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Questions and Answers
Cancer cells exhibit uncontrolled ______ despite normal restrictions.
Cancer cells exhibit uncontrolled ______ despite normal restrictions.
proliferation
Oncogenes promote ______ cell growth and division.
Oncogenes promote ______ cell growth and division.
abnormal
Tumor suppressor genes function to inhibit ______ in cells.
Tumor suppressor genes function to inhibit ______ in cells.
tumorigenesis
______ is the process whereby cancer cells spread from the primary tumor to distant sites.
______ is the process whereby cancer cells spread from the primary tumor to distant sites.
Epithelial-Mesenchymal Transition (EMT) involves the transition from ______ cells to more mobile mesenchymal cells.
Epithelial-Mesenchymal Transition (EMT) involves the transition from ______ cells to more mobile mesenchymal cells.
Secondary tumor cells must cross the ______ to migrate into new tissues.
Secondary tumor cells must cross the ______ to migrate into new tissues.
Cancer cells accumulate mutations that allow them to evade ______.
Cancer cells accumulate mutations that allow them to evade ______.
Cancer cells can have ______ nuclei that are enlarged and irregularly shaped.
Cancer cells can have ______ nuclei that are enlarged and irregularly shaped.
One characteristic of cancer cells is their unlimited ability to ______.
One characteristic of cancer cells is their unlimited ability to ______.
Cells with highly abnormal ______ can indicate genetic instability typical of cancer.
Cells with highly abnormal ______ can indicate genetic instability typical of cancer.
Oncogenes act in a ______ manner: a gain-of-function mutations in a single copy can drive a cell toward cancer.
Oncogenes act in a ______ manner: a gain-of-function mutations in a single copy can drive a cell toward cancer.
Tumor suppressor genes act in a ______ manner: a loss-of-function mutations in both copies can drive a cell toward cancer.
Tumor suppressor genes act in a ______ manner: a loss-of-function mutations in both copies can drive a cell toward cancer.
In normal cells, DNA damage can trigger DNA repair mechanisms, cell cycle arrest, and ______.
In normal cells, DNA damage can trigger DNA repair mechanisms, cell cycle arrest, and ______.
Cancer cells do not repair their DNA damage and do not die as they ______ should.
Cancer cells do not repair their DNA damage and do not die as they ______ should.
Mutations in BRCA 1 and 2 increased risk of ______ cancer and ovarian cancer.
Mutations in BRCA 1 and 2 increased risk of ______ cancer and ovarian cancer.
Normal cells exhibit ______ inhibition, where they stop dividing upon contact with a neighbor.
Normal cells exhibit ______ inhibition, where they stop dividing upon contact with a neighbor.
E-Cadherin is a transmembrane glycoprotein essential for maintaining tissue ______.
E-Cadherin is a transmembrane glycoprotein essential for maintaining tissue ______.
Dominant mutations in the proto-oncogene can lead to the formation of ______ clones within tumors.
Dominant mutations in the proto-oncogene can lead to the formation of ______ clones within tumors.
Half of human tumors contain a mutation in the ______ tumor suppressor gene.
Half of human tumors contain a mutation in the ______ tumor suppressor gene.
Cancer cells grow ______ of each other forming tumors due to loss of contact inhibition.
Cancer cells grow ______ of each other forming tumors due to loss of contact inhibition.
What is one major difference between primary and secondary tumors?
What is one major difference between primary and secondary tumors?
Which characteristic is typical of cancer cells?
Which characteristic is typical of cancer cells?
How do cancer cells achieve an unlimited ability to divide?
How do cancer cells achieve an unlimited ability to divide?
What is the role of cell adhesion molecules in cancer cells?
What is the role of cell adhesion molecules in cancer cells?
What is a consequence of the genetic instability in cancer cells?
What is a consequence of the genetic instability in cancer cells?
What must secondary cancer cells accomplish to establish in a new location?
What must secondary cancer cells accomplish to establish in a new location?
What is an effect of loss-of-function mutations in tumor suppressor genes?
