Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What do proto-oncogenes control

A

Normal cell division
Apoptosis
Differentiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are protooncogenes converted to

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

Tumour supressor genes like p53

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What do undifferentiated stem cells produce in normal tissue

A

Daughter cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What do daughter cells become in normal tissue

A

Mature differentiated cells that perform specialised functions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What cancers usually multiply faster

A

Poorly differentiated cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What activates proliferation in normal cells

A

External mitogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why are tumour cells independent from the external microenvironment

A

They generate their own growth signals (autocrine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What do telomeres do in normal chromosomes

A

Protects against degradation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What do cancer cells produce to overcome cell mortality

A

Telomerase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does the cell cycle control?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When are cells quiescent

A

G0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When do cells divide

A

M phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What comprises interphase

A

G1/S/G2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does S phase involve

A

DNA replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What do cyclin proteins activate

A

Cyclin dependent kinases that drive proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What proteins are antigrowth

A

CDK inhibitors and p53

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are proteins are often defective in cancer

A

CDKs, CDK inhibitors and p53

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is apoptosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is apoptosis triggered by

A

Intracellular stresses or death receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What occurs during apoptosis (4)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How does apoptosis occur

A

Signals that elicit apoptosis converge on the mitochondrion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What proteins have proapoptotic or antiapoptotic functions

A

Multiple bcl-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is released from the mitochondrion to activate executioner protases

A

Cytochome C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How can resistance to apoptosis be acquired

A

Inactivation of proapoptotic factors

Activation of antiapoptotic factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is a common mutation to acquire resistance to apoptosis

A

p53 tumour supressor gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How is the prosurvival PI3-kinase pathway activated

A

Growth factor receptors (EGFR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What does PI3-kinase inhibit

A

Pro-apoptotic bcl-2 proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What must cancers develop to grow in size

A

Angiogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are angiogenesis - initiating signals

A

Vascular endothelial and fibroblast growth factors (VEGF and FGF) that activate receptors on endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are angiogenesis inhibitors

A

Thrombospondin-1 and angiostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Characteristics of blood vessels produced within tumours:

A

Typically aberrant: excessive sprouting and branching, distorted vessels, erratic blood flow and leaky

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How do tumour cells invade without dying upon escape

A

Release of cells and secretion of enzymes that break down the extracellular matrix

37
Q

What is the process of metastasis

A

Local invasion
Intravasation into nearby blood and lymphatic vessels
Escape into distant tissues by extravasation and the formation of micrometastases

38
Q

How do inflammation provided growth factors and cytokines help cancers

A

They limit cell death, proangiogenetic factosr and MMP that facilitate metastasis

39
Q

What do inflammatory cells also provide

A

ROS that damage DNA

40
Q

How does glucose get turned into ATP in a two-step reaction in a normal cell

A

1) Glycolysis in the cytoplasm

2) Oxidative phosphorylation occurs in the mitochondrion

41
Q

Is glygolysis or oxidative phosphorylation less efficient

A

Glycolysis

42
Q

When will glycolysis predominate in a normal cell

A

Low oxygen

43
Q

How do aggressive cancer cells generate ATP

A

Aerobic glycolysis

44
Q

What occurs in cancer cells that use glycolysis as ATP generation

A

Upregulation of glucose influx transporters as glycolysis is inefficient

45
Q

What does increased glycolysis allow for

A

Diversion of intermediates into biosynthetic pathways to produce the macromolecules required for cell replication

46
Q

How do cancer cells evade detection by the immune system

A

By failing to express antigens that are recognised by T-cells
By secreting immunosuppressive cytokinds like IL-10

47
Q

Why do tumour cells contain heterogenous cell populations

A

Susceptible cells are killed but resistant cells survive and repopulate the tumour

