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Carcinogenesis
Pathogenesis of Cancer
Introduction
Carcinogenesis, also called oncogenesis or tumorigenesis, is the
formation of a cancer, whereby normal cells are transformed into cancer
cells. The process is characterized by changes at the cellular, genetic,
and epigenetic levels and abnormal cell division. Cell division is a
physiological process that occurs in almost all tissues and under a
variety of circumstances. Normally the balance between proliferation
and programmed cell death, in the form of apoptosis, is maintained to
ensure the integrity of tissues and organs.
Cancers and tumors are
caused by a series of
mutations. Each mutation
alters the behavior of the
Cancer is fundamentally a disease of regulation of tissue growth. For a
normal cell to transform into a cancer cell, genes that regulate cell growth
and differentiation must be altered. Genetic and epigenetic changes can
occur at many levels, from gain or loss of entire chromosomes, to a mutation
affecting a single DNA nucleotide, or to silencing or activating a microRNA
that controls expression of 100 to 500 genes. There are two broad
categories of genes that are affected by these changes.
Causes
• DNA Damage: DNA damage is the primary cause of
cancer. More than 60,000 new naturally-occurring
instances of DNA damage arise, on average, per
human cell, per day, due to endogenous cellular
processes.
• Field Cancerization: Field defects have been
identified in association with cancers and are
important in progression to cancer.
• Genome Instability: Cancers are known to
exhibit genome instability or a "mutator
phenotype". The protein-coding DNA within the
nucleus is about 1.5% of the total genomic DNA.
• Non-mainstream Theories: There are several
theories of carcinogenesis and cancer treatment
that fall outside the mainstream of scientific
opinion, due to lack of scientific rationale, logic, or
evidence base.
• Genetic and
Epigenetic: There is a
diverse classification scheme
for the various genomic
changes that may contribute
to the generation of cancer
cells. Many of these changes
are mutations, or changes in
the nucleotide sequence of
genomic DNA.
The Horsemen of
the Carcinogenesis
Oncogenes
Oncogenes promote cell growth
through a variety of ways. Many
can produce hormones, a
"chemical messenger" between
cells that encourage mitosis, the
effect of which depends on
the signal transduction of the
receiving tissue or cells.
Proto-
Oncogenes
Proto-oncogenes promote cell growth in
a variety of ways. Many can
produce hormones, "chemical
messengers" between cells that
encourage mitosis, the effect of which
depends on the signal transduction of
the receiving tissue or cells. Some are
responsible for the signal transduction
system and signal receptors in cells and
tissues themselves, thus controlling the
sensitivity to such hormones.
Tumor
Suppressor
Genes
Tumor suppressor genes code for anti-
proliferation signals and proteins that
suppress mitosis and cell growth.
Generally, tumor suppressors
are transcription factors that are
activated by cellular stress or DNA
damage. The functions of such genes is
to arrest the progression of the cell cycle
in order to carry out DNA repair,
preventing mutations from being passed
on to daughter cells.
Multiple
Mutations
In general, mutations in both types
of genes are required for cancer to
occur. For example, a mutation
limited to one oncogene would be
suppressed by normal mitosis
control and tumor suppressor
genes. A mutation to only one
tumor suppressor gene would not
cause cancer either, due to the
presence of many "backup"
genes that duplicate its functions.
Non-Mutagenic Carcinogens
Many mutagens are also carcinogens, but some carcinogens are not
mutagens. Examples of carcinogens that are not mutagens
include alcohol and estrogen. These are thought to promote cancers
through their stimulating effect on the rate of cell mitosis. Faster rates
of mitosis increasingly leave fewer opportunities for repair enzymes to
repair damaged DNA during DNA replication, increasing the likelihood
of a genetic mistake. A mistake made during mitosis can lead to the
daughter cells' receiving the wrong number of chromosomes, which
leads to aneuploidy and may lead to cancer.
