1. Cancer Biology Jasmina Makarevic
ATTA-UR-RAHMAN SCHOOL OF
APPLIED BIOSCIENCES (ASAB)
Cancer Biology Jasmina Makarevic
Fall Semester 2016

2. Infection with Bacteria
At the moment the best know infectins with bacteria causing cancer,
are the infection of Clamydia trochamytis and Helicobacter pylori.
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3. Clamydia Trochamytis
Clamydia trochamatis deals as a possible cofactor of human papillomavirus which leads to cervical cancer.
Chlamydia coat themselves with a growth factor made by
the cells of the organism they are infecting.
This disguise allows the bacteria to infect cells, much like a Trojan horse.
Once inside, Chlamydia induces the host cell to turn out more of the growth factor.
This production of excess growth factor enables more of bacteria to camouflage themselves and infect other cells creating a positive feedback loop which enhances bacterial infection and spread.
The Pgp3 protein is a chlamydial virulence factor that is hypothesized to enhance the bug's ability to initially infect its human host and then evade host defenses.
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4. Helicobacter pylori Two mechanisms are described:
Up to 85% of people infected with H. pylori never experience symptoms or complications.
Acute infection may appear as an acute gastritis with abdominal pain (stomach ache)
or nausea. Where this develops into chronic gastritis.
Individuals infected with H. pylori have a 10 to 20% lifetime risk
of developing peptic ulcers and a 1 to 2% risk of acquiring stomach cancer.
Two mechanisms are described:
One mechanism involves the enhanced production of free radicals near H. pylori
and an increased rate of host cell mutation.
The other proposed mechanism has been called a "perigenetic pathway",
and involves enhancement of the transformed host cell phenotype by
means of alterations in cell proteins, such as adhesion proteins.
H. pylori has been proposed to induce inflammation and locally high levels
of TNF-α and/or interleukin 6 (IL-6). According to the proposed perigenetic mechanism,
inflammation-associated signaling molecules, such as TNF-α, can alter gastric epithelial
cell adhesion and lead to the dispersion and migration of mutated epithelial cells
without the need for additional mutations in tumor suppressor genes,
such as genes that code for cell adhesion proteins.
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5. Growth Factors
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6. Mutations
Def.: Change in the genotype of a species that may involve an alteration
in the nucleotide sequence of a DNA segment, the arrangement of a
segment within a chromosome, the number of copies of a segment, the
physical structure of a chromosome, or even the number of copies of a
structural normal chromosome.
What does this mean?
Mutations are responsible:
Changing content of a gene
Converting one allel into anathor
Creating a new allel frome one previosly widespreaded
Wild-typeMutant
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7. Mutations
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8. Summary statistics (2012)
Mutations
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9. Mutations
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10. Multi- Step Tumorgenesis
Summary statistics (2012)
Multi- Step Tumorgenesis
Tumor progression:
Process of multi-step evolution of a normal cell into a tumor cell.
For this you need a initiation---a promotion---than it leeds to progression.
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11. Adenoma-to-carcinoma
Summary statistics (2012)
Adenoma-to-carcinoma
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12. Adenoma-to-carcinoma
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13. Adenoma-to- carcinoma
Summary statistics (2012)
Adenoma-to- carcinoma
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14. Summary statistics (2012)
Clonal succession
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15. Summary statistics (2012)
Conclusion
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16. Stem cells Def: Cell type within a tissue that is capable
Summary statistics (2012)
Stem cells
Def: Cell type within a tissue that is capable
of selfrenewal and is also capable of generating
daughter cells that develope new phenotypes,
including those that are more differentiated than
the phanotype of stem cell.
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17. Summary statistics (2012)
Conclusion
For the initiation promoting and progression of tumors mutation occurs
in the germ cells and somatic cells. Mutation leeds to a change in proliferation
and apoptosis balance.
In the next lecture we will have a closer look:
Stem cells
What does it mean for cancer?
Growth factors
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18. Thank You for Your Attention!
Jasmina Makarevic