All-domain Anomaly Resolution Office U.S. Department of Defense (U) Case: “Eg...
Tumor Associated Genes
1.
2. PRESENTED BY: ABDUR RAHMAN KHAN/M-
PHILL
DEPT OF BIOTECHNOLOGY
PRESENTED TO : Dr. MASROOR
3. Introduction
Cancer
Proto Oncogenes
Discovery of oncogenes
Oncogenes
Tumor Suppresser Genes
Different Genes
Refrences
4. Cancer is a group of diseases involving abnormal cell
growth with the potential to invade or spread to other
parts of the body.[2][8] These contrast with benign
tumors, which do not spread to other parts of the
body.[8] Possible signs and symptoms include a lump,
abnormal bleeding, prolonged cough
While these symptoms may indicate cancer, they may
have other causes.[1] Over 100 types of cancers affect
humans
5. Normal constituents of cells whose function is to
promote proliferation or cell survival. These genes can
code for growth factors, growth factor receptors, signal
transduction proteins, and transcription factors.
The proto-oncogene can become an oncogene by a
relatively small modification of its original function.
There are three basic methods of activation
6. A mutation within a proto-oncogene, or within a
regulatory region (for example the promoter region),
can cause a change in the protein structure, causing an
increase in protein (enzyme) activity.
An increase in the amount of a certain protein (protein
concentration), caused byan increase of protein
expression (through misregulation)
A chromosomal translocation (another type
of chromosome abnormality)
7.
8. Oncogenes produce proteins that have the capacity to
stimulate growth and proliferation. •
Oncogenes are derived from proto oncogenes which are
genes that encode proteins having function in normal cells
•
They are dominant or “gain of function” mutations. They
may lead to genetic instability, preventing a cell from
becoming a victim of apoptosis or promote metastasis •
Different oncogenes become activated in different types of
tumors, which reflects variations in the signaling pathways
that operate in diverse cell types.
9. First discovered through the ability of Rous sarcoma
virus (RSV) to cause cancer in chickens.
Mutant studies of RSV: the src gene causes cancer
“There is a normal cell equivalent of this so-called
“oncogene” and it codes for a protein that has been
associated with tyrosine kinase activity, that
stimulated growth and proliferation via protein
phosphorylation in signal transduction pathways”.
10. Repression of genes that are essential for
the continuing of the cell cycle.
Coupling the cell cycle to DNA damage. As long as
there is damaged DNA in the cell, it should not divide.
If the damage cannot be repaired, the cell should
initiate apoptosis (programmed cell death)
Some proteins involved in cell adhesion prevent tumor
cells from dispersing, block loss of contact inhibition,
and inhibit metastasis. These proteins are known
as metastasis suppressors.
11. Caretaker genes:
Maintain the integrity of the genome by repairing DNA damage
Gatekeeper genes:
Inhibit the proliferation or promote the death of cells with damaged
DNA
12.
13. Retinoblastoma is a cancerous tumor of the retina. It
occurs in two forms:
Familial retinoblastoma (hereditary)
Sporadic retinoblastoma (nonhereditary)
Mechanism of tumor suppression gene inactivation
Deletion,DNA methylation, binding viral
oncoproteins , loss of heterogeneity.
14. Gene encodes a phosphoprotein with 53 kDa with 375 a.a
It is a transcription factor regulating the cell cycle and
apoptosis.
It block the cells that have damaged DNA by triggering the
production of another protein P21, which blocks cell
division until the damage is repaired.
If DNA damage is serve, P53 directs the cell to commit
suicide by apoptosis program
Most tumors have a complete absence of P53 ,other show
mutation that lead to non function P53
Inheritance of a mutation in p53 leads to Li-Fraumeni
syndrome.