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Questions and Answers
What is the primary function of oncogenes in transformed cells?
What is the primary function of oncogenes in transformed cells?
Which of the following is NOT a characteristic of transformed cells?
Which of the following is NOT a characteristic of transformed cells?
Protooncogenes become oncogenes due to which of the following processes?
Protooncogenes become oncogenes due to which of the following processes?
What does 'anchorage-independent growth' mean in the context of transformed cells?
What does 'anchorage-independent growth' mean in the context of transformed cells?
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Which of the following statements accurately describes protooncogenes?
Which of the following statements accurately describes protooncogenes?
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What is a consequence of gene amplification in tumor cells?
What is a consequence of gene amplification in tumor cells?
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Which mechanism is NOT associated with oncogene activation?
Which mechanism is NOT associated with oncogene activation?
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Which characteristic is associated with the ability to form tumors when injected into immunologically compromised animals?
Which characteristic is associated with the ability to form tumors when injected into immunologically compromised animals?
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What happens as a result of chromosomal translocation involving the MYC gene?
What happens as a result of chromosomal translocation involving the MYC gene?
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What defines the 'gain-of-function mutation' in protooncogenes?
What defines the 'gain-of-function mutation' in protooncogenes?
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What structure do HSRs lack in comparison to normal chromosomal patterns?
What structure do HSRs lack in comparison to normal chromosomal patterns?
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Which mechanism can lead to hematologic malignancies through chromosomal rearrangements?
Which mechanism can lead to hematologic malignancies through chromosomal rearrangements?
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What is a common result of integrating viral DNA into the host genome?
What is a common result of integrating viral DNA into the host genome?
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What classification do growth factor receptors fall under in oncogenes?
What classification do growth factor receptors fall under in oncogenes?
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What type of viruses can cause cellular proliferation leading to cancer?
What type of viruses can cause cellular proliferation leading to cancer?
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Study Notes
Oncogenes and Protooncogenes
- Protooncogenes are normal host genes that can become dysregulated due to mutations.
- When protooncogenes mutate, they become oncogenes, which play a critical role in cancer development.
Role of Oncogenes
- Oncogenes drive the transformation of normal cells by promoting cell proliferation.
- They also help cancer cells evade apoptosis (programmed cell death), allowing for unchecked growth.
Characteristics of Transformed Cells
- Transformed cells can form foci in tissue culture, breaking the typical monolayer structure.
- They exhibit anchorage-independent growth, meaning they can proliferate without being attached to a substrate.
- When introduced into immunocompromised animals, transformed cells can form tumors, demonstrating their oncogenic potential.
Oncogenes and Cancer Transformation
- Protooncogenes are normal host genes that can become oncogenes due to mutations.
- Oncogenes promote cellular proliferation and reduce sensitivity to apoptosis, driving cancerous transformations.
- Characteristics of transformed cells include:
- Formation of foci instead of a single monolayer in tissue cultures.
- Anchorage-independent growth, allowing cells to grow without attachment to a substrate.
- Tumor formation when injected into immunocompromised animal models.
Mechanisms of Oncogene Activation
- Activation can occur through:
- Mutations: Alterations in DNA sequence that can lead to gain-of-function.
- Overexpression: Amplification results in increased gene copies within the cell.
- Chromosomal translocation: Direct exchange of genetic material between chromosomes, commonly seen in haematopoietic malignancies (e.g., MYC gene translocations associated with lymphomas and leukemias).
Gene Amplification
- Gene amplification refers to the increase in copy number of a specific gene, contributing to drug resistance in tumor cell lines.
- Amplification can result in:
- Double-minute chromosomes (DMs): Minichromosomes lacking centromeres.
- Homogeneous staining regions (HSRs): Chromosomal segments with disrupted normal staining patterns.
- Both DMs and HSRs can contain hundreds of gene copies, leading to increased gene expression and growth advantages.
Chromosomal Rearrangements
- Common in hematologic malignancies and some solid tumors, consisting primarily of translocations and inversions.
- Mechanisms of malignancy include:
- Transcriptional activation: Moving a protooncogene near an immunoglobulin or T-cell receptor gene, causing deregulated expression.
- Fusion genes: Resulting from the joining of segments from different genes, which can lead to neoplastic transformation.
Viral Contributions to Cancer
- Both DNA and RNA viruses can induce cancer by integrating viral genetic material into the host genome.
- Mechanisms involve:
- Inducing expression of cellular genes or inactivating them, resulting in uncontrolled cell proliferation.
- Retroviruses reverse transcribe their RNA genome into DNA, which integrates into the host nucleus.
Classes of Oncogenes
- Oncogenes are classified based on their cellular location and biochemical activity into seven categories:
- Growth factors
- Growth factor receptors
- Membrane-associated guanine nucleotide-binding proteins
- Serine-threonine protein kinases
- Cytoplasmic tyrosine kinases
- Nuclear proteins
- Cytoplasmic proteins impacting cell survival
- Each class exhibits unique traits contributing to oncogenesis.
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Description
Explore the key principles of cancer biology, particularly focusing on protooncogenes and oncogenes. This quiz presents concepts related to the dysregulation of host genes and characteristics of transformed cells. Test your understanding of the factors contributing to cell proliferation and transformation processes.