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3921 > 3 Cancer biology and drug targets > Flashcards

3 Cancer biology and drug targets Flashcards

1
Q

How are mutations acquired

A

Exposure to viruses or carcinogens

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2
Q

What do proto-oncogenes control

A

Normal cell division
Apoptosis
Differentiation

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3
Q

What are protooncogenes converted to

A

Oncogenes e.g. Ras and Myc, that induce malignant changes

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4
Q

What do normal cells also contain that can mutate to cause cancer

A

Tumour supressor genes like p53

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5
Q

What do undifferentiated stem cells produce in normal tissue

A

Daughter cells

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6
Q

What do daughter cells become in normal tissue

A

Mature differentiated cells that perform specialised functions

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7
Q

What cancers usually multiply faster

A

Poorly differentiated cancers

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8
Q

What activates proliferation in normal cells

A

External mitogens

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9
Q

What are transmembrane receptors activated by

A

Growth factors, extracellular matrix components or cell adhesion molecules that are external to the cell (paracrine)

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10
Q

Why are tumour cells independent from the external microenvironment

A

They generate their own growth signals (autocrine)

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11
Q

What do telomeres do in normal chromosomes

A

Protects against degradation

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12
Q

What occurs to telomeres during normal cell division

A

Portion of telomere is eroded with loss of function so that cell becomes senescent

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13
Q

What do cancer cells produce to overcome cell mortality

A

Telomerase

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14
Q

What does the cell cycle control?

A

The passage of the cell through phases of DNA replication and mitosis

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15
Q

When are cells quiescent

A

G0

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16
Q

When do cells divide

A

M phase

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17
Q

What comprises interphase

A

G1/S/G2

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18
Q

What does S phase involve

A

DNA replication

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19
Q

What do cyclin proteins activate

A

Cyclin dependent kinases that drive proliferation

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20
Q

What proteins are antigrowth

A

CDK inhibitors and p53

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21
Q

What are proteins are often defective in cancer

A

CDKs, CDK inhibitors and p53

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22
Q

What is apoptosis

A

Normal cell mechanism in which damaged cells are deleted in a regular fashion

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23
Q

What is apoptosis triggered by

A

Intracellular stresses or death receptor

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24
Q

What occurs during apoptosis (4)

A

Cellular membranes are disrupted
Cell structures are degraded The nucleus is fragmented
Residual material is engulfed

