Podcast
Questions and Answers
What is the key difference between a benign and a malignant tumor?
What is the key difference between a benign and a malignant tumor?
- A malignant tumor spreads by invasion and metastasis, while a benign tumor only grows locally. (correct)
- A benign tumor spreads by invasion and metastasis, while a malignant tumor only grows locally.
- Malignant tumors are always more painful than benign tumors.
- Benign tumors are always smaller than malignant tumors.
In the context of tumor development, what is the key difference between linear and parallel tumor development?
In the context of tumor development, what is the key difference between linear and parallel tumor development?
- Linear development involves multiple groups arising simultaneously and parallel development involves a single dominant clone.
- Linear development involves a single dominant clone while parallel development involves multiple groups arising simultaneously. (correct)
- Linear development involves one dominant clone while parallel development involves multiple groups arising simultaneously.
- Linear development involves multiple groups arising simultaneously while parallel development involves one dominant clone.
Which of the following is NOT a characteristic of clonal selection?
Which of the following is NOT a characteristic of clonal selection?
- One change from identical cells becomes a tumor.
- The existing cell population is overtaken by one cell with a specific trait. (correct)
- One cell with a feature gets selected and copied over and over.
- Doesn't affect the existing cell population.
What is the key difference between clonal dominance and clonal selection?
What is the key difference between clonal dominance and clonal selection?
Which step of tumor invasion is described by altering mitotic rate vs. apoptosis?
Which step of tumor invasion is described by altering mitotic rate vs. apoptosis?
During which phase of the cell cycle does the cell prepare for DNA replication?
During which phase of the cell cycle does the cell prepare for DNA replication?
What is the primary function of the G1/S checkpoint?
What is the primary function of the G1/S checkpoint?
Which of the following occurs during the S phase of the cell cycle?
Which of the following occurs during the S phase of the cell cycle?
What is the main function of the G2/M checkpoint?
What is the main function of the G2/M checkpoint?
What is the role of the protein Rb in the G1/S checkpoint?
What is the role of the protein Rb in the G1/S checkpoint?
Which phase of the cell cycle is characterized by the division of the cytoplasm?
Which phase of the cell cycle is characterized by the division of the cytoplasm?
What is the primary role of the Spindle Assembly Checkpoint?
What is the primary role of the Spindle Assembly Checkpoint?
Which of the following best describes the state of a cell in G0?
Which of the following best describes the state of a cell in G0?
What is the role of cyclin in the cell cycle?
What is the role of cyclin in the cell cycle?
How does the phosphorylation of CDK relate to the cell cycle?
How does the phosphorylation of CDK relate to the cell cycle?
Which of these is NOT a mechanism used to prevent the cell cycle?
Which of these is NOT a mechanism used to prevent the cell cycle?
What is the role of Rb in the cell cycle?
What is the role of Rb in the cell cycle?
Which of the following statements about checkpoint inhibitors is TRUE?
Which of the following statements about checkpoint inhibitors is TRUE?
What is the main difference between MCyclin and SCyclin?
What is the main difference between MCyclin and SCyclin?
How does Doxorubicin prevent the cell cycle?
How does Doxorubicin prevent the cell cycle?
What is the connection between cell cycle regulation and cancer development?
What is the connection between cell cycle regulation and cancer development?
Which of the following is NOT a characteristic of a teratogen?
Which of the following is NOT a characteristic of a teratogen?
What is a point mutation, and what impact can it have?
What is a point mutation, and what impact can it have?
Which of the following statements is TRUE regarding carcinogens and mutagens?
Which of the following statements is TRUE regarding carcinogens and mutagens?
Which of the following is NOT an example of a mutagen?
Which of the following is NOT an example of a mutagen?
Which of the following statements about the role of epigenetics in mutations is TRUE?
Which of the following statements about the role of epigenetics in mutations is TRUE?
What type of polyp has a high likelihood of becoming cancerous?
What type of polyp has a high likelihood of becoming cancerous?
Which of the following steps is NOT part of the Three-step Theory of Invasion?
Which of the following steps is NOT part of the Three-step Theory of Invasion?
Which stage of cancer involves spread to distant sites?
Which stage of cancer involves spread to distant sites?
What is the primary function of Invadopodia during cancer invasion?
What is the primary function of Invadopodia during cancer invasion?
What is the significance of the TNM system in cancer staging?
What is the significance of the TNM system in cancer staging?
