Oncogenes promote
cell growth through a variety of ways. Many can produce
hormones, a "chemical messenger" between cells which encourage
mitosis, the effect of which depends on the signal transduction
of the receiving tissue or cells. In other words, when a hormone
receptor on a recipient cell is stimulated, the signal is
conducted from the surface of the cell to the cell nucleus to
effect some change in gene transcription regulation at the
nuclear level. Some oncogenes are part of the signal
transduction system itself, or the signal receptors in cells and
tissues themselves, thus controlling the sensitivity to such
hormones. Oncogenes often produce mitogens, or are involved in
transcription of DNA in protein synthesis, which creates the
proteins and enzymes responsible for producing the products and
biochemicals cells use and interact with.
Mutations in proto-oncogenes, which are the normally quiescent
counterparts of oncogenes, can modify their expression and
function, increasing the amount or activity of the product
protein. When this happens, the proto-oncogenes become oncogenes,
and this transition upsets the normal balance of cell cycle
regulation in the cell, making uncontrolled growth possible. The
chance of cancer cannot be reduced by removing proto-oncogenes
from the genome, even if this were possible, as they are
critical for growth, repair and homeostasis of the organism. It
is only when they become mutated that the signals for growth
become excessive.
One of the first oncogenes to be defined in cancer research is
the ras oncogene. Mutations in the Ras family of proto-oncogenes
(comprising H-Ras, N-Ras and K-Ras) are very common, being found
in 20% to 30% of all human tumours. Ras was originally
identified in the Harvey sarcoma virus genome, and researchers
were surprised that not only was this gene present in the human
genome but that, when ligated to a stimulating control element,
could induce cancers in cell line cultures.
Pathophysiology
Tumor suppressor genes >>
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Cancer
Classification
1. Nomenclature
2. Adult cancers
3. Childhood cancers
Signs and symptoms
Diagnosis
1. Investigation
2. Biopsy
Treatment
1. Surgery
2. Radiation therapy
3. Chemotherapy
4. Targeted therapies
5. Immunotherapy
6. Hormonal therapy
7. Symptom control
8. Complementary and alternative
9. Treatment trials
Prognosis
1. Emotional impact
Causes
1. Chemical carcinogens
2. Ionizing radiation &
Infectious diseases
3. Hormonal imbalances
& Immune system dysfunction
4. Heredity & Other causes
Pathophysiology
1. Epigenetics
2. Oncogenes
3. Tumor suppressor genes
4. Cancer cell biology
4.1 Clonal evolution
4.2 Biological properties of cancer cells
Prevention
1. Modifiable ("lifestyle") risk factors
2. Diet
3. Vitamins
4. Chemoprevention
5. Genetic testing
6. Vaccination
7. Screening
Epidemiology
History
Research |
