetic regulatory network . In recent years, it has become apparent that tumor CSCs are closely related to another self-renewing participant of the tumor mass, namely the reproductive cyst-like structure aCLS  often referred to as PGCC .
It forms numerous monoploid 1C daughter cells microcells, "germ" cells by reductive nuclear division and asymmetric cellularization non-mitotic cell division and daughter cell dissemination. Microcells spread in various tissues and form metastases.
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Tumor hypoxia favors the formation of reproductive aCLSs. The progeny of aCLSs have multipotent stemness and are capable to differentiate multiple cell lineages . Amend  considers the aCLS as a key actuator for tumorigenesis, metastasis and therapy resistance.
A few months ago, Liu J  introduced the term "giant cell life cycle" to describe the developmental pathway between two consecutive aCLSs. In our opinion, the microcell progeny "germ cells" are the precursors of CSCs.
Also, we regard the "giant cell life cycle" as a cancer genetic regulatory network reproductive cancer life cycle that begins with the oncogenic transformation of the cell-of-origin of cancer.
We believe that all eukaryotes including mammals and cancer genetic regulatory network conserve an ancestral unicellular life cycle that can be reactivated under stress and non-Abstract All eukaryotes, from protists to mammalians, preserve a unicellular life cycle inherited from the common ancestor that can be reactivated under unfavorable living conditions.
The cell-of-origin of cancer escapes its death by forming a protected polyploid cyst-like structure CLSthat starts the unicellular life cycle of cancer. The reversal to unicellularity occurs through genomic and epigenetic alterations that activate the MUT switch of early Metazoans and not through mutations. Depending on the environment, the CSC pool differentiates a reproductive cell subline, which cancer genetic regulatory network new aCLSs by cyclic encystment and asymmetric cell division, or a somatic subline, which proliferates strongly by symmetric cell division without cyst differentiation.