Molecular Onco 1 Flashcards
(55 cards)
cancer growth strategies
- signal activation
- deactivation of growth signal controls
- process promotion
- escaping death
- immortalization
genes that have a main role to initiate cellular growth in response to certain scenarios
oncogenes
important characteristics of oncogenes
- dominant expression (need to activate only one gene)
- highly conservative (always off = protooncogene)
- two types: viral and cellular
classification of oncogenes
*secreted growth factors
*cell surface receptors
*intracellular transducers
*dna-binding nuclear proteins
regulators of the cell cycle
- = components of signal transduction pathways
mutations where there is a change in one single dna nucleotide
point mutations
ex. bladder ca hrasa gene point mutation changes glycine to valine
types of point mutations
- transition
- transversion
- nonsense
- silent
- missense: conservative or non conservative
mutation where there is a loss or gain of nucleotide in a given gene
frameshift mutation
- loss or insertion
mutations that occur during the process of extracting the coding portion of genetic code
splice site mutation
- intron not excised
- exon that is removed
mutations that occur as chromosomes start to deteriorate with age
breakage-fusion-bridge cycle
- fraying of the ends of chromosomes = exposure of nucleotides to the environment
attempts of chromosomes to cover breakage-fusion-bridge cycle mutations
- homologous fusion: both chromosomes of a distinct pair
- nonhomologous fusion: occur between chromosomes that are part of a different pair (translocations)
effects of fusion in b-f-b c mutations
- fused chromosomes are under pressure
- bridge will break
- unequal distribution of genetic material
- –> one chromosome will have multiple copies = amplification
- –> lose important genetic material = deletion
t/f in gene amplification, a chromosome acquires multiple copes of a particular gene
true, results in multiple copies of the protein
example of gene amplification
her2 oncogene = increased egfr2 on breast ca
- increased egfr2 = increased proliferation even in physiologic levels of growth factors
- more aggressive disease, poorer prognosis
mutation caused by fusion between nonhomologous pairs of chromosomes
translocation, results in coupling of genes that are normally far apart
- can result to activation of oncogenes
example of translocations
bcr-abl fusion gene
- chromosome 9 and 22 fusion
- coupling generates a proliferative signal = malignancy
- philadelphia chromosome
- hallmark of chronic myelogenous leukemia
what happens in viral activated oncogenes
- virus incorporates genetic profile into nucleus of cell
- viral genome is an oncogene that stimulates proliferation
- oncogene remains incorporated in genome
control signals (genes) that prevent the onset of uncontrolled proliferation, preventing growth of tumors
tumor suppressor genes
characteristics of tumor suppressor gene
- inhibit growth and multiplication of mutated cells
- prevent neoplastic transformation
- recessive and highly conserved (always on)
ex. rb1 and tp53
t/f only one tumor suppressor gene needs to lose activity to initiate malignancy
false! two hit hypothesis
knudson’s two hit hypothesis: two wild type tumor suppressor genes
first hit: mutation in one pair, but the other is still functioning
second hit: mutation in second pair, FUNCTION HAS BEEN LOST
knudson’s two hit hypothesis: one wild type, one inherited mutated gene
first hit: inherited mutated gene, other still intact
second hit: mutation in second gene, FUNCTION HAS BEEN LOST
will acquire disease younger
individuals who have inherited a mutated tumor suppressor gene from their parents are termed ___
heterozygous
when does loss of heterozygosity happen
- when they lose the function of the remaining wild type
- they become homozygous
what is contact inhibition
- body’s way of ensuring that its microscopic architecture remains intact
- normal: cells are side by side, no cell invades neighbors
