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The human cell > Lecture 19 and 20 > Flashcards

Lecture 19 and 20 Flashcards

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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
Name three angiogenesis inhibitors.
Angiostatin Endostatin Thrombospondin
26
What does invasion refer to?
Direct migration and penetration of cancer cells into neighbouring tissues
27
What is metastasis?
The ability of cancer cells to enter the bloodstream and travel to distant sites
28
What 4 factors does cell invasion depend on?
Cell adhesion changes Increased motility Protease production Invasion
29
Give an example of the plasticity of cancer cells during the invasion-metastasis process?
Epithelial-mesenchymal plasticity
30
Give two examples of environmental factors (chemicals, carcinogens) of cancer.
Asbestos (lung cancer) | Benzidine (antioxidant in rubber industry)- metabolised to active from in liver and caused bladder cancer
31
How do environmental factors cause DNA damage?
Genertate cross links between two strands of double helix, or cause breaks in one or both DNA strands
32
What percentage of cancers arise by mechanisms involving viruses/bacteria/parasites?
15%
33
Name the bacteria involved in causing stomach cancer.
Helicobacter pylori
34
What virus is involved in causing cervical cancer?
Human papillomavirus
35
What bacteria is involved in causing cervical cancer?
Chlamydia trachmatis
36
What oncogenic virus is involved in causing liver cancer?
Hepatitis B
37
What virus is involved in causing liver cancer?
Hepatitis C
38
Use of tanning salons increases the chances of developing what types of cancer?
Squamous cell carcinoma Basal cell carcinoma Melanoma
39
The expression of what three genes did Bob Weinberg's lab find resulted in tumorigenic conversion of cells?
Telomerase catalytic subunit Simian virus 40 large T product Oncogenic H-ras protein
40
What are the 5 main mehcanisms of oncogene activation?
Point mutation, gene amplification, chromosomal translocation, local DNA rearrangements, insertional mutagenesis
41
What is a gene amplification?
A copy number increase of a restricted reigion of a chromosome arm
42
What is chromosomal translocation
Rearrangement of parts between non-homologous chromosomes
43
What can chromosomal translocation give rise to?
Increased oncogene expression, fusion gene (chimeric/fusion protein)
44
Give an example of a cancer caused by chromosomal translocation.
Burkitt's lymphoma.
45
What does local DNA rearrangement do?
Disrupt proto-oncogene structure by insertions, deletions, inversions
46
What is insertional mutagenesis?
Viral DNA is intergrated into host chromosome, stimulating expression of proto-oncogene, producing too much protein
47
What do most oncogenes code for?
Components of growth signaling pathways
48
What are the 6 catagories of oncogenes?
``` Growth factors Receptors Plasma membrane GTP-binding proteins Nonreceptor protein kinases Transcription factors Cell cycle or apoptosis regulators ```
49
What experiment demonstrated the suppression of malignancy by cell fusion?
somatic cell hybridization experimnents (some chromosomes are lost during subsequent cell divisions, leading to cancer cell reverting back)
50
Name three tumor suppressor genes.
p53, Rb, APC
51
What does Rb gene regulate?
G1/S progression
52
Who proposed retinoblastoma requires the loss of both functional Rb copies?
Alfred Knudson
53
Deletions of which chromosome was identified suggesting loss of Rb led to tumor development?
13q14
54
How was it demonstrated that Rb is a tumor supressor?
Isolated (found consistently lost/mutated in retinoblastomas) Gene transfer experiments (introducing normal Rb into cell reverses tumorigencity)
55
What is the most frequently mutated gene in human cancer?
p53 (around 50%)
56
What does p53 do?
Respond to DNA damage by arresting cell cycle for DNA repair or triggering apoptosis
57
How does p53 lead to cell cycle arrest>
p21 inhibits Cdk-cyclin, cannot phosphorylate Rb protein, cell cycle arrest
58
How does p53 lead to apoptosis?
Puma inhibits Bcl-2. Bcl-2 cannot inhibit apoptosis
59
How does p53 lead to senescence?
p16^INK4a inhibits cdk-cyclin, which inhibits pRb, leading to senescnece
60
How is cancer diagnosed?
