Cancer
description
Transcript of Cancer
Cancer
By: Aujan M., Zach J., Aditya P.
*Overview
*Genetic disease that results in uncontrolled growth.*Mutation in genetic code results in failure
of cell division control.*~90% of time, cancer mutation due to
external environmental factors. Cancer due to inherited mutations ~10% of time.
*Overview
*Deletion or duplication of nucleotides in genetic sequence can lead to mutation.*Once cell’s life cycle is disrupted,
cancerous cells begin to grow at rapid rate, forming a neoplasm.
*Genetic Basis
*Cell undergoes cell division before cell is fully mature. Since they divide at a rapid rate, successive cancer cells will be immature and dysfunctional.*Mutations occur after birth, not a
hereditary disease.
*Genetic Basis
*Genes that inhibit cell division are proto-oncogenes. These can mutate and become oncogenes.*Oncogenes – mutations causes constant
production of proteins/enzymes stimulating unrestrained cytokinesis.
*Causes of Cancer
*Majority of genetic mutations occur during S phase.* Result of 3 major mechanisms:*1.) Carcinogens – cancer causing agents that cause
mutation to cell’s DNA (anti-oncogenes). i.e.- chemicals and radiation.*2.) Viruses – viruses insert their fragment of DNA
into genetic material of cells they infect. DNA can compromise proto-oncogenes of cell.*3.) Replicative Mutations – during replication,
mutations can affect proto-oncogenes turning them into oncogenes.
*Types of Mutations:
Point Mutations
*Changes to a specific portion of a gene.*May be transmitted to offspring, allowing
it to be found in successive generations.
*Types of Mutations:
Substitutions
*Base Pair Substitution – replacement of one nucleotide and complimentary base with another complimentary pair.*Missense Mutation – altered codon still
codes for amino acid, but amino acid doesn’t make sense with function of protein.*Nonsense Mutation – causes production of
stop codon.
*Substitution
*Types of Mutations:
Insertions/Deletions
*Adding/Losing Nucleotide Pairs – more harmful than substitutions because mRNA coded in series of triplets. Loss/gain causes entire sequence to shift over, resulting in shift in reading frame.*Frameshift Mutation – nucleotides
inserted/deleted don’t come in multiple of three. Alters reading frame. Produces useless protein.
*Insertion/Deletion
*Types of Neoplasms:
Benign
*Benign Neoplasm – mass of cells whose cellular compositions is same as cells of surrounding tissues.*Surrounded by connective tissue, so
metastasis doesn’t occur.*Nuclear fission similar to that of normal
cells.*Since rate of division slightly higher than
that of normal cells, tumor will grow slowly.
*Types of Neoplasms:
Malignant
*Neoplasms whose DNA has mutated. Different from surrounding tissues.*Resemble immature and undifferentiated cells.*Growth is greatly accelerated and can become
detrimental to surrounding tissue.*Neoplasm then breaks out of connective tissue
capsule and can metastasize.*Usually contain degraded chromosomes joined
incorrectly to another gene.
*Benign (top) and Malignant (bottom)
Tumors
*How do cells avoid death?
*Apoptosis- programmed cell death*Inhibit the expression of Apaf-1*Secrete elevated levels of decoy soluble
molecule that binds to Fas-L*Utilization of human proto-oncogene Bcl-2
*Tumor Suppressor Genes
*Inhibit cell division*Contains p53 gene which binds DNA and
stops it from allowing damaged DNA to divide
*Proto-Oncogene
*Stimulates the cell cycle *Ras is a gene turns on other genes
through the signal transduction cascade which tells the cell cycle to go
*Why do cancer cells grow
uncontrollably?
*Divisions determined by telomeres *Cancer cells turn on telomerase*Cancer cells now divide without any limits
*Processing Nutrients
*Cancer cells need nutrients*Blood vessels nourish the tumor*angiogenesis
*Invading Tissues
*Invading tissues and disrupting functions*metastasizing
*Treatments
*There are no cures for cancer but treatment options do exist. *Chemotherapy- poison cancer cells*Radiation- uses x-rays and radio isotopes
to destroy cancer causing cells*Surgery- removes neoplasm and
surrounding tissues