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Questions and Answers
Cancer is solely caused by environmental factors, not genetics.
Cancer is solely caused by environmental factors, not genetics.
False
Most cancers originate from multiple cells rather than a single cell.
Most cancers originate from multiple cells rather than a single cell.
False
The development of cancer is a multistep process that begins with benign growth.
The development of cancer is a multistep process that begins with benign growth.
True
Metastatic cancer refers to cancer that has not invaded surrounding tissue.
Metastatic cancer refers to cancer that has not invaded surrounding tissue.
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Tumor viruses have been identified as direct causes of cancer in humans.
Tumor viruses have been identified as direct causes of cancer in humans.
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Hepatitis B virus is associated with liver cancer in humans.
Hepatitis B virus is associated with liver cancer in humans.
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Rous sarcoma virus is a type of DNA virus that causes cancer.
Rous sarcoma virus is a type of DNA virus that causes cancer.
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Chemical carcinogens can contribute to cancer by damaging DNA and inducing mutations.
Chemical carcinogens can contribute to cancer by damaging DNA and inducing mutations.
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Epstein-Barr virus is a known cause of Burkitt lymphoma primarily in immunocompetent individuals.
Epstein-Barr virus is a known cause of Burkitt lymphoma primarily in immunocompetent individuals.
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Approximately 80% of human cancers are induced by viruses.
Approximately 80% of human cancers are induced by viruses.
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Oncogenes can transform normal cells into cancerous cells when mutated.
Oncogenes can transform normal cells into cancerous cells when mutated.
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The first oncogene identified was the Rb gene.
The first oncogene identified was the Rb gene.
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Proto-oncogenes mutate to become tumor suppressor genes.
Proto-oncogenes mutate to become tumor suppressor genes.
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Tumor suppressor genes promote tumor development by enhancing cell growth.
Tumor suppressor genes promote tumor development by enhancing cell growth.
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The p53 gene product plays a role in apoptosis when DNA damage occurs.
The p53 gene product plays a role in apoptosis when DNA damage occurs.
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Loss of function in tumor suppressor genes like Rb and p53 contributes to the development of cancer.
Loss of function in tumor suppressor genes like Rb and p53 contributes to the development of cancer.
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Rb and p16 are classified as oncogenes.
Rb and p16 are classified as oncogenes.
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Wild-type p53 is necessary for inducing apoptosis after DNA damage.
Wild-type p53 is necessary for inducing apoptosis after DNA damage.
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Cdk4 and cyclin D promote the passage through the G1 restriction point by activating Rb.
Cdk4 and cyclin D promote the passage through the G1 restriction point by activating Rb.
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Mutations in tumor suppressor genes have no impact on cancer development.
Mutations in tumor suppressor genes have no impact on cancer development.
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Gain-of-function mutations in proto-oncogenes typically increase protein activity.
Gain-of-function mutations in proto-oncogenes typically increase protein activity.
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Ras protein is a type of tumor suppressor.
Ras protein is a type of tumor suppressor.
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The Bcl-2 family members PUMA and Noxa are inhibitors of cell cycle arrest.
The Bcl-2 family members PUMA and Noxa are inhibitors of cell cycle arrest.
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Proto-oncogenes are normal genes that can become oncogenes through mutation.
Proto-oncogenes are normal genes that can become oncogenes through mutation.
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Cyclin D functions solely as a tumor suppressor in the cell cycle.
Cyclin D functions solely as a tumor suppressor in the cell cycle.
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Accumulated damage to multiple oncogenes is sufficient to cause cancer.
Accumulated damage to multiple oncogenes is sufficient to cause cancer.
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Missense mutations are a type of genetic change that can lead to the activation of tumor-suppressor genes.
Missense mutations are a type of genetic change that can lead to the activation of tumor-suppressor genes.
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The retinoblastoma gene was the first identified tumor-suppressor gene in humans.
The retinoblastoma gene was the first identified tumor-suppressor gene in humans.
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Knudson's two-hit model suggests that only one mutation is necessary for retinoblastoma to develop.
Knudson's two-hit model suggests that only one mutation is necessary for retinoblastoma to develop.
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The p53 gene is associated with 50% of all human cancers due to defects.
The p53 gene is associated with 50% of all human cancers due to defects.
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The Rb protein promotes cell cycle progression by activating transcription factor E2F.