Which of the following cellular changes is directly associated with increased cancer cell motility?
Which of the following cellular changes is directly associated with increased cancer cell motility?
What is the primary difference between benign and malignant tumors?
What is the primary difference between benign and malignant tumors?
Which of the following is NOT a factor that can contribute to cancer cell invasion?
Which of the following is NOT a factor that can contribute to cancer cell invasion?
What is the meaning of M-0 in the TNM system?
What is the meaning of M-0 in the TNM system?
In the TNM system, what does a T-3 tumor indicate?
In the TNM system, what does a T-3 tumor indicate?
Which of the following accurately describes the role of tumor suppressor genes in the regulation of the cell cycle?
Which of the following accurately describes the role of tumor suppressor genes in the regulation of the cell cycle?
What is the primary function of p53 in relation to DNA damage?
What is the primary function of p53 in relation to DNA damage?
Which of the following statements correctly describes the relationship between proto-oncogenes and oncogenes?
Which of the following statements correctly describes the relationship between proto-oncogenes and oncogenes?
Why are germline mutations generally associated with a higher risk of developing cancer than somatic mutations?
Why are germline mutations generally associated with a higher risk of developing cancer than somatic mutations?
Which of the following situations can lead to an accumulation of damaged cells, potentially increasing the risk of cancer development?
Which of the following situations can lead to an accumulation of damaged cells, potentially increasing the risk of cancer development?
What is the primary mechanism by which increased mutation rates contribute to cancer development?
What is the primary mechanism by which increased mutation rates contribute to cancer development?
What is the main difference between a germline mutation and a somatic mutation?
What is the main difference between a germline mutation and a somatic mutation?
How does p53 contribute to the regulation of the cell cycle?
How does p53 contribute to the regulation of the cell cycle?
Flashcards
Benign Tumor
Benign Tumor
A tumor that does not invade nearby tissues and cannot metastasize.
Malignant Tumor
Malignant Tumor
A cancerous tumor that invades surrounding tissues and can spread through the bloodstream (metastasis).
Clonal Selection
Clonal Selection
A process where one cell with a beneficial change is selected and proliferates, forming a tumor without affecting the wider population.
Clonal Dominance
Clonal Dominance
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Linear Tumor Development
Linear Tumor Development
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Point Mutation
Point Mutation
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Mutagen
Mutagen
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Carcinogen
Carcinogen
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Clastogen
Clastogen
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Teratogen
Teratogen
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Cellular Death Rate Ratios
Cellular Death Rate Ratios
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Three-step Theory of Invasion
Three-step Theory of Invasion
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Tumor Cell Attachment
Tumor Cell Attachment
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Degradation of Matrix
Degradation of Matrix
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Benign Colonic Neoplasms
Benign Colonic Neoplasms
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Villous Adenoma
Villous Adenoma
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Carcinoma in Situ (CIS)
Carcinoma in Situ (CIS)
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TNM System
TNM System
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Oncogenes
Oncogenes
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Mutation Rate
Mutation Rate
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Protooncogenes
Protooncogenes
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Tumor Suppressor Gene
Tumor Suppressor Gene
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p53
p53
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Germline Mutation
Germline Mutation
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Somatic Mutation
Somatic Mutation
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Apoptosis
Apoptosis
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Cyclin
Cyclin
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Cell Cycle
Cell Cycle
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G0 Phase
G0 Phase
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Restriction Point
Restriction Point
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G1 Phase
G1 Phase
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S Phase
S Phase
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G2 Phase
G2 Phase
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G1/S Checkpoint
G1/S Checkpoint
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G2/M Checkpoint
G2/M Checkpoint
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CDK
CDK
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Checkpoint Inhibitors
Checkpoint Inhibitors
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Phosphorylation
Phosphorylation
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Negative Regulation
Negative Regulation
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Retinoblastoma
Retinoblastoma
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Mechanisms to Prevent Cell Cycle
Mechanisms to Prevent Cell Cycle
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Doxorubicin
Doxorubicin
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Study Notes
Cancer Biology
- Cancer is a genetic disease, caused by uncontrolled cell division in a part of the body.
- Cancer cells tend to cause death and deterioration.
- They are invasive, metastasize, and can terminate a malignant tumor.
- Changes in DNA sequence of key genes (cancer genes) cause abnormal behavior of cancer cells.
- Biopsy is the only way to confirm uncontrolled cell division.
