Chapter 18 : Uncontrolled Cell Division & Differentiation
Two characteristics of normal cells :
Have regulatory mechanisms to keep rate of cell division appropriate (hormones, inhibition by signals nearby cells)
Remain in one location thru lifetime (except blood cells)
Tumors can be benign or cancerous
HYPERPLASIA = Substantial increase in cell division (eg breast tissue during pregnancy). Can be signal of control loss
NEOPLASM = Tumor = discrete mass
Benigm tumors :
Cells still look like the original cells & remain in one location
Stay together and may be surrounded by a layer of connective tissue
o LIPOMA (tumor of fat cells)
o ADENOMA (tumor of gland cells)
o Moles on the skin (but CAN become melonoma)
In most cases, surgery !
Cancerous cells lose control of their functions & structures
DYSPLASIA = Abnormal structural change :
Nucleus becomes larger
Less cytoplasm
Cell loses its functions & structures
= Often signal that tumor cells are “pre-cancerous”. Becomes more&more disorganised as cells pile on top of
eachother in seemingly random fashon.
Eg ACTINIC KERATOSIS : dry, scaly, rough skin lesions on areas exposed to sun. May grow slowly, even disappear and
returnr. Only 10-20% becomes cancerous.(treatment : peeling, freezing, scraping)
How cancer develops
At least 2 things must happen :
The cell must grow and divide uncontrollably (ignore inhibitory signals from nearby cells)
The cell must undergo physical changes that allow it to break away from surrounding cells.
Mutant forms of proto-oncogenes, tumor suppressor genes, and mutator genes contribute to cancer
Structural genes control the activities of the cell (Cell growth, Differentiation, Cell adhesion). Regulatory genes code
for proteins that activate OR repress the expression of structural genes :
PROTO-ONCOGENES : code for proteins “growth factors” => promote activitity. If damaged or mutated called
ONCOGENES. Some oncogenes :
o drive internal rate of cell growth faster than normal
o produce damaged protein receptors that fail to heed inhibitory growth signals from other cells
BUT one oncogene does not cause cancer => many processes, controlled by multiple genes, must be distrupted !
Two characteristics of normal cells :
Have regulatory mechanisms to keep rate of cell division appropriate (hormones, inhibition by signals nearby cells)
Remain in one location thru lifetime (except blood cells)
Tumors can be benign or cancerous
HYPERPLASIA = Substantial increase in cell division (eg breast tissue during pregnancy). Can be signal of control loss
NEOPLASM = Tumor = discrete mass
Benigm tumors :
Cells still look like the original cells & remain in one location
Stay together and may be surrounded by a layer of connective tissue
o LIPOMA (tumor of fat cells)
o ADENOMA (tumor of gland cells)
o Moles on the skin (but CAN become melonoma)
In most cases, surgery !
Cancerous cells lose control of their functions & structures
DYSPLASIA = Abnormal structural change :
Nucleus becomes larger
Less cytoplasm
Cell loses its functions & structures
= Often signal that tumor cells are “pre-cancerous”. Becomes more&more disorganised as cells pile on top of
eachother in seemingly random fashon.
Eg ACTINIC KERATOSIS : dry, scaly, rough skin lesions on areas exposed to sun. May grow slowly, even disappear and
returnr. Only 10-20% becomes cancerous.(treatment : peeling, freezing, scraping)
How cancer develops
At least 2 things must happen :
The cell must grow and divide uncontrollably (ignore inhibitory signals from nearby cells)
The cell must undergo physical changes that allow it to break away from surrounding cells.
Mutant forms of proto-oncogenes, tumor suppressor genes, and mutator genes contribute to cancer
Structural genes control the activities of the cell (Cell growth, Differentiation, Cell adhesion). Regulatory genes code
for proteins that activate OR repress the expression of structural genes :
PROTO-ONCOGENES : code for proteins “growth factors” => promote activitity. If damaged or mutated called
ONCOGENES. Some oncogenes :
o drive internal rate of cell growth faster than normal
o produce damaged protein receptors that fail to heed inhibitory growth signals from other cells
BUT one oncogene does not cause cancer => many processes, controlled by multiple genes, must be distrupted !