The Rb protein promotes cell cycle progression by activating transcription factor E2F.
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Apoptosis is a process that helps in the formation of new cells by suppressing caspases.
Apoptosis is a process that helps in the formation of new cells by suppressing caspases.
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Inherited retinoblastoma typically appears in later stages of life compared to non-inherited forms.
Inherited retinoblastoma typically appears in later stages of life compared to non-inherited forms.
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Tumor-suppressor genes are responsible for promoting uncontrollable cell division.
Tumor-suppressor genes are responsible for promoting uncontrollable cell division.
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Proteases known as caspases play a role in apoptosis by facilitating cell shrinkage and DNA degradation.
Proteases known as caspases play a role in apoptosis by facilitating cell shrinkage and DNA degradation.
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Gene amplification leads to the inactivation of tumor-suppressor genes.
Gene amplification leads to the inactivation of tumor-suppressor genes.
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Inhibition of E2F promotes the transcription of genes required for DNA replication and cell division.
Inhibition of E2F promotes the transcription of genes required for DNA replication and cell division.
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The protein kinase p16 regulates cyclin-dependent kinases to control the transition from G1 to S phase of the cell cycle.
The protein kinase p16 regulates cyclin-dependent kinases to control the transition from G1 to S phase of the cell cycle.
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Loss of NF1 function leads to the deactivation of the Ras protein.
Loss of NF1 function leads to the deactivation of the Ras protein.
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P53 acts as a sensor of DNA damage and can promote apoptosis if necessary.
P53 acts as a sensor of DNA damage and can promote apoptosis if necessary.
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BRCA1 and BRCA2 proteins are involved in promoting DNA damage by inhibiting DNA repair processes.
BRCA1 and BRCA2 proteins are involved in promoting DNA damage by inhibiting DNA repair processes.
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Tumor-suppressor genes are responsible for promoting cell division.
Tumor-suppressor genes are responsible for promoting cell division.
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Epigenetics refers to stable changes in cell function without alterations to the DNA sequence.
Epigenetics refers to stable changes in cell function without alterations to the DNA sequence.
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Checkpoint proteins have no role in detecting genetic abnormalities and preventing cell division.
Checkpoint proteins have no role in detecting genetic abnormalities and preventing cell division.
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DNA methylation is a mechanism that alters gene expression without changing the underlying DNA sequence.
DNA methylation is a mechanism that alters gene expression without changing the underlying DNA sequence.
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Epigenetic changes can only contribute directly to disease symptoms and cannot arise from them.
Epigenetic changes can only contribute directly to disease symptoms and cannot arise from them.
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Histone modification can involve the addition of acetyl groups to histones.
Histone modification can involve the addition of acetyl groups to histones.
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Chromatin remodeling does not play a role in cancer.
Chromatin remodeling does not play a role in cancer.
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Environmental agents can affect the functions of chromatin-modifying proteins.
Environmental agents can affect the functions of chromatin-modifying proteins.
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Tobacco smoke is associated with epigenetic changes that can lead to lung cancer.
Tobacco smoke is associated with epigenetic changes that can lead to lung cancer.
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Mutations in genes that encode chromatin-modifying proteins can influence gene expression.
Mutations in genes that encode chromatin-modifying proteins can influence gene expression.
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All environmental agents associated with cancer directly cause epigenetic changes.
All environmental agents associated with cancer directly cause epigenetic changes.
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5-azacytidine and decitabine are scholars known to inhibit cancer cell growth through DNA methylation modulation.
5-azacytidine and decitabine are scholars known to inhibit cancer cell growth through DNA methylation modulation.
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Benzene exposure has been linked to multiple myeloma and lymphoma.
Benzene exposure has been linked to multiple myeloma and lymphoma.
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Histone kinases add phosphate groups to histones as part of histone modification.
Histone kinases add phosphate groups to histones as part of histone modification.
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Chromatin modifications have no relevance to cancer pathology.
Chromatin modifications have no relevance to cancer pathology.
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The presence of toxic agents can indirectly cause disease without altering genetic changes.
The presence of toxic agents can indirectly cause disease without altering genetic changes.
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Histone demethylases are involved in removing methyl groups from histones.
Histone demethylases are involved in removing methyl groups from histones.
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Study Notes
Genetic Basis of Cancer
- Cancer is a disease characterized by uncontrolled cell division.
- It's a genetic disease at the cellular level.
