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Questions and Answers
What is the common feature of cancers?
What is the common feature of cancers?
Uncontrolled abnormal cell growth.
What is the primary cause of cancer?
What is the primary cause of cancer?
Genetic changes (mutation).
Which of the following are hallmarks of cancer? (Select all that apply)
Which of the following are hallmarks of cancer? (Select all that apply)
What are the three ways mutations can cause cancer?
What are the three ways mutations can cause cancer?
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What is a proto-oncogene?
What is a proto-oncogene?
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What is an oncogene?
What is an oncogene?
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Which of these is NOT a type of Ras GTPase?
Which of these is NOT a type of Ras GTPase?
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What percentage of colorectal cancers have activating mutations in the K-Ras gene?
What percentage of colorectal cancers have activating mutations in the K-Ras gene?
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What percentage of Burkitt Lymphoma cases have mutations in the Myc oncogene?
What percentage of Burkitt Lymphoma cases have mutations in the Myc oncogene?
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What is the name of the transcription factor that is upregulated in response to oncogenic stimuli in the Myc oncogene?
What is the name of the transcription factor that is upregulated in response to oncogenic stimuli in the Myc oncogene?
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What can happen when there is a mutation in the MYC gene, especially in childhood glioblastoma?
What can happen when there is a mutation in the MYC gene, especially in childhood glioblastoma?
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What is the name of the single subunit small GTPase that belongs to a family of related proteins: N-Ras, K-Ras, and H-Ras ?
What is the name of the single subunit small GTPase that belongs to a family of related proteins: N-Ras, K-Ras, and H-Ras ?
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What is the name of the pathway activated by Ras GTPases?
What is the name of the pathway activated by Ras GTPases?
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What percentage of all cancers have mutations in the Ras gene?
What percentage of all cancers have mutations in the Ras gene?
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What is the role of EGFR (Epidermal Growth Factor Receptor) in signaling pathways?
What is the role of EGFR (Epidermal Growth Factor Receptor) in signaling pathways?
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What are genes that make proteins called tumor suppressor proteins?
What are genes that make proteins called tumor suppressor proteins?
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What are the names of the proteins involved in DNA repair/stability that maintain DNA stability by repairing DNA and protecting against the accumulation of mutations?
What are the names of the proteins involved in DNA repair/stability that maintain DNA stability by repairing DNA and protecting against the accumulation of mutations?
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What gene encodes the transcription factor P53?
What gene encodes the transcription factor P53?
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What is the most frequently mutated gene in cancer?
What is the most frequently mutated gene in cancer?
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What is the name of the transcription factor that regulates expression of genes involved in proliferation and apoptosis to reduce the likelihood of cancer developing, encoded by the TP53 gene?
What is the name of the transcription factor that regulates expression of genes involved in proliferation and apoptosis to reduce the likelihood of cancer developing, encoded by the TP53 gene?
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What gene is mutated in retinoblastoma and other cancers?
What gene is mutated in retinoblastoma and other cancers?
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What process inhibits E2F transcription factors and cell cycle progression?
What process inhibits E2F transcription factors and cell cycle progression?
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What is the name of the family of proteins that regulate programmed cell death?
What is the name of the family of proteins that regulate programmed cell death?
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What is the name of the protein that is involved in inhibiting apoptosis?
What is the name of the protein that is involved in inhibiting apoptosis?
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What is the name of the protein that is involved in promoting apoptosis?
What is the name of the protein that is involved in promoting apoptosis?
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BH3-only proteins are a distinct and structurally diverse class of proteins that share one motif, the BH3 domain, with BCL-2 family proteins.
BH3-only proteins are a distinct and structurally diverse class of proteins that share one motif, the BH3 domain, with BCL-2 family proteins.
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The gene for BCL2 is found on chromosome 18 and is not transferred to a different chromosome in many B-cell leukemias and lymphomas.
The gene for BCL2 is found on chromosome 18 and is not transferred to a different chromosome in many B-cell leukemias and lymphomas.
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Mutations in the BCL2 gene lead to the BCL2 protein to be made in smaller amounts, which may keep cancer cells from dying.
Mutations in the BCL2 gene lead to the BCL2 protein to be made in smaller amounts, which may keep cancer cells from dying.
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What are the names of the two processes that can trigger programmed cell death (apoptosis)?
What are the names of the two processes that can trigger programmed cell death (apoptosis)?
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The extrinsic pathway starts with external signals binding to death receptors on the cell surface.
The extrinsic pathway starts with external signals binding to death receptors on the cell surface.
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The intrinsic pathway is initiated from within the cell due to stress signals, causing mitochondria to release pro-apoptotic proteins, like SMAC and cytochrome C, that activate caspases, resulting in apoptosis.