- KI 67 is a marker of cell division.
Hallmarks of Cancer
- Self-sufficiency in growth signals
- Insensitivity to antigrowth signals
- Evading apoptosis
- Limitless replicative potential
- Sustained angiogenesis (formation of new blood vessels)
- Tissue invasion and metastasis
Cancer Cells
- Cancer cells arise from single cells.
- Their genomes are altered.
- They lose contact inhibition.
- They are usually clonal in origin (replicated clones).
Normal vs. Cancer Cells
- Normal cells exhibit contact inhibition, while cancer cells do not.
- Normal cells have large cytoplasm, single nucleus, and fine chromatin.
- Cancerous cells have multiple nuclei, coarse chromatin, and small cytoplasm.
Tumour Cell Biological Markers
- Substances produced by cancer cells or found on plasma cell membranes, in blood, CSF, or urine.
- These include hormones, enzymes, genes, antigens and antibodies.
Neoplasia
- Any abnormal new growth of cells.
- Increased number of cells in one area describes hyperplasia.
- Increased size of cells describes hypertrophy.
- Disordered proliferation of cells, and changed cell form is called dysplastic.
In Situ Cancer
- Cancer-looking cells are present in the original site, but no spread to nearby tissue.
- These cells may become cancerous and spread into nearby tissue eventually.
Benign Tumors
- Benign tumor cells grow locally and cannot spread by invasion or metastasis.
Malignant Tumors
- Cancer cells invade surrounding tissues.
- They enter blood vessels and become metastasized.
- Primary tumor development is linear, arising from a single dominant clone.
- Parallel tumor development occurs with multiple groups of cancer cells that arise simultaneously.
Clonal Selection
- A change from identical cells can become a tumor.
- One cell, with a characteristic, is selected and copied many times, replacing the original population.
- When a cell trait is replicated enough, it can become the dominant cell/trait.
Invasion
- Tumour invasion involves steps including cellular multiplication.
- Altered mitotic rate, lytic enzymes release, and decreased cell-cell adhesion increase mobility in tumour cells.
- Intravasation and extravasation processes allow entry and exit from blood vessels.
Benign Colonic Neoplasms
- Tubular adenomas and villous adenomas are precancerous polyps.
- About 15-25% of villous adenomas and 10% of tubular adenomas become cancerous.
- Hyperplastic polyps are located in the colon rectum and sigmoid colon.
- Dysplastic polyps display abnormal cell characteristics.
Essential TNM
- A registry tool to reduce errors in cancer staging.
- Metastasis is checked for using M status (M0 or M1) and determined
- Tumor size (T status) is checked
- Lymph node involvement is checked (N status)
Oncogenes, Protooncogenes, Tumor Suppressor Genes
- Mutations in oncogenes increase the frequency of cancer.
- Protooncogenes can become oncogenes.
- Tumor suppressor genes usually suppress tumors.
p53
- Master regulator of cell cycle.
- Regulates DNA replication and repair.
Germline and Somatic Mutations
- Germline mutations can be inherited from parents.
- Somatic mutations are present in all body cells, except reproductive cells.
DNA Damage Repair Mechanisms
- Base excision repair, mismatch repair, and nucleotide excision repair.
Chromosomal Mutations
- Rearrangements include inversions and translocations; deletions, insertions, and duplications and substitutions; aneuploidy; and polyploidy.
Aneuploidy
- Irregular number of chromosomes.
Mutagens, Carcinogens, Clastogens, Teratogens
- Mutagens cause mutations.
- Carcinogens cause cancer.
- Clastogens produce chromosome breaks.
- Teratogens cause congenital malformations.
Cell Cycle
- A series of events that occur in a cell as it grows and divides.
Checkpoints
- Control points in the cell cycle to ensure DNA replication and cell division proceed accurately.
Cyclins and CDKs
- Cyclins are proteins that regulate CDKs (cyclin-dependent kinases) which are involved in regulating the cell cycle.
- Phosphorylation activates proteins, thus enabling cell cycle progression.
Apoptosis
- Regulated cell death (and sometimes an unregulated process), with mechanisms that destroy cells.
Intrinsick and Extrinsic Pathways to Apoptosis
- Intrinsic - signals that trigger programmed cell death from inside the cell.
- Extrinsic - signals outside of the cell trigger programmed cell death.
Cancer Cells and Membrane Flipping
- Tumor Cells are often associated with membrane flipping.
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