- Human cancers are classified according to the type of cell that becomes cancerous, with over 100 identified types.
- Most cancers originate from a single cell; growth is clonal in origin.
- A cancer cell divides to produce two cancer cells
- Cancer is a multistep process.
- Begins as a benign growth (not invasive).
- Additional genetic changes lead to cancerous growth.
- Cancers can be staged (malignant - invasive - Invades surrounding tissue; metastatic - Moves to a different site in body).
Characteristics of Cancer
- Cancer development is a multistep process, starting from a single cell to uncontrolled growth.
- Cancer initially develops as a benign growth that isn't invasive.
- Further genetic changes transform the growth into a cancerous one.
- Cancer cells can spread locally and distantly (metastasize), showcasing malignant behavior.
Causes of Cancer
- Radiation and many chemical carcinogens damage DNA, inducing mutations.
- Other chemical carcinogens stimulate cell proliferation, contributing to cancer development.
- Viruses can cause cancer in both humans and other species.
Tumor Viruses
- Some animal viruses, called tumor viruses, can directly cause cancer in animals and humans.
- Different viral families exhibit various genome sizes and cause diverse human cancers.
- Around 80% of human cancers aren't caused by viruses and arise from other causes like radiation and chemical carcinogens.
Oncogenes
- Specific genes (oncogenes) induce cell transformation, providing insight into cancer's molecular basis.
- Studies of viral oncogenes helped identify cellular oncogenes involved in non-virus-induced cancers.
- Retroviruses are crucial in linking viral and cellular oncogenes.
- The first oncogene identified was the src gene of Rous sarcoma virus (RSV).
- Subsequent research recognized dozens of distinct oncogenes.
Proto-Oncogenes
- Proto-oncogenes are normal genes that can become oncogenes through mutations.
- Proto-oncogene mutations manifest as increased protein amounts, altered protein structures (overactivity), or protein expression in inappropriate cell types.
Tumor Suppressor Genes
- Tumor suppressor genes play a vital role in regulating growth control, inhibiting cell division and tumor development.
- The prototypical tumor suppressor gene, Rb, was identified through retinoblastoma studies
- The loss or inactivation of tumor suppressor genes can lead to various human cancers.
- The proteins encoded by most tumor suppressor genes act as inhibitors of cell proliferation or survival, mainly negative regulators of cell cycle progression.
- Some examples are Rb, p16, NF1, APC, p53, and BRCA-1 / BRCA-2.
p53 Gene
- A prominent role of p53 is its ability to detect DNA damage and promote cellular pathways. Some of these pathways include DNA repair, arresting cell division, and promoting apoptosis.
- About 50% of cancers display defects in the p53 gene function.
Apoptosis
- Apoptosis is a process of programmed cell death, facilitated by proteases (caspases).
- Apoptosis's role involves shrinking cells, condensing chromatin, and breaking down DNA.
- Consequently, the cell is broken into small vesicles and then removed by the immune system.
Epigenetics
- Epigenetics is the study of heritable traits controlled by changes in cell function. These changes occur without alteration in the DNA's nucleotide sequence.
- Epigenetic changes, which include mechanisms such as DNA methylation, histone modification, and chromatin remodeling, might contribute to various health issues.
Association Between Epigenetics and Disease
- Epigenetic changes in various ways can influence disease in humans from directly contributing to symptoms to symptoms leading to changes, and ultimately indirect involvement via third factors.
Environmental Agents and Cancer
- Some environmental agents alter chromatin-modifying proteins' function, potentially leading to cancer.
Cancer Treatments
- Researchers are exploring DNA methylation or covalent histone modification-inhibiting drugs, especially 5-azacytidine and decitabine.
Mutations Changing Proto-oncogenes to Oncogenes
- Four types of mutations frequently convert proto-oncogenes to oncogenes:
- Missense mutations
- Gene amplification
- Chromosomal translocation
- Viral integration
Rb Protein Regulates Cell Division
- Recent studies demonstrate how the Rb protein's activity impacts cancer-cell proliferation by regulating the transcription factor E2F.
- Rb's interaction with E2F inhibits the activation of genes related to cell-cycle progression.
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Description
Explore the intricate genetic factors that contribute to the development of cancer. This quiz covers the characteristics of cancer, its multistep process, and how benign growths can progress to invasive and metastatic stages. Test your knowledge on different types and classifications of cancer.