The intrinsic pathway is initiated from within the cell due to stress signals, causing mitochondria to release pro-apoptotic proteins, like SMAC and cytochrome C, that activate caspases, resulting in apoptosis.
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Both the extrinsic and intrinsic pathways play crucial roles in maintaining cellular homeostasis and eliminating damaged or unwanted cells.
Both the extrinsic and intrinsic pathways play crucial roles in maintaining cellular homeostasis and eliminating damaged or unwanted cells.
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Cancer survival rates have not changed much in the last 40 years.
Cancer survival rates have not changed much in the last 40 years.
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Over 50% of patients with cancer survive for more than 10 years.
Over 50% of patients with cancer survive for more than 10 years.
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Cancer death rates are rising.
Cancer death rates are rising.
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Less than 40% of cancers are preventable.
Less than 40% of cancers are preventable.
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The increase in cancer rates is due to the fact that we're not dying from other causes.
The increase in cancer rates is due to the fact that we're not dying from other causes.
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Study Notes
Learning Objectives
- Describe the key features of cancer cells
- Understand how mutations affect protein and cell behaviour
- Describe oncogenes and tumour suppressor genes
- Explain their roles in cell proliferation and death
What is Cancer?
- Cancer is a group of >200 diseases
- Characterized by uncontrolled abnormal cell growth
- Life-threatening if untreated
- Driven by genetic changes (mutations)
Hallmarks of Cancer
- Genome instability & mutation
- Resisting cell death
- Evading growth suppressors
- Sustained proliferative signalling
- Enabling replicative immortality
- Inducing angiogenesis
- Activating invasion and metastasis
- Deregulating cellular energetics
- Tumour-promoting inflammation
- Avoiding immune destruction
Cancer Caused by Mutations
- Mutations alter bases (adding, deleting, substituting)
- Increase promoter activity
- Increase transcription factor function
- Alter protein activity
Cancer Genes
Proto-Oncogenes
- Genes involved in normal cell growth
- Mutations can transform them into oncogenes, promoting cancer cell growth
- Examples: c-Myc, K-Ras
Oncogenes
- Mutated forms of proto-oncogenes
- Promote cancer cell growth
- Examples: Activating mutations in K-Ras (found in 30-50% of colorectal cancers), mutations of c-myc (common in Burkitt Lymphoma)
Myc Oncogenes
- Transcription factors upregulated by oncogenic stimuli
- Three family members: c-Myc, N-Myc, and L-Myc
- MYC gene mutations lead to excessive Myc protein, causing overactivity
- Amplification of N-Myc in childhood glioblastoma has poor prognosis
Ras GTPase
- Small GTPase protein family (N-Ras, K-Ras, H-Ras)
- Active when bound to GTP
- Inherent GTPase activity
- Activates the MAP Kinase pathway
- K-Ras mutations are found in 20-30% of all cancers (especially colorectal)
Signalling Pathways from EGFR
- Complex pathway involving EGFR, Ras, and multiple kinases (e.g., Raf, MEK, ERK)
- Initiated by growth factors like EGF
Tumour Suppressor Genes
- Genes encoding proteins that control cell growth
- Mutations lead to uncontrolled cell growth
- Examples: RB1, TP53
TP53 and P53
- TP53 gene encodes the tumour protein p53
- Most frequently mutated gene in cancers
- p53 is a transcription factor
- Regulates proliferation and apoptosis, reducing cancer development
- P53 is vital in regulating cell division, ensuring cells don't replicate with damage
RB1 (retinoblastoma)
- Inhibited by phosphorylation
- Inhibits E2F transcription factors and cell cycle progression
- Phosphorylation of RB1 causes dissociation of RB-repressor complex; releasing E2F which controls cell cycle progression
BCL-2 Proteins
- Regulate programmed cell death (apoptosis)
- Some inhibit apoptosis (e.g., BCL-2), others promote it (e.g., BAX)
- BCL-2 gene found on chromosome 18, its amplification seen in leukemias and lymphomas, leading to increased amounts of BCL-2 (can prevent cell death)
Propogated Cell Death (Apoptosis)
- Extrinsic pathway: External signals activate caspase cascade
- Intrinsic pathway: Intracellular stress signals initiate caspase activation
- Both pathways crucial for homeostasis and eliminating damaged cells
Cancer Optimism
- Cancer survival has doubled in the past 40 years
- 50% of patients survive for >10 years
- Death rates are falling
- ~40% of cancers are preventable
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Description
This quiz explores the fundamental aspects of cancer biology, covering key features of cancer cells, the impact of genetic mutations, and the roles of oncogenes and tumor suppressor genes in cell behavior. You'll enhance your understanding of how these elements contribute to uncontrolled cell growth and cancer progression.
