Topic 25 - Cancer Flashcards
Cancer can result from
A transformation of a single cell in any tissue of the body
A family of diseases characterized by uncontrolled cell proliferation (growth or division)
Cancer
If the tumor stays confined it is considered
Benign
Cancer cells may ___________ by leaving their original location to colonize other areas of the body
Metastasize
Metastasizing is dependent on
The actin cytoskeleton
Cells normally stop dividing when they contact neighboring cells
Contact inhibition
Transformed cells lose
Contact inhibition
Metastasizing cancer cells secrete
Matrix Metalloproteases
Special enzymes that digest the extracellular matrix components promoting migration through tissues
Matrix Metalloproteases
Activation of matrix metalloproteases and loss of contact inhibition alls tumor cells to
Colonize other tissues
Involved in the ability of cancer cells to metastasize
Actin Cytoskeleton
Matrix Metalloproteases
Loss of Contact inhibition
Six cellular properties of deadly cancers
Self-sufficiency in growth signals Insensitivity to antigrowth signals Evasion of Apoptosis Limited replicative potential Tissue Invasion and Metastasis Sustained Angiogenesis
Cancer is a progressive disease cause by
An accumulation of mutations
Genes that promote cell survival and cell proliferation
Proto-oncogenes
Mutation of proto-oncogenes results in
Gain of function mutations
Encode proteins with unregulated permanently activated activity
Gain of Function mutations
Gain of function mutated genes are called
oncogenes
_________________ are genes that promote cell proliferation and when mutated with a “gain of function” mutation can result in cancer
Proto-oncogenes
Three main ways that pro to-oncogenes are turned into oncogenes
- Mutation in coding sequence
- Gene amplification
- Chromosome Rearrangement
Tyrosine Receptor Kinase (Trk)
Proto-oncogene
Activates cell division in response to extracellular growth factors
Trk
A chromosomal rearrangement with _____________ makes a chimeric protein
Tropomyosin
Permanent receptor dimerization and cell proliferation even in the absence of a signal
Chimeric protein made by Tropomyosin-Trk
Gene whose normal function is to stimulate the cell to divide
Proto-oncogene
Mutation of a proto-oncogene to an oncogene results in
“Gain of Function” = unregulated cell proliferation
Normally inhibit events in the cell cycle until feedback control stimulates passage through a cell cycle checkpoint
Tumor Suppressor genes
In tumore suppressor genes, inactivates this activity which leads to cancer formation
“Loss of function” mutation
Typically a “recessive” mutation because both alleles need to be lost
Loss of Function
“Loss of Function” mutations of ______________ can result in cancer formation
Tummor Suppressors
“Loss of function” mutations in p53 would result in
The inability to halt the cell cycle in the presence of damaged DNA
Replication of damaged DNA can lead to
Mutations that lead to cancer
Gene that inhibits cell proliferation
Retinoblastoma (Rb)
Can be hereditary and usually forms as a child
Rb mutation of both genes - adult onset
Sporadic Tumor Formation
When the cell is not proliferating active Rb proteins binds to and inhibits transcriptional activator
E2F
In response to mitogen (growth factor):
- G1-Cdk and G1/S-Cdk are activated
- G1-Cdk and G1/S-Cdk phosphorylate Rb and inactivate it
This frees E2F to activate genes for cell proliferation
Loss of function mutation of Rb results in
The inability to inhibit E2F
Two proto-oncogenes
Myc (transcriptional factor)
Ras (major growth facto signal pathway component)
Gain of function mutations of Myc and Ras are
More tumorigenic than either alone
