Several people from a single family are diagnosed with the same cancer type at an unusually early age. Factors causing cancer are either environmental or genetic (molecular). The general indication of cancer is abnormal cell division (when cells do not stick to the predesigned process of controlled cell division). Cancer can either be hereditary or nonhereditary. Nonhereditary cancer arises from somatic mutations while hereditary cancer arises from a biased mutation in the germline. Most types of cancer stem from an individual cell and successive clonal progress of cells that are not genetically stable.
Passarge informs us that the human genome has more than one hundred genes, which contribute to cancer if modified by mutations. Passarge further classifies these genes into three main groups depending on the outcome of their mutations. The first type is the proto-oncogene. The distorted forms of proto-oncogenes are the oncogenes. Oncogenes force the cells to divide unnecessarily. An individual mutation usually triggers the beginning of cancer. Oncogenes work in sign pathways controlling cell division. Several mechanisms activate oncogenes. Such mechanisms include rearrangement of chromosomes, point mutations, and augmentation of genes.
In this case, members of the given family develop cancer at an early age. Since there is no environmental cause for cancer, it follows that the cause is genetic (molecular). The cancer gene affected is the proto-oncogene. Ras-genes show how oncogenes cause cancer. Ras-genes instruct a group of connected proteins that control growth. They bind to proteins and function in a manner similar to switches. They are active when attached to guanosyltriphosphate (GTP) and become dormant when connected to guanosyldiphosphate (GDP).
A tyrosine kinase receptor triggers the activation of Ras-genes. The deactivation process of Ras-genes involves GTPase-activating proteins (GAPs), which facilitate the removal of GTP. Distorted variants of Ras-genes are extremely active and have a poor response to GAPs. Consequently, they stay attached to GTP and continue sending signals that encourage cell division. This uncontrolled cell division is what causes cancer. For this family, the activating factor for cancer is possibly a mutation in the genes of a given protein, probably a growth hormone produced at an early stage in life.