24 Questions
What is the Knudson 2 hit hypothesis in the context of tumor suppressor genes?
Most tumor suppressor genes require both alleles to be inactivated.
Explain how Retinoblastoma (Rb) acts as a tumor suppressor gene.
Single phosphorylated Rb sequesters E2F proteins while multiply phosphorylated Rb cannot bind and sequester E2F, allowing them to send the cell into S phase.
What is the significance of mitotic recombination in familial cancers with mutated tumor suppressor genes?
Early cancer cells aim to eliminate wild type copies of TSG through mitotic recombination.
How does methylation of the promoter affect tumor suppressor genes?
Methylation of the promoter causes gene silencing.
What does it mean for a tumor suppressor gene to be haploinsufficient?
It means that only 1 mutation in the gene is required for its function to be affected.
Explain how p53 functions as a tumor suppressor gene in response to DNA damage and dysregulated growth signals.
P53 stabilizes in response to DNA damage, forms a homotetramer, and blocks cell cycle progression, leading to senescence or apoptosis.
Distinguish between oncogenes and tumor suppressor genes, highlighting their roles in cancer development.
Oncogenes are genes that increase selective growth advantage, leading to cancer, whereas tumor suppressor genes prevent uncontrolled growth when functional, but lead to cancer when inactivated.
Describe the mechanism of the Src protein in cancer development, including its effects on downstream signaling pathways.
The Src protein, a tyrosine kinase, phosphorylates and activates AKT and PKB, promoting cell proliferation and survival.
Explain the process of anchorage-independent growth in cancer cells, and its significance in cancer development.
Cancer cells can grow without attachment to a solid substrate, allowing them to proliferate in suspension, a hallmark of cancer.
Discuss the role of the Rous sarcoma virus in cancer development, including the genetic material it transmits to host cells.
The Rous sarcoma virus (RSV) transmits the src gene, a proto-oncogene, into host cells, leading to uncontrolled growth and cancer.
Distinguish between immortalization and replicative immortality in cancer cells, highlighting their implications for cancer development.
Immortalization refers to the ability of cancer cells to proliferate indefinitely, while replicative immortality refers to the ability to bypass normal limits on cell division.
Discuss the significance of evading growth suppressors and inducing angiogenesis in cancer development, highlighting their roles in tumor progression.
Evasion of growth suppressors allows cancer cells to bypass normal growth controls, while inducing angiogenesis provides a blood supply for tumor growth.
What type of mutation directly or indirectly confers a selective growth advantage, leading to the formation of cancer?
Driver mutation
What is the result of the translocation between chromosomes 9 and 22, leading to chronic myeloid leukemia?
Formation of the BCR-ABL fusion protein
How does the inhibition of erbB2/HER2 by Herceptin/Traztuzumab prevent proliferative signaling?
By preventing dimerization of erbB2
What type of mutation in the Ras protein can turn it from a proto-oncogene into an oncogene?
Missense mutation in G12 and Q61
What is the effect of overexpression of erbB2/HER2 in cancer cells?
Increased dimerization and proliferative signaling
What is the mechanism of action of Gleevec/Imatinib in inhibiting the BCR-ABL fusion protein?
Competitive binding to the phosphorylation site
What are the two types of repairs that are hindered in cancer cells with undruggable targets, leading to cell death?
base excision repair (PARP1) and homologous recombination (BRCA)
What are the two major barriers to cell immortalization, and how do cancer cells bypass them?
Replicative senescence and crisis; cancer cells bypass them by reactivating telomerase to lengthen telomeres.
What are the three types of cellular adaptations that can occur in response to cellular stress, and how do they differ?
Atrophy (smaller cells), hypertrophy (larger cells), and hyperplasia (more cells); they differ in cell size and number.
What is the key feature that distinguishes benign tumors from malignant tumors?
Malignant tumors are invasive and may metastasize, whereas benign tumors are confined to a specific tissue and have not penetrated the basement membrane.
What is EMT, and what are the key changes that occur in epithelial cells that undergo EMT?
EMT is epithelial-to-mesenchymal transition; key changes include cytoskeletal remodeling, weakening of cell-cell adhesion, and acquisition of cell motility.
What is the role of telomerase in cancer cells, and how does it contribute to tumorigenesis?
Telomerase reactivates to lengthen telomeres, allowing cancer cells to bypass crisis and achieve immortality, contributing to tumorigenesis.
Test your knowledge on what causes cancer, including factors such as viruses, chemical carcinogens, and radiation, as well as the key hallmarks of cancer cells. Learn about identifying cancerous cells through characteristics like immortalization and altered morphology.
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