Complete summary of the Oncology course (AB_1184) from the 2nd year of biomedical sciences, VU Amsterdam. This summary contains all information needed for partial exam 1 and 2, and includes all the material from the lectures and the book that was required for this course, together with the seminars...
Oncogenic mutations sites in relevant proto and oncogenes
Leerstof Oncology Ch7/14
Oncology exam 2 full summary of lectures + practice exam and answers
All for this textbook (29)
Written for
Vrije Universiteit Amsterdam (VU)
Biomedical Sciences
Oncology (AB_1184)
All documents for this subject (41)
Seller
Follow
SummaryLin
Reviews received
Content preview
Oncology summary (exam 1+2)
1
,Ch1 | Introduction: The Nature of Cancer 3
Ch2a | DNA Structure and Stability: Mutations vs. Repair 6
Ch2b | Radiation and Chemical Carcinogenesis 11
Ch3 | Regulation of Gene Expression 16
Ch4 | Growth Factor Signaling and Oncogenes 22
Ch5 | The Cell Cycle 28
Ch6 | Growth Inhibition and Tumor Suppressor Genes 33
Molecular Diagnostics in Pathology 39
Ch7 | Apoptosis 42
Ch8 | Stem cells and di erentiation 49
Ch9 | Metastasis 54
Ch14 | Technology, and drug and diagnostics development 59
Ch10 | Angiogenesis 62
Ch11 | Nutrients, hormones, and gene interactions 65
Ch12/13 | In ammation, immunotherapy, and cancer 70
Ch13 | Infectious agents and cancer 76
BMW seminar 1 | Proteomics, global analysis of the functionally relevant
OME in cancer 81
BMW seminar 2 | Let’s kill the tumor vasculature 85
BMW seminar 3 | MicroRNA from trash to treasure 87
BMW seminar 4 | Functional oncogenomics 89
BMW seminar 5 | History of sequencing 91
BMW seminar 6 | Advances in pancreatic cancer translational research 94
2
fl ff
, Ch1 | Introduction: The Nature of Cancer
CANCER EPIDEMIOLOGY: DEFINITIONS & TRENDS
- Incidence of cancer: the number of new cases diagnosed with cancer that is registered within
a certain period (mostly 1 year)
- To be able to follow the incidence in time, or to enable comparison between regions, the
incidence is mostly expressed as the number of new cases per 100,000 inhabitants/
persons each year: the crude incidence rate
- Cancer incidence in the Netherlands in 2021: ~124,000 (i.e. 1/137)
- ~1/3 chance to get cancer someday
- Trend: increase in cancer incidence over time, except for 2020 (due to covid)
- Prevalence of cancer: all persons who somewhere in time have been diagnosed with cancer,
and are still living at a certain date
- Hence, this is a diverse group, ranging from persons who have been cured from cancer in
the past to persons who just have been diagnosed with cancer
- The period can be unlimited, but also de ned: e.g. the 5-year prevalence on January 1st,
2010, comprises all still living people who have been diagnosed with cancer during the
previous 5 years
- 5-year cancer prevalence in the Netherlands in 2021: ~380,000
- Trend: cancer mortality slightly increased over time (but not as steep as the incidence), but
has not increased in the last 4 years
- Cancer incidence increases, while the mortality levels o
- Mortality of cancer: the number of patients who died as a result of cancer within a certain
period (mostly 1 year)
- Are not necessarily the same cases that were diagnosed that year: incidence vs. mortality
- Cancer mortality in the Netherlands in 2021: ~46,000
- In the Western world, cancer mortality is 1st/2nd cause of premature death: top ranking of
cancer as leading cause of premature death partly re ects marked declines in mortality
rates of stroke and coronary heart disease in many countries
- Regional di erences in cancer mortality: the cancer mortality in Southern (and South-
Eastern) countries is not as high as in the Western world, due to other leading causes
of death (infectious diseases, etc.)
- Trends (2010 vs. 2000): relative mortality due to cancer decreases, but there are some
striking di erences (e.g. increase in lung cancer among women due to increased smoking,
and increase in melanoma)
- Survival of cancer: the percentage of patients still living at a certain period after diagnosis
- The presented survival is a relative survival that approaches the ‘cancer-speci c
survival’: this means that the survival observed is corrected for the expected death within
a comparable population (with respect to country/region, gender, age, and calendar year)
- Trend of survival in time as function of time after diagnosis: 5-year survival improved ~30%
since 1980
CHARACTERISTICS OF CANCER
- Clinical de nition of cancer:
- Cancer is a group of diseases
- More than 100 cancer types can be distinguished (or even every tumor is di erent?)
