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The human cell > Lecture 19 and 20 > Flashcards

Lecture 19 and 20 Flashcards

1
Q

Name three differences in the growth of normal cells and cancer cells.

A

Cancer cells form tumors
Anchorage independent growth
Density dependent inhibition of growth

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2
Q

What is anchorage dependence?

A

Normal cells require a matrix (cancer cells can grow in suspension)

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3
Q

Why do cancer cells have unusual metabolism?

A

They rely on oxidative phosphorylation as well as aerobic glycolysis

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4
Q

Why are cancer cells less likely to die?

A

Abnormal stress response, less prone to apoptosis, escape replicative cell senescence

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5
Q

What are the differences in genes involved in the cell cycle expressed by normal cells vs cancer cells?

A

Cancer cells increase oncogene expression and do not express tumour suppressor genes

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6
Q

What are the 6 most common cancers?

A

Breast, colon/rectum, prostate, lung, stomach, uterine/cervix

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7
Q

Total number of deaths from cancer in 2018?

A

9.6 million

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8
Q

What is the type of cancer that arises from epithelial cells?

A

Carcinoma

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9
Q

What % of cancers does carcinoma make up?

A

around 80-90%

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10
Q

What is the type of cancer that develops from supporting and connective tissues (such as bones, cartilages, fat and muscles)?

A

Sarcomas

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11
Q

What cancer arises from cells of lymphatic and blood origin?

A

Lymphomas and leukemias

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12
Q

What cancers arise from blasts (precursor cells) of embryonic tissue?

A

Blastomas

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13
Q

Give two examples of blastomas.

A

Retinoblastoma (affects the eye)

Nephroblastoma (effects the kidney)

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14
Q

What % of cancers does lymphomas and leukemias make up?

A

around 7%

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15
Q

Where do osteosarcoma develop and who does this effect?

A

Growing bones

Teenagers and young adults

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16
Q

Where do lymphomas develop?

A

Any organ lymphoid tissue is present (lymph nodes, spleen, tonsil, gus skin etc.)

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17
Q

What can lymphomas be further catagorised into?

A

B-cell
T-cell
Hodgkin lymphoma

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18
Q

What 4 things does the spread of cancer cells require?

A
  1. Brake off tumor
  2. Invade local tissue
  3. Penetrate endothelia
  4. Spread via blood or lymph
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19
Q

What 4 factors affect cancer spreading?

A

Tumor microenvironment (influences cancer development)
Angiogenesis
Invasion
Metastasis

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20
Q

What makes up the tumor microenvironment?

A

Endothelial cells, stromal fibroblasts, bone marrow derived cells, macrophages, monocytes, mesenchymal stem cells

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21
Q

In what way do tumors and microenvironments (stroma) interact?

A

They communicate two ways to influence growth (e.g. cancer cells release growth factors and signal proteins, stroma releases signal proteins that stimlate growth and division, as well as proteases)

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22
Q

How is angiogenesis regulated?

A

Angiogenesis promoters make blood vessels grow towards tumor, controlled by balance of opposing factors

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23
Q

Name two activators of angiogenesis.

A

Basic fibroblast GF

Vascular endothelial GF

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24
Q

What happens once cancer cells release angiogenesis activators and these bind to receptor proteins on the lining of blood vessels?

A

Endothelial cells are synthesised, metalloproteases are secreted

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25
Q

Name three angiogenesis inhibitors.

A

Angiostatin
Endostatin
Thrombospondin

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26
Q

What does invasion refer to?

A

Direct migration and penetration of cancer cells into neighbouring tissues

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27
Q

What is metastasis?

A

The ability of cancer cells to enter the bloodstream and travel to distant sites

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28
Q

What 4 factors does cell invasion depend on?

A

Cell adhesion changes
Increased motility
Protease production
Invasion

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29
Q

Give an example of the plasticity of cancer cells during the invasion-metastasis process?

A

Epithelial-mesenchymal plasticity

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30
Q

Give two examples of environmental factors (chemicals, carcinogens) of cancer.

A

Asbestos (lung cancer)

Benzidine (antioxidant in rubber industry)- metabolised to active from in liver and caused bladder cancer

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31
Q

How do environmental factors cause DNA damage?

