In general, the severity of cancer increases with a shorter duration of time between initial treatment and its return.
CSCs have so far been found in a variety of tumors, including those of the brain, breast, ovary, head and neck, etc.
Therefore, even decades after the primary cancer has been fully treated, the reactivation of the inactive CSCs may lead to tumor recurrence.
[22][23] Hypoxia, chemotherapeutic agents, and radiation can generate Polyploid Giant Cancer Cells (PGCC).
[28][29] In fact, the effects of therapy that kills most cancer cells, may cause a few of them to pause proliferation instead of dying.
[30] While the precise mechanism of growth arrest is not entirely clear and may not be uniform across cancer cases, malignant cells that survive chemotherapy make several metabolic adaptations and possess altered configuration of key positions of their chromatin, the material that packages their DNA.
This has as result that certain conditions can trigger expression of genes that reignite cancer cell growth, causing proliferation, and additionally these conditions may trigger aberrant expression of genes that cause changes in the host tissue, which also permit cancer growth.
These markers might ideally be used to screen for cancer, diagnose it, and track how effectively it responds to treatment.