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25
How does apoptosis occur
Signals that elicit apoptosis converge on the mitochondrion
26
What proteins have proapoptotic or antiapoptotic functions
Multiple bcl-2
27
What is released from the mitochondrion to activate executioner protases
Cytochome C
28
How can resistance to apoptosis be acquired
Inactivation of proapoptotic factors | Activation of antiapoptotic factors
29
What is a common mutation to acquire resistance to apoptosis
p53 tumour supressor gene
30
How is the prosurvival PI3-kinase pathway activated
Growth factor receptors (EGFR)
31
What does PI3-kinase inhibit
Pro-apoptotic bcl-2 proteins
32
What must cancers develop to grow in size
Angiogenesis
33
What are angiogenesis - initiating signals
Vascular endothelial and fibroblast growth factors (VEGF and FGF) that activate receptors on endothelial cells
34
What are angiogenesis inhibitors
Thrombospondin-1 and angiostatin
35
Characteristics of blood vessels produced within tumours:
Typically aberrant: excessive sprouting and branching, distorted vessels, erratic blood flow and leaky
36
How do tumour cells invade without dying upon escape
Release of cells and secretion of enzymes that break down the extracellular matrix
37
What is the process of metastasis
Local invasion Intravasation into nearby blood and lymphatic vessels Escape into distant tissues by extravasation and the formation of micrometastases
38
How do inflammation provided growth factors and cytokines help cancers
They limit cell death, proangiogenetic factosr and MMP that facilitate metastasis
39
What do inflammatory cells also provide
ROS that damage DNA
40
How does glucose get turned into ATP in a two-step reaction in a normal cell
1) Glycolysis in the cytoplasm | 2) Oxidative phosphorylation occurs in the mitochondrion
41
Is glygolysis or oxidative phosphorylation less efficient
Glycolysis
42
When will glycolysis predominate in a normal cell
Low oxygen
43
How do aggressive cancer cells generate ATP
Aerobic glycolysis
44
What occurs in cancer cells that use glycolysis as ATP generation
Upregulation of glucose influx transporters as glycolysis is inefficient
45
What does increased glycolysis allow for
Diversion of intermediates into biosynthetic pathways to produce the macromolecules required for cell replication
46
How do cancer cells evade detection by the immune system
By failing to express antigens that are recognised by T-cells By secreting immunosuppressive cytokinds like IL-10
47
Why do tumour cells contain heterogenous cell populations
Susceptible cells are killed but resistant cells survive and repopulate the tumour
48
How do cytotoxic drugs work
Kill cells non-specifically by binding to DNA and preventing replication
49
What are some cytotoxic drug
Alkylating agents Antimetabolites Cytotoxic antibiotics and plant-derived agents
50
How do targeted agents work
Selective inhibition of a pathway utilised by the cancer cell
51
What are some targeted agents
Hormones and hormone antagonists Kinase inhibitors Monoclonal antibodies
52
How does melphalan work
Generates cross-links with adjacent DNA strands which prevents replication
53
What displaces the chloro-substituents in mustard/alkylating agents
Nitrogens from DNA bases
54
What is the most commonly used alkylating agent
Cyclophosphamide
55
What is cyclophosphamide used for
Treatment of lymphomas, brain cancer and solid tumours
56
What does busulphan do and its application
Alkylating agent that attacks DNA, produces selective bone marrow suppression to prepare recipients for bone marrow transplants
57
What is cisplatin
Platinum compound
58
What is cisplatin used for (3)
Ovarian, testicular, oesophageal
59
How does cisplatin work
Interacts with nitrogens in DNA bases to produce cross-linked strands
60
What is required for purine and DNA production
Folic acid
61
What is a folic acid antagonist
Methotrexate
62
Methotrexate MOA
Replaces folic acid in the active site of dihydrofolate reductase and prevents DNA synthesis
63
What are some other anticancer antimetabolite rugs
5-flurouracil Cytarabine Gemcitabine
64
What are some anthracycline antibiotics
Doxorubicin Epirubicin Mitosantrone
65
How does doxorubicin work
Intercalates DNA and prevents repair of tangled DNA in rapidly dividing cells
66
What is a significant side-effect of anthracycline antibioitics
Dose-related cardiotoxicity
67
What must be monitored when patients are prescribed anthracycline antibiotics
Lifetime intake
68
What are some natural cytotoxic drugs (4)
Vinca alkaloids Taxanes Etoposide Camptothecins
69
Where are vinca alkaloids from and examples (3)
Periwinkle Vincristine Vinblastine Vinorelbine
70
Where are taxanes from and examples (2)
Pacific yew bark | Paclitaxel and docetaxel
71
Where is etoposide
Mandrake root
72
What is etoposide MOA
Inhibits DNA untangling during proliferation
73
What is a camptothecin
Irinotecan
74
What controls signal transduction
Post-translational modification (usually phosphorylation)
75
How are signal transductions terminated
Phosphatase
76
What are some kinase inhibitors (3)
Gefitinib Imatinib Sorafenib
77
What does gefitinib target?
EGFR
78
What is gefitinib used for
Non-small cell lung cancer advanced locally into adjacent tissue
79
What does imatinib target
bcr-acl and c-kit kinases
80
What is imatinib used for
Chronic myelogenous leukaemia and GI stromal tumours
81
What is sorafenib used for
advanced renal cell carcinoma and liver cancer
82
What is sorafenib
Multi-kinase inhibitor
83
What do monoclonal antibodies target
Plasma receptors that promote tumour growht
84
How do monoclonal antibodies work
Prevent ligand activation and growth factor receptors
85
What does trastuzumab/herceptin target
HER2 receptor
86
What is a major side effect of trastuzumab
Cardiotoxicity
87
What are some methods of resistance to anticancer drugs (2)
Over-expression of efflux transporters Enzyme degradation Defective apoptotic pathway Increased DNA repair pathways
88
What is a problem with combination therapies
Difficult to detect efficacy and devise drug regimen

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