Biopsy (large nuclear size, pleomorphic nuclear shape, high mitotic index, disorganised tissue etc.)
61
What are the treatment options for cancer?
Surgery (of primary tumors) Radio-therapy (ionizing radiations damage/destroy cancer cells) Chemotherapy
62
What are the 4 major catagories of chemotherapeutic drugs?
Antimetabolites Alkylating agents Antibiotics Plant derived drugs
63
What do antimetabolites do?
Inhibit metabolic pathways required for DNA synthesis
64
What do alkylating agents do?
Inhibit DNA function (X-linking double DNA helix)
65
What do antibiotics do?
Inhibit DNA function (block topoisomerases etc.)
66
What do plant derived drugs do?
Block specific phases of cell cycle progression- proliferation
67
What is targeted therapy?
Drugs or other substances that attack cancer cells more precisely
68
What is immunotherapy?
Treatment that uses your body's own immune system to help fight cancer
69
What is hyperhtermia?
High temperatures to kill cancer cells
70
What is a stem cell transplant?
Peripheral blood, bone marrow or cord blood transplants
71
What is photodynamic therapy?T
Treatment using photosensitizing agents along with light to kill cancer cells
72
What is the first antibody approved for use in cancer patients?
Herceptin
73
What does herceptin do?
Binds and inactivates the human epidermal growth factor receptor-2(HER2)
74
How does Ipilimumab work
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
What cancer is ipilmumab used to treat?
Metastatic melanoma
76
Give an example of a targeted therapy.
Imatinib blocks chimeric Bcr-Abl tyrosine kinase in chronic myelogenous leukeamia
77
How many adult human body cells undergo apoptosis a day?
50-70 billion
78
During development, what does apoptosis play a major role in?
Morphogenesis and tissue remodelling (elimination of organs and tissues useful only during the embryonic stage)
79
What pathologies has excessive apoptosis been associated with?
Neurodegenerative diseases and organ failure after infarction or toxic insult
80
What induces apoptosis?
DNA damage, hypoxia, oxidative stress, death receptor ligands and drug treatments
81
What induces necrosis?
Accidents/trauma Infections Physical damage Chemical damage
82
What happens to the contents of cells that have died by apoptosis?
Apoptotic bodies are phagocytosed by macrophages and neighbouring cells
83
What are some hallmarks of apoptosis?
Cellular and nuclear shrinkage, apoptotic bodies, chromatin condensation, DNA fragmentation, mitochondrial membrane permeabilization, release of cytochrome c into cytoplasm, caspases cascade
84
What change occurs in the plasma membrane before apoptosis occurs>
Externalization of phosphatidylserine (phospholipid flipping)
85
What ion is involved in triggering and regulating apoptosis?
Calcium
86
How is the mitochondrial membrane potential lost?
Cytochrome c is released from the mitchondria into the cytosol
87
What does caspases mediate during apoptosis?
Intracellular protelytic cascade
88
What does active initator capase activate?
Executioner caspases
89
What do executioner caspases do?
Cleave cytosolic protein | Cleave nuclear lamin
90
What are the two pathways that activate apoptosis?
Cell-surface death receptors activate extrinsic pathway | Mitochondria activates intrinsic pathway
91
Briefly describe the death receptor pathway.
Fas ligand on killer lymphocyte binds to Fas death receptor. Death inducing signalling complex activates caspases.
92
What molecule is assembled during the intrinsic pathway that becomes caspase 9?
Apotosome
93
What protiens control apoptosis?
Bcl-2 family (anti and pro apoptotic)
94
How does Bcl2 anti-apoptotic mechanism work?
Reduces permability of mitochondria, stops release of cytochrome c
95
Name 2 Bcl2 pro-apoptotic protiens.
Bax and Bak, both trigger cytochrome c release
96
What does IAP stand for and what is it?
Inhibitor of apoptosis protein | Family of endogenous inhibitor of caspases

The human cell (10 decks)

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