A

Genertate cross links between two strands of double helix, or cause breaks in one or both DNA strands

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32
Q

What percentage of cancers arise by mechanisms involving viruses/bacteria/parasites?

A

15%

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33
Q

Name the bacteria involved in causing stomach cancer.

A

Helicobacter pylori

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34
Q

What virus is involved in causing cervical cancer?

A

Human papillomavirus

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35
Q

What bacteria is involved in causing cervical cancer?

A

Chlamydia trachmatis

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36
Q

What oncogenic virus is involved in causing liver cancer?

A

Hepatitis B

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37
Q

What virus is involved in causing liver cancer?

A

Hepatitis C

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38
Q

Use of tanning salons increases the chances of developing what types of cancer?

A

Squamous cell carcinoma
Basal cell carcinoma
Melanoma

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39
Q

The expression of what three genes did Bob Weinberg’s lab find resulted in tumorigenic conversion of cells?

A

Telomerase catalytic subunit
Simian virus 40 large T product
Oncogenic H-ras protein

40
Q

What are the 5 main mehcanisms of oncogene activation?

A

Point mutation, gene amplification, chromosomal translocation, local DNA rearrangements, insertional mutagenesis

41
Q

What is a gene amplification?

A

A copy number increase of a restricted reigion of a chromosome arm

42
Q

What is chromosomal translocation

A

Rearrangement of parts between non-homologous chromosomes

43
Q

What can chromosomal translocation give rise to?

A

Increased oncogene expression, fusion gene (chimeric/fusion protein)

44
Q

Give an example of a cancer caused by chromosomal translocation.

A

Burkitt’s lymphoma.

45
Q

What does local DNA rearrangement do?

A

Disrupt proto-oncogene structure by insertions, deletions, inversions

46
Q

What is insertional mutagenesis?

A

Viral DNA is intergrated into host chromosome, stimulating expression of proto-oncogene, producing too much protein

47
Q

What do most oncogenes code for?

A

Components of growth signaling pathways

48
Q

What are the 6 catagories of oncogenes?

A 
Growth factors
Receptors
Plasma membrane GTP-binding proteins
Nonreceptor protein kinases
Transcription factors
Cell cycle or apoptosis regulators
49
Q

What experiment demonstrated the suppression of malignancy by cell fusion?

A

somatic cell hybridization experimnents (some chromosomes are lost during subsequent cell divisions, leading to cancer cell reverting back)

50
Q

Name three tumor suppressor genes.

A

p53, Rb, APC

51
Q

What does Rb gene regulate?

A

G1/S progression

52
Q

Who proposed retinoblastoma requires the loss of both functional Rb copies?

A

Alfred Knudson

53
Q

Deletions of which chromosome was identified suggesting loss of Rb led to tumor development?

A

13q14

54
Q

How was it demonstrated that Rb is a tumor supressor?

A

Isolated (found consistently lost/mutated in retinoblastomas)
Gene transfer experiments (introducing normal Rb into cell reverses tumorigencity)

55
Q

What is the most frequently mutated gene in human cancer?

A

p53 (around 50%)

56
Q

What does p53 do?

A

Respond to DNA damage by arresting cell cycle for DNA repair or triggering apoptosis

57
Q

How does p53 lead to cell cycle arrest>

A

p21 inhibits Cdk-cyclin, cannot phosphorylate Rb protein, cell cycle arrest

58
Q

How does p53 lead to apoptosis?

A

Puma inhibits Bcl-2. Bcl-2 cannot inhibit apoptosis

59
Q

How does p53 lead to senescence?

A

p16^INK4a inhibits cdk-cyclin, which inhibits pRb, leading to senescnece

60
Q

How is cancer diagnosed?

A

Biopsy (large nuclear size, pleomorphic nuclear shape, high mitotic index, disorganised tissue etc.)

61
Q

What are the treatment options for cancer?

A

Surgery (of primary tumors)
Radio-therapy (ionizing radiations damage/destroy cancer cells)
Chemotherapy

62
Q

What are the 4 major catagories of chemotherapeutic drugs?