What is an effect of loss-of-function mutations in tumor suppressor genes?
What is the primary mechanism that enables cancer cells to proliferate despite DNA damage?
What is the primary mechanism that enables cancer cells to proliferate despite DNA damage?
Which of the following describes oncogenes?
Which of the following describes oncogenes?
What does the process of Epithelial-Mesenchymal Transition (EMT) enable cancer cells to do?
What does the process of Epithelial-Mesenchymal Transition (EMT) enable cancer cells to do?
Which type of gene requires mutations in both copies to drive a cell toward cancer?
Which type of gene requires mutations in both copies to drive a cell toward cancer?
What is the primary consequence of somatic mutations in cancer cells?
What is the primary consequence of somatic mutations in cancer cells?
Which of the following is a characteristic behavior of cancer cells compared to normal cells?
Which of the following is a characteristic behavior of cancer cells compared to normal cells?
What role do oncogenes play in cancer development?
What role do oncogenes play in cancer development?
How do BRCA 1 and BRCA 2 mutations influence cancer risk?
How do BRCA 1 and BRCA 2 mutations influence cancer risk?
What is the role of E-Cadherin in normal cells?
What is the role of E-Cadherin in normal cells?
Which event distinguishes primary tumor formation from normal cell division?
Which event distinguishes primary tumor formation from normal cell division?
What is the consequence of a gain-of-function mutation in an oncogene?
What is the consequence of a gain-of-function mutation in an oncogene?
What is a common feature of malignant clones in tumors?
What is a common feature of malignant clones in tumors?
What happens to the progeny cells when a cancer cell with DNA damage proliferates?
What happens to the progeny cells when a cancer cell with DNA damage proliferates?
Flashcards
Cancer Cell Characteristics
Cancer Cell Characteristics
Cancer cells exhibit uncontrolled proliferation, metastasis (spread), and lack of differentiation, unlike normal cells.
Tumorigenesis
Tumorigenesis
The process of developing a tumor; caused by accumulated mutations in cells.
Oncogenes
Oncogenes
Genes that promote cell growth and division.
Tumor Suppressor Genes
Tumor Suppressor Genes
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Metastasis
Metastasis
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Primary Tumor
Primary Tumor
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Secondary Tumor
Secondary Tumor
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Genetic Instability
Genetic Instability
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Epithelial-Mesenchymal Transition (EMT)
Epithelial-Mesenchymal Transition (EMT)
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Cell Adhesion Molecules
Cell Adhesion Molecules
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Mutation in Oncogenes
Mutation in Oncogenes
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Cell Proliferation
Cell Proliferation
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Primary Tumor Formation
Primary Tumor Formation
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Contact Inhibition
Contact Inhibition
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E-Cadherin
E-Cadherin
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DNA Damage Repair Mechanism
DNA Damage Repair Mechanism
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Apoptosis
Apoptosis
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Mutation in Tumor Suppressor Gene
Mutation in Tumor Suppressor Gene
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What makes cancer cells unique?
What makes cancer cells unique?
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Telomerase
Telomerase
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What happens to DNA damage in normal cells?
What happens to DNA damage in normal cells?
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What happens to DNA damage in cancer cells?
What happens to DNA damage in cancer cells?
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BRCA 1 and 2
BRCA 1 and 2
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What happens to contact inhibition in cancer cells?
What happens to contact inhibition in cancer cells?
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How do tumor-suppressor genes act?
How do tumor-suppressor genes act?
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Study Notes
Cancer Cell Biology
- Learning Outcomes: Explain the molecular basis of tumorigenesis, distinguish between oncogenes and tumor suppressor genes, outline the mechanisms of epithelial-mesenchymal transition (EMT) and metastasis, and describe methods for cancer diagnosis and treatment.
- Overview: Two key properties of cancer cells are uncontrolled proliferation and metastasis. Cells that only proliferate form primary, often benign, tumors that can be removed surgically.
Cancer Overview
- Cancer Characteristics: Cancer cells proliferate beyond normal constraints; they metastasize by invading and colonizing new tissues.
