Week 13

Question 1

Neoplasm

Answer 1

New growth; tumor.

Question 2

Metastasis

Answer 2

Formation of secondary tumors

Question 3

Hallmark of cancer 1: sustained growth and proliferation

Answer 3

• Promote paracrine signaling by neighbors
• Acquire autocrine signaling
• Become more sensitive to mitogens
• Constitutive activation of growth and proliferation promoting factors

Question 4

Cancer cells and contact-mediated inhibition

Answer 4

in a tissue-culture dish, normal cells form a monolayer of contact-inhibited cells. Cancer (transformed) cells lose contact inhibition and grow more than a monolayer.

Question 5

How do cancer cells achieve replicative immortality (ie, avoid replicative senescence)?

Answer 5

• There is a short stretch of DNA at the chromosomal ends that fails to get replicated. This results in shortening of chromosomal ends with every round of replication. Provides a check on cellular replication.
• Cancer cells either turn on expression of telomerase (enzyme that elongates telomeres) or use homologous recombination to elongate their chromosomal ends.

Question 6

How do cancer cells alter their metabolism?

Answer 6

Through the Warburg effect. Normal cells fully oxidize glucose to carbon dioxide and want to extract as much energy from the sugar molecule as possible–done by oxidizing all the way to carbon dioxide. In contrast, cancer cells rely on glycolysis over oxidative phosphorylation and end up producing a lot of lactate and inefficient energy.

Question 7

How do cancer cells coopt blood vessels or induce angiogenesis?

Answer 7

They either grow near existing vessels (cooption) or promote angiogenesis whereby they promote the growth of vessels to the area occupied by cancer cells (angiogenic growth)

Question 8

How are cancer cells able to do things that normal cells cannot?

Answer 8

• Somatic cells are evolutionary ‘dead-ends’, but are genetically identical to germ cells (i.e., the vehicles that ensure transmission of the genetic material) and hence are committed to cooperate
• By acquiring mutations, cancer cells become genetically distinct. Changes the paradigm from one of cooperation to that of conflict
• At its core, cancer is product of an evolutionary process driven by natural selection that selects for the ‘fittest’ cells and takes place within the course of a human lifespan.
• Explains why cancer is not a single disease and is so hard to cure.

Question 9

Why does the incidence of cancer rise steeply (non-linearly) with age?

Answer 9

It takes multiple mutations to cause cancer. If the cause of cancer was only one mutation, then the graph would be a straight line across.

Question 10

How are cancers traditionally classified?

Answer 10

Cancers traditionally classified according to tissue or cell type from which they arise. Can also be classified according to the mutations cancers carry.

Question 11

How is the lethality of a type of cancer assessed?

Answer 11

The ratio of new cases to deaths gives an idea of how lethal a particular cancer.

Question 12

Which type of cells are most susceptible to becoming cancerous?

Answer 12

Highly proliferative cells.

Question 13

Why does tumor progression tend to speed up?

Answer 13

Cancer cells acquire mutations that increase genetic instability, which increases the mutation rate and speeds up the process of tumor progression.