Cancer stem cells have been found in tumors from two distinct sources. Transit-amplifying cells give rise to tumors by continuing to proliferate without entering the postmitotic differentiated state. This process creates a pool of self-renewing cells. These cells then accumulate mutations and give rise to cancer stem cells from more differentiated cells. Here are the two main sources of cancer stem cells. This article will discuss both sources and their implications.
One potential mechanism of cancer stem cells is their high tumorigenicity. This feature was originally attributed to only a small population of cells, but later discovered to be widespread among cancer cells. The term cancer stem cell has since evolved to mean a cell that has stem cell-like properties, such as unlimited self-renewal and pluripotency. The new definition of cancer stem cells is more specific, however. This new definition also reflects the fact that cancer stem cells cannot be derived from tissue stem cells.
It has been suggested that the process by which leukemia blood cells form starts with mutations in the bone marrow. This mutation in the blood stem cell changes it into an abnormal blood stem cell, which gives rise to leukemia blood cells. Then, a subsequent mutation can reprogram leukemia stem cells into cancer stem cells, which are responsible for the re-emergence of cancer blood cells. The cancer stem cells will then give rise to more cancer blood cells, unless they are removed or cured.
While it may be difficult to eliminate cancer stem cells completely, a treatment that targets a large proportion of cancer stem cells can be highly effective. Chemotherapy may target cancer cells that don’t differentiate, but the population of CSCs that gave rise to the tumor could be untouched, leading to a relapse. In addition, conventional chemotherapies only kill differentiated cells, which don’t generate new cells. This could cause the tumor to recur and cause the treatment to fail again.
While human cancer cells are able to differentiate from normal stem cells, incompatible cytokines and receptors have also been reported. Incompatible cytokines and receptors can hinder critical interactions between cancer cells and their host. Even if the immune system of the NOD/SCID mouse is weakened, the human cells can still be rejected and mounted as rejections. This can lead to inaccurate estimates of cancer stem cell number.
The two main features of cancer stem cells are their ability to generate more SCs and to produce differentiated cells. Both tasks are achieved by asymmetric cell division, which enables one progeny to retain SC identity while the other undergoes rounds of cell division and post-mitotic differentiation. However, there is no consensus on the definition of CSCs. It is important to note that these cancer stem cells are constantly changing, and a treatment targeting their growth and resistance cannot be 100% effective.
The discovery of cancer stem cells has led to a shift in the way we view tumors. They contain DNA from the cancer cells and a large number of changes in their genome. Thus, these cells behave like true stem cells, but are not actually true ones. This has lead to the development of several strategies for treating cancer. But, before we move forward with the treatment of cancer stem cells, we must understand how they change the environment around them.