48
Q

How do cytotoxic drugs work

A

Kill cells non-specifically by binding to DNA and preventing replication

49
Q

What are some cytotoxic drug

A

Alkylating agents
Antimetabolites
Cytotoxic antibiotics and plant-derived agents

50
Q

How do targeted agents work

A

Selective inhibition of a pathway utilised by the cancer cell

51
Q

What are some targeted agents

A

Hormones and hormone antagonists
Kinase inhibitors
Monoclonal antibodies

52
Q

How does melphalan work

A

Generates cross-links with adjacent DNA strands which prevents replication

53
Q

What displaces the chloro-substituents in mustard/alkylating agents

A

Nitrogens from DNA bases

54
Q

What is the most commonly used alkylating agent

A

Cyclophosphamide

55
Q

What is cyclophosphamide used for

A

Treatment of lymphomas, brain cancer and solid tumours

56
Q

What does busulphan do and its application

A

Alkylating agent that attacks DNA, produces selective bone marrow suppression to prepare recipients for bone marrow transplants

57
Q

What is cisplatin

A

Platinum compound

58
Q

What is cisplatin used for (3)

A

Ovarian, testicular, oesophageal

59
Q

How does cisplatin work

A

Interacts with nitrogens in DNA bases to produce cross-linked strands

60
Q

What is required for purine and DNA production

A

Folic acid

61
Q

What is a folic acid antagonist

A

Methotrexate

62
Q

Methotrexate MOA

A

Replaces folic acid in the active site of dihydrofolate reductase and prevents DNA synthesis

63
Q

What are some other anticancer antimetabolite rugs

A

5-flurouracil
Cytarabine
Gemcitabine

64
Q

What are some anthracycline antibiotics

A

Doxorubicin
Epirubicin
Mitosantrone

65
Q

How does doxorubicin work

A

Intercalates DNA and prevents repair of tangled DNA in rapidly dividing cells

66
Q

What is a significant side-effect of anthracycline antibioitics

A

Dose-related cardiotoxicity

67
Q

What must be monitored when patients are prescribed anthracycline antibiotics

A

Lifetime intake

68
Q

What are some natural cytotoxic drugs (4)

A

Vinca alkaloids
Taxanes
Etoposide
Camptothecins

69
Q

Where are vinca alkaloids from and examples (3)

A

Periwinkle
Vincristine
Vinblastine
Vinorelbine

70
Q

Where are taxanes from and examples (2)

A

Pacific yew bark

Paclitaxel and docetaxel

71
Q

Where is etoposide

A

Mandrake root

72
Q

What is etoposide MOA

A

Inhibits DNA untangling during proliferation

73
Q

What is a camptothecin

A

Irinotecan

74
Q

What controls signal transduction

A

Post-translational modification (usually phosphorylation)

75
Q

How are signal transductions terminated

A

Phosphatase

76
Q

What are some kinase inhibitors (3)

A

Gefitinib
Imatinib
Sorafenib

77
Q

What does gefitinib target?

A

EGFR

78
Q

What is gefitinib used for

A

Non-small cell lung cancer advanced locally into adjacent tissue

79
Q

What does imatinib target

A

bcr-acl and c-kit kinases

80
Q

What is imatinib used for

A

Chronic myelogenous leukaemia and GI stromal tumours

81
Q

What is sorafenib used for

A

advanced renal cell carcinoma and liver cancer

82
Q

What is sorafenib

A

Multi-kinase inhibitor

83
Q

What do monoclonal antibodies target

A

Plasma receptors that promote tumour growht

84
Q

How do monoclonal antibodies work

A

Prevent ligand activation and growth factor receptors

85
Q

What does trastuzumab/herceptin target

A

HER2 receptor

86
Q

What is a major side effect of trastuzumab

A

Cardiotoxicity

87
Q

What are some methods of resistance to anticancer drugs (2)

A

Over-expression of efflux transporters
Enzyme degradation
Defective apoptotic pathway
Increased DNA repair pathways

88
Q

What is a problem with combination therapies

A

Difficult to detect efficacy and devise drug regimen

3921 (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions