This article is about cancer cells. For the scientific journal, see Cancer Cell (journal).
Cancer cells are cells that divide continually, forming solid tumors or flooding the blood or lymph with abnormal cells. Cell division is a normal process used by the body for growth and repair. A parent cell divides to form two daughter cells, and these daughter cells are used to build new tissue or to replace cells that have died because of aging or damage. Healthy cells stop dividing when there is no longer a need for more daughter cells, but cancer cells continue to produce copies. They are also able to spread from one part of the body to another in a process known as metastasis.[1]
Classification
There are different categories of cancer cell, defined according to the cell type from which they originate.[2]
epithelial
in origin, beginning in a tissue that lines the inner or outer surfaces of the body.
histological features visible under the microscope. The nucleus is often large and irregular, and the cytoplasm may also display abnormalities.[3]
Nucleus
The shape, size, protein composition, and texture of the nucleus are often altered in
malignant cells. The nucleus may acquire grooves, folds or indentations, chromatin may aggregate or disperse, and the nucleolus can become enlarged. In normal cells, the nucleus is often round or solid in shape, but in cancer cells the outline is often irregular. Different combinations of abnormalities are characteristic of different cancer types, to the extent that nuclear appearance can be used as a marker in cancer diagnostics and staging.[4]
Causes
Life cycle of a cancer cell
Main article:
Malignant tumors can invade other organs, spread to distant locations (metastasis
) and become life-threatening.
More than one mutation is necessary for carcinogenesis. In fact, a series of several mutations to certain classes of genes is usually required before a normal cell will transform into a cancer cell.[5]
Damage to
DNA transcription, making age another risk factor. Oncoviruses can cause certain types of cancer, and genetics are also known to play a role.[6]
Stem cell research suggests that excess
stem cells into cancer cells.[7] However, a lack of particular co-stimulated molecules that aid in the way antigens react with lymphocytes can impair the natural killer cells' function, ultimately leading to cancer.[8][failed verification
]
DNA repair and mutation
When a cell is deficient in the capacity to
germ-line. However, DMC1 is also expressed in various cancer cell lines including cervical, breast, and lymphoma cancer cell lines.[9] Expression of meiotic DNA repair genes such as DMC1 may promote tumor cell growth by dealing with endogenous DNA damage within the tumor, and may also diminish the effectiveness of anticancer therapy, such as radiation therapy.[9]
Cancer cells have unique features that make them "immortal" according to some researchers. The enzyme telomerase is used to extend the cancer cell's life span. While the telomeres of most cells shorten after each division, eventually causing the cell to die, telomerase extends the cell's telomeres. This is a major reason that cancer cells can accumulate over time, creating tumors.
Cancer stem cells and drug resistance
Scientists have discovered a molecule on the surface of tumors that appears to promote drug resistance—by converting the tumor cells back into a stem cell-like state.
When the tumor cells began to exhibit drug resistance, the cells were simultaneously transforming into a stem cell-like state, which made them impervious to the drugs. It appeared that the treatment itself was driving this transformation by activating a specific molecular pathway. Luckily, several existing drugs, such as Bortezomib for example, can attack this pathway and reverse the cellular transformation, thus 're-sensitizing' the tumor to treatment.[19][20][21]
Treatment
In February 2019, medical scientists announced that
cancer cells and, after being irradiated with light (a process called photodynamic therapy), destroy the cancer cells.[22][23]