What is meant by the term 'genomic instability' in the context of cancer development?
Explanation
Genomic instability is a core characteristic of cancer cells. It refers to the high frequency at which their genomes acquire mutations, ranging from point mutations to large-scale chromosomal rearrangements. This instability is driven by defects in DNA repair and cell cycle checkpoints and accelerates the accumulation of other cancer-promoting mutations.
Other questions
What is the primary function of the HPV E6 protein in the context of oncogenesis?
What is the estimated percentage of human cancers that have mutations in the p53 gene?
How does homology-directed repair (HR) differ from non-homologous end-joining (NHEJ) in repairing double-strand DNA breaks?
Which of the following describes a key characteristic of a proto-oncogene?
What is the primary mechanism of base excision repair (BER)?
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?
How does the drug imatinib function as a targeted cancer therapy?
What is the role of the Retinoblastoma (Rb) protein in a healthy cell?
Why are people with Xeroderma Pigmentosum (XP) extremely sensitive to UV light and have a high risk of skin cancer?
What is the definition of a malignant tumor as opposed to a benign tumor?
How do elephants, which are large and long-lived, exhibit a lower-than-expected cancer incidence?
Which of the following is considered a 'gatekeeper' function of a tumor suppressor, as opposed to a 'caretaker' function?
According to the text, what is the average number of driving mutations typically found in most cancers?
In mismatch repair in prokaryotes, how is the newly synthesized daughter strand distinguished from the parental template strand?
Which of the following is NOT listed as one of the original Hallmarks of Cancer proposed by Hanahan and Weinberg?
What is gene conversion in the context of double-strand break repair?
The fusion protein BCR-ABL, targeted by the drug imatinib, is the result of what type of genetic event?
Why are germline mutations in proto-oncogenes typically embryonic lethal?
What is metastasis?
In the progression of colon cancer shown in Figure 18, which gene is an example of a proto-oncogene that becomes activated?
What is the key difference between how traditional chemotherapy and radiation therapy work?
Which of the following cellular processes does the p53 protein promote when a cell sustains excessive DNA damage?
What type of DNA lesion is repaired by photolyase enzymes, a mechanism not found in humans?
Why is cancer considered a genetic disease?
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?
What is the main reason that liquid tumors like leukemias are not solid masses?
What is the function of the MSH and MLH protein families in humans?
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?
What is the defining characteristic of a 'familial' cancer?
How do naked mole rats appear to resist cancer, according to the text?
What is the consequence of the HPV E7 protein's interaction with the Rb protein?
What is the key limitation of non-homologous end-joining (NHEJ) as a DNA repair mechanism?
Children who inherit a germline disease-associated variant of the Rb gene have what approximate chance of developing retinoblastoma?
What does the term 'oncogenesis' refer to?
Which of the following is an example of a gain-of-function mutation leading to an oncogene?
Why do patients undergoing traditional chemotherapy often experience side effects like hair loss and digestive issues?
What is the consequence of epigenetic silencing of a tumor suppressor gene like BRCA1?
Which DNA repair pathway would most likely be responsible for fixing a mismatched base pair that occurred during DNA replication?
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?
The cells in a single tumor are often genetically different from one another. What is this phenomenon called?
What is the function of the cell cycle checkpoints at G1, S, and G2/M?
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?
Which of the following describes the difference in tumors seen in sporadic versus familial retinoblastoma?
A translocation brings a proto-oncogene next to the regulatory region of a highly active gene. What is the likely outcome?
What is the general sequence of events in most indirect DNA repair pathways like BER and NER?
What happens when a loss-of-function mutation occurs in both copies of a tumor suppressor gene in a somatic cell?
Which statement accurately describes the relationship between age and cancer incidence within a species?
What is the function of the enzyme family known as glycosylases?
What is a major reason why familial cancers associated with proto-oncogenes are not observed?