Neoplasia Flashcards
In the cell cycle, what does g1 do
making proteins, energy and normal stuff
What does the g1s check point do
looking for dna damage, size, environment, growth signals (internal and external)
What does S do
double dna in synthesis
what does g2 do
double the dna and preparing to divide
What does the g2m checkpoint do
final check, everythings okay
Whats different about the cycle in cancer
there’s NO checkpoints: like an amusement park with no security at gates
keeps dividing to form a tumor
What are the two main charecteristics of cancer cells?
1) Abnormal and Rapid Proliferation
2) Loss of Differentiation and Normal Properties (Anaplasia)
What is growth factor independence
It keeps growing and pays no attention to anything else
Cell Density-Dependent Inhibition
It doesnt stop when theres too many cells in an area
What does immortal lifespan mean
the telomere makes it live forever
What does evasion of immune response mean?
it wont go into apoptosis when the immune tells it to
What are some other charecteristics of cancer?
Reduced Cell Cohesiveness and Adhesion
Loss of Anchorage Dependence
Faulty Cell-to-Cell Communication
Expression of Foreign Antigens
Production of Enzymes, Hormone, and Other Substances
Cytoskeletal Abnormalities that Allow Metastasis
Angiogenesis Capabilities
What is metastasis?
the development of a secondary
tumor at a location distant from the primary tumor.
What do metastatic cancer cells take advantage of?
the blood or lymph to
transport them to a different location
What is a sentinel node?
the initial node where a tumor drains.
Tumor growth is dependent on what three factors?
1) The number of cells actively moving through the Cell Cycle
2) The duration of the Cell Cycle
3) The number of cells being lost relative to the number produced
The ratio of dividing cells to resting cells is called what?
Growth Faction
What are DNA repair defects
when p53 is silenced and the cell is unable to fix itself
Defects in Growth Factor Signaling Pathways
growth signals are hardwired on bc of mutations in Tyrosine Kinase
Defects in Growth Factor Signaling Pathways
mutations have hijacked and turned
‘OFF’ the Apoptosis pathways
Evasion of Cellular Senescence
Increased production of Telomerase means
Chromosomes don’t age
Development of Sustained Angiogenesis
mutations turn on the genes that
produce hormones which stimulate the growth of blood vessels to feed the
growing cells
Defects in Density and Environment Dependent Controls
mutations have turned
“OFF’ the genes which tell cells to stop growing when their density is too high
and to stop growing in certain environments they are not suited for
What is carcinogenesis?
cancer causing agents make normal cells
become cancerous. Promoters are agents that accelerate
unregulated growth.
