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Presentation on oncogene with respect to cancer
1. SAHYADRI SCIENCE COLLEGE, SHIVAMOGGA-577
203
PG DEPARTMENT OF BIOTECHNOLOGY
SEMINAR TOPIC ON – “ONCOGENES”
SUBMITTED BY:-
BALAJI G K
I MSc I SEM
PG Department of
Biotechnology
Sahyadri Science College
Shivamogga-577203
KUVEMPU UNIVERSITY
3. Cancer is a complex disease characterized by the
abnormal growth and spread of cells.
Cells normally grow, divide, and die in a regulated
manner.
Tumor can be divided in to tow category;
• Benign (non-cancerous).
• Malignant (cancerous).
Generally mutation leads to the
• Expression of altered gene products.
• Decreased or increased gene expression.
INTRODUCTION
4. Two classes of genes affected by genetic and epigenetic alterations in cancer cells are oncogenes and tumor
suppressor genes.
Oncogenes contribute to tumor development by increased or misdirected activity.
Tumor suppressors insufficient or lost function supports tumor development.
Oncogenes
Tumor
Suppressor
genes
Stimulate Proliferation
Inhibit Differentiation
Inhibit Apoptosis
Inhibit Proliferation
Promote Differentiation
Stimulate Apoptosis
7. ONCOGENES
Oncogenes are activated versions of normal cellular
genes involved in
Regulating cell replication
Growth
Survival
Differentiation
Motility
Oncogenes become activated by;
Genetic mutation
Chromosomal translocation
Gene amplification
An oncogene is a gene that has the potential to cause
cancer. In tumor cells, these genes are often mutated, or
expressed at high levels.
9. PROTO-ONCOGENE V/S ONCOGENE
PROTO-ONCOGENE ONCOGENE
A group of genes that cause normal cell to
become cancerous when they are mutated.
A gene having the potential to cause a normal
cell to become cancerous.
Unmutated cancer causing genes. Mutated cancer causing genes.
It doesn't under go rapid replication. It undergoes rapid replication, and becoming out
of control.
They are not cancer causing genes. They are cancer causing genes.
11. MYC ONCOGENE
The cellular proto-oncogene, c-MYC, encodes the
protein c-MYC - promote cell cycle progression,
differentiation, cell death and angiogenesis.
In normal dividing cells, c-MYC expression is
maintained at a relatively constant intermediate level
throughout the cell cycle, whereas in its oncogenic form
c-MYC might be constitutively expressed at levels
ranging from moderate to very high, and is non-
responsive to external signals.
12. RAS ONCOGENE
The Ras is a protein subfamily of small GTPases
that are involved in cellular signal transduction
pathways that control actin cytoskeletal integrity,
proliferation, differentiation, cell adhesion,
apoptosis, and cell migration.
Ras communicates signals from outside the cell
to the nucleus. Mutations in ras genes can
permanently activate it and cause inappropriate
transmission inside the cell even in the absence of
extracellular signals.
These signals result in cell growth and division.
Ultimately lead to oncogenesis, decreased
apoptosis and cancer.
13. The most important tumor suppressor is p53
(molecular weight 53 kDa).
It is located on band p13 of chromosome 17.
Also called "Guardian of the Genome".
In 1990, p53 was recognized as the tumor-
suppressor gene.
Mutation in p53 is the cause of Li-Fraumeni
syndrome, which is rare form of inherited cancer.
Functions;
• DNA repairing.
• Apoptosis.
• Regulation of cell cycle.
• Prevent neoplastic transformation either by cell
cycle arrest or by triggering apoptosis.
P53 - TUMOR SUPPRESSOR GENE
14. CONCLUSION
A mutated (changed) form of a type of gene called a proto-oncogene, which is
involved in normal cell growth and division.
When a proto-oncogene is changed so that too many copies are made or it becomes
more active than normal, it is called an oncogene.
Several viruses with oncogenic potential stimulate cell proliferation and cause tumors
or cancers in animals and humans.
They act with different mechanisms depending on different factors.
15. REFERENCE
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Giovannucci, E., E. B. Rimm, et al. (1994). “Intake of fat, meat, and fiber in relation to
risk of colon cancer in men.” Cancer Res 54(9):2390-7.
Baron,J.A., B. F. Cole, et al. (2003). “A randomized trial of aspirin to prevent colorectal
adenomas.” N Engl Med 348(10): 891-9