BIOL 311 Lecture Notes - Lecture 34: Ras Subfamily, Tumor Suppressor Gene, Bladder Cancer

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Published on 13 Dec 2017
Department
Course
Professor
Hot topic Tu rning to th e Ge n e tic s o f Ca nc e r
WHAT IS CANCER?
- A malignant tumor or cance r is an aggregate of ce lls
- All of these ce lls us ually des cend from a n initial a berra nt founder cell that ha d at least one
mutation
- What s e ts them a part from “normal” cells is their a cce le ra te d division ra te , the a bility to
invade ne w cellula r te rritories, high metabolic rate, and a n a bnorma l s hape
- Ma ny ca nce r ce lls have much longer longevity a nd are re s is ta nt to a poptosis
- In which ge nes do ca ncer muta tions usually occur?
- Mutations leading to cancer usua lly occur in one of the following two ge nes : porto-
oncoge nes or tumor-s uppressor gene s
- Mutations in thes e gene s include S NP s , S S LP s, and CNVs
- Proto-oncogenes
- Wild type : re s ulting in prote ins that a re involve d in inducing the ce ll cycle or inhibiting
apoptos is ; highly regula ted
- Oncogenes (cancer cells ): muta te d proto-oncogenes , which re s ult from a gain-of-
function muta tion
- Tumor-suppre ssor gene s
- Wild type : encode proteins that inhibit the cell cycle a nd activate apoptos is if cell
damage is dete cted; als o include s repa ir e nzymes for DNA
- Oncogene (cancer cells ):
mutations promote tumor
formation, re s ult of loss -of-
function re cess ive mutation
- Exa mple : the ras oncogene
(muta tion s ingle S NP in this
gene re s ults in human bladde r
cancer)
- Ke y points on oncoge nes :
- Proteins e ncode d by
oncoge nes a re a c tiva ted in
tumor ce lls
- Only one copy is required
- Mutated oncoge ne results in a protein that now have u n regulated e xpression
- Example : p53 gene
- 50% human tumors la ck a functiona l p53 gene
- WT p53 gene e ncodes a tra nscriptiona l re gulator that is a ctivated in re s ponse to DNA
damage
- Functions to prevent progression of cell cycle until DNA dama ge is re paired a nd induces
apoptos is
- In ce lls with a mutant p53 ge ne, the cell cycle progresses even if damaged DNA ha s not
bee n re paired
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