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Questions

Question 1

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

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Question 2

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

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Question 3

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

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Question 4

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

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Question 5

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

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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?

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Question 7

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

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Question 8

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

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Question 9

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

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Question 10

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

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Question 11

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

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Question 12

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

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Question 13

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

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Question 14

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

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Question 15

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

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Question 16

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

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Question 17

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

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Question 18

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

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Question 19

What is metastasis?

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Question 20

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

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Question 21

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

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Question 22

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

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Question 23

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

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Question 24

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

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Question 25

Why is cancer considered a genetic disease?

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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?

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Question 27

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

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Question 28

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

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Question 29

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?

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Question 30

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

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Question 31

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

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Question 32

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

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Question 33

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

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Question 34

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

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Question 35

What does the term 'oncogenesis' refer to?

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Question 36

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

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Question 37

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

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Question 38

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

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Question 39

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

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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?

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Question 41

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

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Question 42

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

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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?

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Question 44

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

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Question 45

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

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Question 46

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

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Question 47

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

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Question 48

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

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Question 49

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

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Question 50

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

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