- Uncontrolled cell growth
- Invasive and forming metastases
- A patient with a tumor does not always have cancer:
- A tumor is a mass of cells
- Not every tumor is invasive and metastasizing
- Benign tumors are no cancer, only malignant tumors are cancer
3
ff fi
ff fi fl ff ff fi
, - Why is a malignant tumor life-threatening?
- Invasion of organs disturbs organ function
- Cancer cells compete with normal cells for nutrients and oxygen
- Growing tumors can cause obstructions (e.g. in blood vessels)
- (Some benign tumors can also be life-threatening because of their location)
- The di erence between carcinoma, adenocarcinoma, sarcoma and lymphoma:
- Carcinomas arise from epithelial cells (85% of all cancers)
- Incidence of carcinomas is much higher than of other cancers, because: carcinomas
are derived from epithelial cells, which align our body (inside and outside), and are
most exposed to carcinogens (e.g. gut, lungs, etc.)
- Adenocarcinomas arise from glandular tissues (e.g. breast)
- Sarcomas arise from mesodermal tissues (e.g. bone, muscle)
- Lymphomas arise from (progenitors of) white blood cells
- Cancer is a disease of the genome:
- What is a carcinogen?
- A carcinogen is an agent causing cancer (compound, radiation, etc.)
- A carcinogen causes alterations in the DNA of a cell: most carcinogens are mutagens
- Cancer cells contain many alterations in the DNA
- The accumulation of mutations in the DNA of a cell causes stepwise development of
cancer: oncogenesis, carcinogenesis
- Development of cancer (oncogenesis):
- Genetic progression model: progression model based on gene expression
- Normal epithelium -> hyperplasia -> dysplasia -> carcinoma in situ -> invasive
carcinoma -> lymph node and distant metastases
- Because oncogenesis is the stepwise accumulation of mutations in di erent parts of
the genome over time, a tumor is always clonal and heterogeneous
- Clonal: oncogenesis always starts with a rst mutation, and all cancer cells later
on are daughter cells of this one cell
- Heterogeneous: during growth, di erent daughter cells can get other di erent
mutations, resulting in sub-clones with more mutations accumulated
- This classi es the mechanism of cancer as a complex Darwinian adaptive
system, with sub-clonal selection and survival of the ttest
- Is cancer inheritable?
- No: almost all of the mutations develop in somatic cells and will not be passed to the
next generation of o spring
- However: some inherited germ-line mutations can increase the chance to develop
cancer and can be passed on to the next generation of o spring
- These mutations are rarely involved in causing cancer immediately
- Why does the risk to develop cancer increase at older age?
- An accumulation of mutations in the DNA is needed for the development of cancer
- It is a matter of chance and time (~exposure to carcinogens)
- The incidence of cancer is increasing due to longer life expectancy
- The main characteristics of cancer are described in the 6 ‘Hallmarks of Cancer’, de ned by
Hanahan and Weinberg: sustaining proliferative signaling, evading growth suppressors,
resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating
invasion and metastasis
- Renewed and 4 extra ones added:
- Enabling characteristics: genome instability and mutation, and tumor-promoting
in ammation
- Emerging hallmarks: reprogramming energy metabolism, and avoiding immune
destruction
- In 2022, renewed and 4 extra ones added: ‘New dimensions’ by Hanahan
- Unlocking phenotypic plasticity, senescent cells, polymorphic microbiomes, and non-
mutational epigenetic reprogramming
- All these hallmarks distinguish a cancer cell from a normal healthy cell, and are potential
target pathways for the design of new therapeutics
4
fl
ff fi ff ff fi fi ff ff ff fi
The benefits of buying summaries with Stuvia:
Guaranteed quality through customer reviews
Stuvia customers have reviewed more than 700,000 summaries. This how you know that you are buying the best documents.
Quick and easy check-out
You can quickly pay through credit card for the summaries. There is no membership needed.
Focus on what matters
Your fellow students write the study notes themselves, which is why the documents are always reliable and up-to-date. This ensures you quickly get to the core!
Frequently asked questions
What do I get when I buy this document?
You get a PDF, available immediately after your purchase. The purchased document is accessible anytime, anywhere and indefinitely through your profile.
Satisfaction guarantee: how does it work?
Our satisfaction guarantee ensures that you always find a study document that suits you well. You fill out a form, and our customer service team takes care of the rest.
Who am I buying these notes from?
Stuvia is a marketplace, so you are not buying this document from us, but from seller SummaryLin. Stuvia facilitates payment to the seller.
Will I be stuck with a subscription?
No, you only buy these notes for £8.54. You're not tied to anything after your purchase.
