cancer hallmarks and traits

Question 1

What are the hallmarks of cancer?

Answer 1

The eight hallmarks are sustained proliferative signaling, evasion of growth suppressors, resistance to apoptosis, enabling of replicative immortality, induction of angiogenesis, activation of invasion and metastasis, reprogramming of energy metabolism, and evasion of immune destruction.

Question 2

What is sustained proliferative signaling?

Answer 2

Cancer cells continuously proliferate due to activation of oncogenes, which promote abnormal growth, often through mutations, gene amplifications, or chromosomal translocations that affect growth factor pathways.

Question 3

What are proto-oncogenes and oncogenes?

Answer 3

Proto-oncogenes are normal genes regulating cell proliferation. When mutated or overexpressed, they become oncogenes, leading to uncontrolled cell growth.

Question 4

What is evasion of growth suppressors?

Answer 4

Cancer cells deactivate tumor suppressor genes, which normally inhibit proliferation, regulate the cell cycle, and prevent mutations. The inactivation of these genes enables unchecked cancer cell growth.

Question 5

What role do tumor suppressor genes play?

Answer 5

They act as cell cycle “brakes,” halting cell division when cells are damaged and preventing mutations in DNA.

Question 6

What happens when proto-oncogenes and tumor suppressor genes are mutated?

Answer 6

Proto-oncogenes become oncogenes (over-activation of growth) and inactivation of tumor suppressor genes removes the “brakes,” leading to uncontrolled growth.

Question 7

How do cancer cells resist apoptotic cell death?

Answer 7

Mutations in cancer cells lead to suppression of apoptosis and overexpression of anti-apoptotic molecules, allowing damaged, non-functional cells to survive.

Question 8

What is apoptosis?

Answer 8

Apoptosis is programmed cell death that removes aged, damaged, or abnormal cells.

Question 9

How do cancer cells enable replicative immortality?

Answer 9

Cancer cells produce the enzyme telomerase, which restores telomeres, allowing them to divide indefinitely.

Question 10

What are telomeres, and what is their role in cell division?

Answer 10

Telomeres are protective caps on chromosomes that shorten with each division. Short telomeres signal cells to stop dividing; however, cancer cells produce telomerase to restore them, enabling unlimited division.

Question 11

What is induced angiogenesis?

Answer 11

Cancer cells promote the growth of new blood vessels by increasing angiogenic growth factors and reducing inhibitors, ensuring a continuous supply of oxygen and nutrients.

Question 12

How does angiogenesis support cancer growth?

Answer 12

It allows tumors to generate their own blood supply, facilitating growth beyond what would be limited by the surrounding tissue’s nutrient and oxygen supply.

Question 13

How do cancer cells activate invasion and metastasis?

Answer 13

Cancer cells break down structural barriers and invade local tissues, allowing them to spread to distant organs through lymphatic and vascular systems.

Question 14

What is metastasis?

Answer 14

Metastasis is the spread of cancer cells from the original tumor to distant tissues and organs.

Question 15

What is epithelial-mesenchymal transition (EMT)?

Answer 15

EMT is the loss of normal epithelial characteristics, increasing cell migratory capacity, resistance to apoptosis, and dedifferentiation into stem-like cells, aiding in metastasis.

Question 16

How do cancer cells reprogram energy metabolism?

Answer 16

Cancer cells use aerobic glycolysis (Warburg effect) to produce energy even in oxygen-rich environments, supporting rapid proliferation by generating byproducts for cell growth.

Question 17

What is the Warburg effect?

Answer 17

The Warburg effect describes cancer cells using aerobic glycolysis (without oxygen) to generate energy, even when oxygen is available, producing byproducts that fuel cell proliferation.

Question 18

How do cancer cells evade immune destruction?

Answer 18

Cancer cells manipulate T-regulatory cells to suppress the immune response against tumors and to support a pro-cancer immune environment that remodels tissue, promotes blood vessel formation, and enhances metastasis.

Question 19

What role do T-regulatory cells play in immune evasion?

Answer 19

T-reg cells normally control immune responses, but tumors can alter them to block anti-tumor immunity and to promote tissue remodeling, angiogenesis, and metastasis.

Question 20

What are the two traits associated with an increased risk for cancer?

Answer 20

Genomic instability and inflammation.

Question 21

What is genomic instability in cancer?

Answer 21

Genomic instability refers to an increased frequency of mutations within the genome, often due to damage in caretaker genes that would normally repair DNA and maintain genomic integrity.

Question 22

What role do caretaker genes play in cancer prevention?

Answer 22

Caretaker genes protect genome integrity by repairing damaged DNA. They help prevent mutations that can lead to cancer.

Question 23

How does a mutation in caretaker genes increase cancer risk?

Answer 23

Mutations in caretaker genes impair DNA repair mechanisms, allowing other mutations to accumulate, which increases genomic instability and the risk for cancer.

Question 24

How does UV light increase the risk of skin cancer?

Answer 24

UV light can damage caretaker genes, leading to defects in DNA repair, which increases the risk of mutations and skin cancer development.

Question 25

What are BRCA1 and BRCA2, and how are they linked to cancer risk?

Answer 25

BRCA1 and BRCA2 are tumor-suppressor and caretaker genes involved in DNA repair. Mutations in these genes prevent proper DNA repair, increasing the risk of breast, ovarian, and other cancers.

Question 26

What is epigenetic silencing?

Answer 26

Epigenetic silencing is the inactivation of genes due to environmental factors rather than direct mutations, leading to reduced expression of genes that could protect against cancer.

Question 27

What are some examples of conditions associated with genomic instability?

Answer 27

Down syndrome, where structural chromosome abnormalities increase predisposition to other diseases, including cancer.

Question 28

How does inflammation contribute to cancer development?

Answer 28

Inflammation can cause genetic and epigenetic changes in cells, leading to cellular dysplasia. Chronic inflammation from infections, chemical exposure, or diseases is associated with increased cancer risk.

Question 29

What are some examples of infections linked to cancer?

Answer 29

Hepatitis B and C increase liver cancer risk; H. pylori increases stomach cancer risk; and long-term ulcerative colitis raises the risk of colon cancer.

Question 30

How do tumors manipulate inflammation to aid their growth?

Answer 30

Tumors produce cytokines and chemokines that attract immature immune cells (monocytes), maturing them into altered macrophages that block immune responses, produce tumor-spreading cytokines, and secrete growth factors that support tumor growth, angiogenesis, and tissue remodeling.

Question 31

What role do tumor-associated macrophages play in cancer progression?

Answer 31

Tumor-associated macrophages (TAMs) inhibit immune responses by blocking T-cytotoxic and NK cells, promoting tumor cell survival and spread. They also secrete growth factors that aid in angiogenesis and tissue remodeling, benefiting tumor progression.

Question 32

How does chronic inflammation from disease contribute to cancer?

Answer 32

Diseases like ulcerative colitis and chronic pancreatitis cause persistent inflammation, increasing cellular turnover and genetic alterations that can lead to cancer.

Question 33

What cellular changes occur as a result of inflammation that increase cancer risk?

Answer 33

Inflammation can lead to genetic mutations, epigenetic changes, and cellular dysplasia, all of which promote abnormal cell growth and increase cancer risk.