Professional Documents
Culture Documents
Gen Molekuler Carsinogesis
Gen Molekuler Carsinogesis
PROTEIN
Enzyme
Receptor
Hormone
Growth Factor
Immunoglobulin
Interferon, Interleukin, Cytokine
Adhesions molecules
HLA/MHC
STRUKTUR
PROTEIN
SIFAT PROTEIN
FUNGSI PROTEIN
PEMBENTUKAN PROTEIN
DISTRIBUSI PROTEIN
PEMERIKSAAN PROTEIN
Biokimia
Genes
Segments of DNA code for proteins (or
parts of proteins)
Each coding segment is called a gene
One gene codes one protein (or part of)
Genes contain the information which
makes us what we are
Gene Structure
Every
ATC G G
UAG C C
Nukleotida 1.
(5)
U
Nukleotida 2.
Nukleotida 3.
Phe
Ser
Tyr
Cys
Phe
Ser
Tyr
Cys
Leu
Ser
STOP
STOP
Leu
Ser
STOP
Trp
Leu
Pro
His
Arg
Leu
Pro
His
Arg
Leu
Pro
Gln
Arg
Leu
Pro
Gln
Arg
(3)
Ile
Thr
Asn
Ser
Ile
Thr
Asn
Ser
Ile
Thr
Lys
Arg
Met
Thr
Lys
Arg
Val
Ala
Asp
Gly
Val
Ala
Asp
Gly
Val
Ala
Glu
Gly
Val
Ala
Glu
Gly
Protein Synthesis
transcription
DNA
RNA
Protein
translation
Mutations
A change in the DNA sequence of the
gene
All cells acquire mutations as they
divide
-6
Types of Mutation
Deletion
- DNA missing
Insertion - extra DNA inserted
Expansion (Amplification) - DNA
repeat size has increased
Point Mutation - change in one base
Types of Mutation
(in coding sequence)
POINT MUTATION
UAA
(Termination Codon)
UCA
(Codon for Serine)
UCU
(Codon for Serine)
CCA
(Codon for Proline)
Cancer
Cancer is a group of diseases in which
genetically damaged cells proliferate
autonomously
The genetic damage consists of mutations
(eg.point mutation, deletion, insertion) and
chromosomal rearrangements or losses
Such changes result in the loss or altered
function of molecules involved in cell growth
or proliferation.
Genes in Cancer
Mutations could affect Protooncogenes
or Tumorsuppressor genes.
Protooncogenes code for a variety of
growth factors, growth factor receptors,
enzymes or transcription factors that
promote cell growth and/or cell division.
Mutated version of Protooncogenes
(erbB, ras, jun, fos, myc, etc) are called
Oncogenes
Genes in Cancer
Proto-oncogenes
are activated to
oncogenes by various mechanisms.
1. Promoter insertion
2. Enhancer insertion
3. Chromosomal translocations
4. Gene amplification
5. Point mutation
Oncogen
Cancer
abl
Translocation
CML
myc
Translocation
Burkitts Lymphoma
erb B
Amplification
Epithelcarcinoma,
Astrocytoma,
Ca Oesophagus
neu
Amplification
Adeno Ca (Mammae,
Ovarium, Gaster)
myc
Amplification
Ca- Mammae, Lung,
Uterus, Oes
N-myc
Amplification
Neuroblastoma, Ca.Paru
Int-2
Amplification
Ca-Oesophagus
Apoptosis
Programmed
cell death
Intracellular machinery responsible for
apoptosis is called caspases.
Caspases
Carcinogenics
Radiant energy
Chemical compounds
Viruses ( DNA virus,RNA virus, Adeno
virus)
Photodimerizatio
n
Exposure to UV light
can cause adjacent
thymines to
covalently link.
This results in a
distortion of the DNA
molecule and
breaks the hydrogen
bonding with the
adenine.
UV light
|
| |
A C T
|
T
T
|
A C G T
| |
| |
G A
| |
| |
| |
G C A T
A
|
thymine
dimer
|
|
A C
| |
| |
G C A T
T
|
C G T
|
| |
G
|
A
|
Carcinogenesis (Colorectal
Cancer)
Tumor metastasis
Metastasis is the most dangerous
property of tumor cells
The cell grow as secondary tumors
Many changes have been documented at
the surfaces of malignant cells
Some are: alterations in transport
property, diminished adhesion, loss of
certain antigens etc.