Chapter 1: Introduction (Book) Flashcards
What is cancer (what is it characterised by)?
A group of diseases characterized by unregulated cell grwoth and the invasion and spread of cells from the site of origin to other sites in the body.
Cancer is characterised as a group of diseases. What does this mean?
That over 100 types of cancers have been classified that each have their own origin, cause, phenotype, molecular mechanism and treatment. (E.g. lung cancer caused by smoke inhalation compared to skin cancer caused by UV-radiation).
Hanahan and Weinberg defined six hallmarks of cancers. Besides this, they modified their concept to include two enabling characteristics and two emerging hallmarks. Name the six hallmarks, two enabling characteristics and two emerging hallmarks.
- Six hallmarks: autonomous growth signals, evasion of growth inhibitory signals, evasion of apoptotic cell death, unlimited replicative potential, angiogenesis and invasion and metastasis.
- Two enabling characteristics: genome instability and tumor-promoting inflammation.
- Two emerging hallmarks: reprogramming energy metabolism and avoiding immune destruction.
Why are malignant tumors life-threatening and how can benign tumors be life-threatening?
Malignant tumors are life-threatening because they’re physical obstructions and compromise function of other organs upon invasion. They also compete fierely with healthy tissue for nutrients and oxygen. Benign tumors can be life-threatening because of their location (e.g. in the brain).
(I didn’t discuss this properly in the lecture part of chapter 1, so the following cards are a bit of a repetition). What is meant by contact inhibition?
Contact with neighboring cells inhibits growth. Normal cells grow as a single layer (monolayer) due to contact inhibition.
So what happens when normal cells transform to cancer cells (what phenotype do they acquire) in cell culture?
- No contact inhibition -> cancer cells grow as piles of cells (foci) against a monolayer of normal cells.
- They can grow in conditions of low serum.
- They adopt round morphology (rather than flat and extended).
- They are able to grow without attaching to a substrate (e.g. surface petri dish) -> anchorage independence.
Fill in: Most agents that cause cancer, called … (1), are agents that cause alterations to the DNA sequence, called mutations (e.g. … (2).
- carcinogens 2. mutagens
What are two factors that contribute to the increasing risk of cancer development during aging?
Mutations in cells accumulate over time and the world life expectancy has more than doubled.
Fill in: Interestingly, only … (1)% of the mutations observed are thought to be directly involved in causing cancer.
5-10%
True or false: Clonal evolution explains the heterogeneous population of cells within a tumor.
True
What process is explained by the fact that clonal evolution explains the heterogeneous population of cells within a tumor.
Darwinian evolution, the additional mutations give the cancer cells a growth advantage over its normal neighbors.
When can mutations accumulate in a cell?
When the cell’s defence mechanism (e.g. DNA repair) have been evaded.
What three important processes contribute to the overall net cell number in an individual?
Cell proliferation, apoptosis and differentiation (make sure you can understand how an increase/decrease/imbalance in these processes can result in more/less cells.
Why does a oncogene “act” dominant?
An oncogene is a gene mutated such that its protein product is produced in higher quantaties or has increased activity and therefore acts in a dominant manner to initiate further tumor formation.
Why are tumor suppressor mutations mainly recessive?
Because one intact allele is usually sufficient to inhibit growth and so one mutated allele is insufficient to stimulate growth.
What is Knudson’s two-hit hypothesis?
It states that both alleles need to be mutated (recessive) to trigger carcinogenesis.
Why do patients with one inherited mutated tumor suppressor allele have a “head start” towards a cancer phenotype?
Because these patients only need to acquire a second somatic mutation, the first mutation is already there.
What is haploinsufficiency?
Only one mutated tumor suppressor allele can lead to the cancer phenotype.
Why do normal stem cells seem to be a main starting point for carcinogenesis in some cancers?
Both cancer cells and stem cells utilize and rely on self-renewal molecular programs. Also, cancer is more likely to develop in cells that are actively proliferating, as there is a greater chance for mutations to accumulate.
What is correlative evidence?
The observation between two events and weakly intimates that one may cause the other. (For example, a gene from a tumor has a mutation, compared with the same gene isolated from healthy tissue –> keep in mind that this kind of evidence has a good starting point, but is not strong evidence (and may even be coincidental))