- Primary Tumors: Cells that only proliferate produce primary (benign) tumors.
- Secondary Tumors (Malignant): Tumor cells must cross basal lamina, migrate through connective tissue, and enter blood or lymphatic vessels. They then exit these vessels and proliferate at a new location, forming a secondary tumor.
Cancer Cells Accumulate Mutations
- Development: Cancers arise through the accumulation of mutations, mostly somatic.
- Oncogene Mutations (Gas Pedals): Gain-of-function mutations in oncogenes drive increased cell division.
- Tumor Suppressor Gene Mutations (Brakes): Loss-of-function mutations in tumor suppressor genes lead to uncontrolled cell division.
Tumor Suppressor Genes
- Recessive Manner: Loss-of-function mutations in both copies of a tumor suppressor gene are required for cancer development.
- Examples: Rb, p53, and p27 are examples of tumor suppressor genes.
Cancer Growth
- Oncogenes' Role: Mutations in oncogenes act like "jammed gas pedals".
- Tumor Suppressor genes' Role: Mutations in tumor suppressor genes act like "defective brakes".
- Uncontrolled Growth: Mutations in both lead to potentially uncontrolled cell division and tumor formation.
Primary Tumor Formation
- Uncontrolled Cell Division: In normal cells, DNA damage triggers a DNA repair mechanism, cell cycle arrest, or apoptosis.
- Cancer Cell Response to Damage: In cancer cells, damaged DNA is not repaired. The damaged cell continues proliferating, and all of the progeny cells carry the mutation.
- Triggers: DNA damage, replication stress are examples.
p53
- Cell Repair Mechanism: p53 gene helps with cellular repair after minor damage triggering the cell cycle to stop until repair is complete.
- Heavy Damage: Heavy damage triggers p53 to signal the cell to initiate apoptosis
BRCA 1 & 2
- DNA Repair: BRCA1 and BRCA2 are involved in DNA repair.
- Increased Risk: Mutations in either gene increase the risk of breast and ovarian cancer.
Contact Inhibition
- Normal Cell Behavior: Normal cells adhere to their neighbors, and contact with a neighbor halts cell division.
- Cancer Cell Behavior: Cancer cells lack restraint and grow on top of each other, leading to tumors.
E-Cadherin and Contact Inhibition
- Transmembrane Glycoprotein: E-cadherin is a transmembrane glycoprotein part of adherens junctions.
- Essential for integrity: Maintaining tissue architecture, integrity, and cell polarity.
- Cell Cycle Arrest: Triggers cell cycle arrest when cells are crowded.
EMT (Epithelial-Mesenchymal Transition)
- Loss of Characteristics: Epithelial cells lose their characteristics and gain motility.
- Epithelial Markers: Examples include E-cadherin, β-catenin, Claudin-1, and Occludin.
- Mesenchymal Markers: Examples include N-cadherin, vimentin, Fibronectin, and S100A4
Metastasis
- Cell Spreading: Cancer cells spread from the primary tumor to distant sites.
- Stages: Degradation of basal membrane, local invasion, entering blood vessels, circulation, exit from blood vessels, and angiogenesis and secondary tumor formation.
Melanoma
- Stages: Cell invasion is a major pathway.
Cancer Diagnosis
- Techniques: Imaging (X-ray, CT, MRI, ultrasound), blood tests (tumor biomarkers), and genetic tests (mutations in proto-oncogenes and tumor suppressors).
Cancer Treatment
- Local Treatment: Surgery, and Radiation.
- Metastatic Treatment: Chemotherapy, Immunotherapy (boost immune system to fight cancer via vaccines, antibodies, and CAR-T cell therapy).
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Description
Explore the fundamental concepts of cancer cell biology, focusing on tumorigenesis, the distinction between oncogenes and tumor suppressor genes, and the processes of metastasis. This quiz also covers the methods for diagnosing and treating various cancers. Test your knowledge of cancer characteristics and the dynamics of tumor formation.
