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PRESENTED BY: ABDUR RAHMAN KHAN/M-
PHILL
DEPT OF BIOTECHNOLOGY
PRESENTED TO : Dr. MASROOR
 Introduction
 Cancer
 Proto Oncogenes
 Discovery of oncogenes
 Oncogenes
 Tumor Suppresser Genes
 Different Genes
 Refrences
 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
 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
 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)
 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.
 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”.
 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.
 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
 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.
 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.
 Wikipedia
(https://en.wikipedia.org/wiki/Oncogene#Proto-
oncogene)
 Slide Share
(https://www.slideshare.net/search/slideshow?searchf
rom=header&q=ONCOGENES)
Tumor Associated Genes
Tumor Associated Genes

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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.
  • 15.
  • 16.  Wikipedia (https://en.wikipedia.org/wiki/Oncogene#Proto- oncogene)  Slide Share (https://www.slideshare.net/search/slideshow?searchf rom=header&q=ONCOGENES)