Thank
You
A project summitted in fulfillment for
the requirements of the Value-Added
Course - Cancer Awareness and Therapy
By
MOHD AZHAN
Department of Computer Applications
Enrollment No. 2000100767

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Carcinogenesis.pptx

  • 2. Introduction Carcinogenesis, also called oncogenesis or tumorigenesis, is the formation of a cancer, whereby normal cells are transformed into cancer cells. The process is characterized by changes at the cellular, genetic, and epigenetic levels and abnormal cell division. Cell division is a physiological process that occurs in almost all tissues and under a variety of circumstances. Normally the balance between proliferation and programmed cell death, in the form of apoptosis, is maintained to ensure the integrity of tissues and organs.
  • 3. Cancers and tumors are caused by a series of mutations. Each mutation alters the behavior of the
  • 4. Cancer is fundamentally a disease of regulation of tissue growth. For a normal cell to transform into a cancer cell, genes that regulate cell growth and differentiation must be altered. Genetic and epigenetic changes can occur at many levels, from gain or loss of entire chromosomes, to a mutation affecting a single DNA nucleotide, or to silencing or activating a microRNA that controls expression of 100 to 500 genes. There are two broad categories of genes that are affected by these changes.
  • 5. Causes • DNA Damage: DNA damage is the primary cause of cancer. More than 60,000 new naturally-occurring instances of DNA damage arise, on average, per human cell, per day, due to endogenous cellular processes. • Field Cancerization: Field defects have been identified in association with cancers and are important in progression to cancer. • Genome Instability: Cancers are known to exhibit genome instability or a "mutator phenotype". The protein-coding DNA within the nucleus is about 1.5% of the total genomic DNA. • Non-mainstream Theories: There are several theories of carcinogenesis and cancer treatment that fall outside the mainstream of scientific opinion, due to lack of scientific rationale, logic, or evidence base. • Genetic and Epigenetic: There is a diverse classification scheme for the various genomic changes that may contribute to the generation of cancer cells. Many of these changes are mutations, or changes in the nucleotide sequence of genomic DNA.
  • 6. The Horsemen of the Carcinogenesis
  • 7. Oncogenes Oncogenes promote cell growth through a variety of ways. Many can produce hormones, a "chemical messenger" between cells that encourage mitosis, the effect of which depends on the signal transduction of the receiving tissue or cells.
  • 8. Proto- Oncogenes Proto-oncogenes promote cell growth in a variety of ways. Many can produce hormones, "chemical messengers" between cells that encourage mitosis, the effect of which depends on the signal transduction of the receiving tissue or cells. Some are responsible for the signal transduction system and signal receptors in cells and tissues themselves, thus controlling the sensitivity to such hormones.
  • 9. Tumor Suppressor Genes Tumor suppressor genes code for anti- proliferation signals and proteins that suppress mitosis and cell growth. Generally, tumor suppressors are transcription factors that are activated by cellular stress or DNA damage. The functions of such genes is to arrest the progression of the cell cycle in order to carry out DNA repair, preventing mutations from being passed on to daughter cells.
  • 10. Multiple Mutations In general, mutations in both types of genes are required for cancer to occur. For example, a mutation limited to one oncogene would be suppressed by normal mitosis control and tumor suppressor genes. A mutation to only one tumor suppressor gene would not cause cancer either, due to the presence of many "backup" genes that duplicate its functions.
  • 11. Non-Mutagenic Carcinogens Many mutagens are also carcinogens, but some carcinogens are not mutagens. Examples of carcinogens that are not mutagens include alcohol and estrogen. These are thought to promote cancers through their stimulating effect on the rate of cell mitosis. Faster rates of mitosis increasingly leave fewer opportunities for repair enzymes to repair damaged DNA during DNA replication, increasing the likelihood of a genetic mistake. A mistake made during mitosis can lead to the daughter cells' receiving the wrong number of chromosomes, which leads to aneuploidy and may lead to cancer.
  • 12. Thank You A project summitted in fulfillment for the requirements of the Value-Added Course - Cancer Awareness and Therapy By MOHD AZHAN Department of Computer Applications Enrollment No. 2000100767