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These cells are termed cancer stem cells (CSCs), and are marked by the ability to both self-renew and differentiate into non-tumourigenic progeny. The CSC model posits that the heterogeneity observed between tumour cells is the result of differences in the stem cells from which they originated.
Molecular cytogenetics combines two disciplines, molecular biology and cytogenetics, and involves the analysis of chromosome structure to help distinguish normal and cancer-causing cells. Human cytogenetics began in 1956 when it was discovered that normal human cells contain 46 chromosomes.
Plasmacytoma is a plasma cell dyscrasia in which a plasma cell tumour grows within soft tissue or within the axial skeleton.. The International Myeloma Working Group lists three types: solitary plasmacytoma of bone (SPB); extramedullary plasmacytoma (EP), and multiple plasmacytomas that are either primary or recurrent. [1]
A transmissible cancer is a cancer cell or cluster of cancer cells that can be transferred between individuals without the involvement of an infectious agent such as an oncovirus. [ 1 ] [ 2 ] The evolution of transmissible cancer has occurred naturally in other animal species, but human cancer transmission is rare. [ 2 ]
Warburg regarded the fundamental difference between normal and cancerous cells to be the ratio of glycolysis to respiration; this observation is also known as the Warburg effect. In the somatic mutation theory of cancer, malignant proliferation is caused by mutations and altered gene expression, in a process called malignant transformation ...
Cancer/testis (CT) antigens are a group of proteins united by their importance in development and in cancer immunotherapy. In general, expression of these proteins is restricted to male germ cells in the adult animal. However, in cancer these developmental antigens are often re-expressed and can serve as a locus of immune activation.
The remaining copy of the tumor suppressor gene can be inactivated by a point mutation or via other mechanisms, resulting in a loss of heterozygosity event, and leaving no tumor suppressor gene to protect the body. Loss of heterozygosity does not imply a homozygous state (which would require the presence of two identical alleles in the cell).
As another example, certain ligand-receptor interactions are incompatible between mice and humans. Additionally, experiments have demonstrated important and significant differences in the ability to transform cells, compared with cells of murine origin. For these reasons, it remains essential to develop models of cancer that employ human cells. [3]