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Chapter 20: Cellular Communites

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Todd Stotlar

on 5 December 2013

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Transcript of Chapter 20: Cellular Communites

Chapter 20: Cellular Communities
Tissues, Stem Cells, and Cancer
Many diverse types of genes are critical for cancer
Two types of mutations
Dominant
Only one gene copy needs to be mutated
Product is hyperactive
Mutated gene called an oncogene
ONCO(relating to tumors)gene
Normal form is a proto-oncogene
PROTO(before)-oncogene
Recessive
Both copies mutated
Hereditary
Colorectal Cancer Illustrates how loss of a Gene Can Lead to Growth of a Tumor
Colorectal Cancer
Most cases not hereditary
Some families are more prone to the disease and have an earlier onset
Two families were studied
Family #1
Inherited mutation in a DNA repair enzyme
Family #2
Mutation with a distinct phenotypic result
Deletion or inactivation of Adenomatous Polyposis Coli (APC) gene
One normal and one mutant
Colorectal Cancer (cont.)
People who have 2 good copies of the gene can still get colorectal cancer
Tumor cells would have lost both copies of gene
An Understanding of Cancer CEll BIology Opens The Way to New Treatments
Cancer is hard to treat
Cells are mutable and evolve resistance
Each has its own combination of mutated genes
Not detected until it has begun to metastasize
Classic Treatments
Surgical techniques improving
Radiotherapy and chemotherapy take advantage of cells' properties
Lack checkpoint mechanisms
Keep dividing, producing damaged daughter cells
new treatments
Targets cells that lack protein for repair of double strand breaks, raising cell instability
Blocks off blood supply to cancer cells in a tumor
Produce immune response using tumor-specific cell surface molecules
Target oncogene products to block their actions
Chronic Myeloid Leukemia (CML)
Cancer cells depend on a tyrosine protein kinase that causes unnecessary proliferation
Gleevec designed to block kinase's activity
Inhibits survival of leukemic cells
Causes a prolonged remission of symptoms
Determining Gene Function
Most proteins do not function in isolation
Partner proteins are looked at for potential related functions
One way to find partner proteins is co-immunoprecipitation

APC and Beta Catenin
Using co-immunoprecipitation, these were found to be linked
Beta-catenin functions to connect cadherin molecules at adherens junctions between cells
Scientists thought APC was involved in cell adhesion
WRONG
aRMADILLO
Key protein in signaling pathway for normal development in Drosophila
Pathway activated by Wnt proteins
Wnt proteins bind to cells, activating genes that influence cell growth, division, and differentiation
Homolog is beta-catenin
Suggests it is important in gene expression
LEF-1/TCF
Found to be linked to beta-catenin through immunoprecipitation
Transcription regulator
Wnt promotes accumulation of free beta-catenin, which moves into the nucleus
Binds to TCF regulator, creating a complex
Complex activates Wnt-responsive genes
APC's Function
Regulates this pathway by helping to degrade beta-catenin
Loss of APC causes beta-catenin concentration to rise, TCF activates, and Wnt-responsive genes are turned on
How does this cause colorectal cancer?
Knockout Mice
Mice lacking TCF4 did not develop intestinal crypts
TCF4 maintains the pool of proliferating gut stem cells
Missing APC
Beta-catenin accumulates
Binds to TCF4 transcription regulator
Overactivates TCF4-responsive genes
Excessive proliferation of stem cells
Forms polyps
What happens when a single mutation event occurs in a proto-oncogene?
A) Proto-oncogene reverts to original state
B) A dominant mutation can occur
C) Nothing will happen...yet
D) B and C are both correct
How can colorectal tumors come about?
A) APC is missing
B) Beta-catenin is mutated
C) Both A and B
D) Neither A nor B
Full transcript