A

Antimetabolites
Alkylating agents
Antibiotics
Plant derived drugs

63
Q

What do antimetabolites do?

A

Inhibit metabolic pathways required for DNA synthesis

64
Q

What do alkylating agents do?

A

Inhibit DNA function (X-linking double DNA helix)

65
Q

What do antibiotics do?

A

Inhibit DNA function (block topoisomerases etc.)

66
Q

What do plant derived drugs do?

A

Block specific phases of cell cycle progression- proliferation

67
Q

What is targeted therapy?

A

Drugs or other substances that attack cancer cells more precisely

68
Q

What is immunotherapy?

A

Treatment that uses your body’s own immune system to help fight cancer

69
Q

What is hyperhtermia?

A

High temperatures to kill cancer cells

70
Q

What is a stem cell transplant?

A

Peripheral blood, bone marrow or cord blood transplants

71
Q

What is photodynamic therapy?T

A

Treatment using photosensitizing agents along with light to kill cancer cells

72
Q

What is the first antibody approved for use in cancer patients?

A

Herceptin

73
Q

What does herceptin do?

A

Binds and inactivates the human epidermal growth factor receptor-2(HER2)

74
Q

How does Ipilimumab work

A

CTLA4 is an inhibitory receptor on the surface of T cells. When blocked, T cells are more reactive and attack tumor cells that were recognized abnormal but tolerated

75
Q

What cancer is ipilmumab used to treat?

A

Metastatic melanoma

76
Q

Give an example of a targeted therapy.

A

Imatinib blocks chimeric Bcr-Abl tyrosine kinase in chronic myelogenous leukeamia

77
Q

How many adult human body cells undergo apoptosis a day?

A

50-70 billion

78
Q

During development, what does apoptosis play a major role in?

A

Morphogenesis and tissue remodelling (elimination of organs and tissues useful only during the embryonic stage)

79
Q

What pathologies has excessive apoptosis been associated with?

A

Neurodegenerative diseases and organ failure after infarction or toxic insult

80
Q

What induces apoptosis?

A

DNA damage, hypoxia, oxidative stress, death receptor ligands and drug treatments

81
Q

What induces necrosis?

A

Accidents/trauma
Infections
Physical damage
Chemical damage

82
Q

What happens to the contents of cells that have died by apoptosis?

A

Apoptotic bodies are phagocytosed by macrophages and neighbouring cells

83
Q

What are some hallmarks of apoptosis?

A

Cellular and nuclear shrinkage, apoptotic bodies, chromatin condensation, DNA fragmentation, mitochondrial membrane permeabilization, release of cytochrome c into cytoplasm, caspases cascade

84
Q

What change occurs in the plasma membrane before apoptosis occurs>

A

Externalization of phosphatidylserine (phospholipid flipping)

85
Q

What ion is involved in triggering and regulating apoptosis?

A

Calcium

86
Q

How is the mitochondrial membrane potential lost?

A

Cytochrome c is released from the mitchondria into the cytosol

87
Q

What does caspases mediate during apoptosis?

A

Intracellular protelytic cascade

88
Q

What does active initator capase activate?

A

Executioner caspases

89
Q

What do executioner caspases do?

A

Cleave cytosolic protein

Cleave nuclear lamin

90
Q

What are the two pathways that activate apoptosis?

A

Cell-surface death receptors activate extrinsic pathway

Mitochondria activates intrinsic pathway

91
Q

Briefly describe the death receptor pathway.

A

Fas ligand on killer lymphocyte binds to Fas death receptor. Death inducing signalling complex activates caspases.

92
Q

What molecule is assembled during the intrinsic pathway that becomes caspase 9?

A

Apotosome

93
Q

What protiens control apoptosis?

A

Bcl-2 family (anti and pro apoptotic)

94
Q

How does Bcl2 anti-apoptotic mechanism work?

A

Reduces permability of mitochondria, stops release of cytochrome c

95
Q

Name 2 Bcl2 pro-apoptotic protiens.

A

Bax and Bak, both trigger cytochrome c release

96
Q

What does IAP stand for and what is it?

A

Inhibitor of apoptosis protein

Family of endogenous inhibitor of caspases

The human cell (10 decks)

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