The development of a tumor is described as a multi-stage process. What does the loss of the APC tumor suppressor gene typically lead to in the colon?

Correct answer: The growth of a polyp.

Explanation

The progression of colon cancer from a normal cell to a metastatic tumor often follows a model of sequential mutations. The loss of the APC tumor suppressor gene is a very common initiating event, which gives the cell a slight growth advantage and leads to the formation of a small, benign growth called a polyp. Further mutations are required for progression to malignancy.

Other questions

Question 1

What is the primary function of the HPV E6 protein in the context of oncogenesis?

Question 2

What is the estimated percentage of human cancers that have mutations in the p53 gene?

Question 3

How does homology-directed repair (HR) differ from non-homologous end-joining (NHEJ) in repairing double-strand DNA breaks?

Question 4

Which of the following describes a key characteristic of a proto-oncogene?

Question 5

What is the primary mechanism of base excision repair (BER)?

Question 6

In the context of Knudson's two-hit hypothesis, how many mutations are typically required for cancer to develop in an individual with a familial cancer syndrome like inherited retinoblastoma?

Question 7

How does the drug imatinib function as a targeted cancer therapy?

Question 8

What is the role of the Retinoblastoma (Rb) protein in a healthy cell?

Question 9

Why are people with Xeroderma Pigmentosum (XP) extremely sensitive to UV light and have a high risk of skin cancer?

Question 10

What is the definition of a malignant tumor as opposed to a benign tumor?

Question 11

How do elephants, which are large and long-lived, exhibit a lower-than-expected cancer incidence?

Question 12

Which of the following is considered a 'gatekeeper' function of a tumor suppressor, as opposed to a 'caretaker' function?

Question 13

According to the text, what is the average number of driving mutations typically found in most cancers?

Question 14

In mismatch repair in prokaryotes, how is the newly synthesized daughter strand distinguished from the parental template strand?

Question 15

Which of the following is NOT listed as one of the original Hallmarks of Cancer proposed by Hanahan and Weinberg?

Question 16

What is gene conversion in the context of double-strand break repair?

Question 17

The fusion protein BCR-ABL, targeted by the drug imatinib, is the result of what type of genetic event?

Question 18

Why are germline mutations in proto-oncogenes typically embryonic lethal?

Question 19

What is metastasis?

Question 20

In the progression of colon cancer shown in Figure 18, which gene is an example of a proto-oncogene that becomes activated?

Question 21

What is the key difference between how traditional chemotherapy and radiation therapy work?

Question 22

What is meant by the term 'genomic instability' in the context of cancer development?

Question 23

Which of the following cellular processes does the p53 protein promote when a cell sustains excessive DNA damage?

Question 24

What type of DNA lesion is repaired by photolyase enzymes, a mechanism not found in humans?

Question 25

Why is cancer considered a genetic disease?

Question 26

What is the key functional difference between a gain-of-function mutation in a proto-oncogene and a loss-of-function mutation in a tumor suppressor?

Question 27

What is the main reason that liquid tumors like leukemias are not solid masses?

Question 28

What is the function of the MSH and MLH protein families in humans?

Question 30

What is the defining characteristic of a 'familial' cancer?

Question 31

How do naked mole rats appear to resist cancer, according to the text?

Question 32

What is the consequence of the HPV E7 protein's interaction with the Rb protein?

Question 33

What is the key limitation of non-homologous end-joining (NHEJ) as a DNA repair mechanism?

Question 34

Children who inherit a germline disease-associated variant of the Rb gene have what approximate chance of developing retinoblastoma?

Question 35

What does the term 'oncogenesis' refer to?

Question 36

Which of the following is an example of a gain-of-function mutation leading to an oncogene?

Question 37

Why do patients undergoing traditional chemotherapy often experience side effects like hair loss and digestive issues?

Question 38

What is the consequence of epigenetic silencing of a tumor suppressor gene like BRCA1?

Question 39

Which DNA repair pathway would most likely be responsible for fixing a mismatched base pair that occurred during DNA replication?

Question 40

What is the term for a nonfunctional gene that persists in the genome and is structurally related to a functional gene, often arising from gene duplication followed by inactivating mutations?

Question 41

The cells in a single tumor are often genetically different from one another. What is this phenomenon called?

Question 42

What is the function of the cell cycle checkpoints at G1, S, and G2/M?

Question 43

Loss-of-function mutations in the tumor suppressor BRCA1 are linked with about half of all familial breast cancers. What is a mechanism that can lead to loss of BRCA1 function in sporadic (non-familial) breast cancers?

Question 44

Which of the following describes the difference in tumors seen in sporadic versus familial retinoblastoma?

Question 45

A translocation brings a proto-oncogene next to the regulatory region of a highly active gene. What is the likely outcome?

Question 46

What is the general sequence of events in most indirect DNA repair pathways like BER and NER?

Question 47

What happens when a loss-of-function mutation occurs in both copies of a tumor suppressor gene in a somatic cell?

Question 48

Which statement accurately describes the relationship between age and cancer incidence within a species?

Question 49

What is the function of the enzyme family known as glycosylases?

Question 50

What is a major reason why familial cancers associated with proto-oncogenes are not observed?