Brainscape's Knowledge GenomeTM

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


See full index

biology > COD Cancer > Flashcards

COD Cancer Flashcards

You may prefer our related Brainscape-certified flashcards:
AP® Biology flashcards Biology 101 flashcards
1
Q

Name some changes in cellular properties that promote cancer

A 
Resisting cell death
Evading growth suppressors
Sustaining proliferative signaling
Inducing angiogenesis
Enabling replicative immortality
Activating invasion and metastasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Normal cells require external stimulation from growth factors to promote entry into the cell cycle
How is this different from cancer cells?

A

They may have enhanced external stimulation eg mutations in gfr
They may have lost this dependency due to activating mutations in signal transduction components or mutations in cell cycle components

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

In order to maintain homeostasis, normal cells respond to inhibitory signals which regulate growth, differentiation and apoptosis
How have cancer cells lost this ability?

A

Loss of activity of tumour suppressor genes such as p53, PTEN & Retinoblastoma (Rb)
Aberration in developmental signalling pathways e.g. Hedgehog, Wnt and Transforming growth factor-b (TGF-b)

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

In order to maintain fidelity, normal cells with DNA damage are removed via apoptosis
How do cancer cells avoid apoptotic signals?

A

Via
Mutations that affect the intrinsic pathway of apoptosis i.e. Loss of p53 activity, upregulation of anti-apoptotic members of the BCL-2 family; down regulation of pro-apoptotic BCl-2 family members

Mutations that affect the extrinsic pathway e.g. aberrations in death receptor regulation

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

In normal cells & tissue, angiogenesis only occurs under very specific physiological conditions such as?

A

e.g. active periods of growth, female reproductive organs and wound healing.

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

What is the diffusion limit of oxygen through solid tissue?

A

200 micrometres

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

What is necrosis caused by?

A

hypoxia or lack of oxygen

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

True or false

Tumours require vascularisation to grow into a large mass and to prevent of necrotic cell death

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Angiogenesis is regulated by a balance between the levels of angiogenic inducers and what?

A

angiogenic inhibitors

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

Many proangiogenic molecules are growth factors – key player is what?

A

vascular endothelial growth factor (VEGF)

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

What is VEGF expression regulated by?

A

hypoxia and over-activation of other growth factor signalling pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Normal cells shorten the ends of their chromosomes (telomeres) during every round of DNA replication which defines a finite number of cell doublings
Describe telomeres

A

Composed of repetitive DNA sequences (TTAGGG) and associated proteins
Protect ends of chromosomes and control chromosomal length
Shorten by 100-200 bp each DNA replication round due to limits of DNA polymerase needing an RNA primer

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

What is telomerase?

A

A form of reverse transcriptase that also contains the RNA template for the telomere repeat DNA (a)

Maintains telomere length

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

How do cancer cells and stem cells maintain telomere length and immortality

A

Produce telomerase

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

Cancer cells have gained the ability to invade and spread (metastasise) to distant sites by what?

A

Breaking cell- cell and cell –ECM attachment
Becoming more motile
Inducing angiogenesis to support ‘secondary’ tumour growth

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

Metastatic cells show preferential spread to particular sites - what is this known as?

A

organotropism

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

Where is the site of spread usually?

A

Close proximity to primary tumour
Direction of blood flow
Tumour cells get trapped in capillary bed

Distal/ non-obvious
Seed and soil hypotheses (Paget)
(cells need to match with optimum environment)

Premetastatic niche (Lynden)
(distant site  is prepared via circulating tumour derived fact
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

True or false

Less than 1:10,000 circulating tumour cells will survive to set up a secondary metastatic tumour

A

True

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

what helps mediate breakdown of cell:cell contacts and cell:ECM contact?

A

Src

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

EMT- Key regulators are transcription factors what?

A

SNAIL and TWIST

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

What are some Emerging Hallmarks and Enabling Characteristics of tumours?

A

Hallmarks: Avoiding immune destruction
Deregulating cellular energetics

Enabling characteristics: Tumor promoting inflammation
Genome instability and mutation

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

What is the rationale for cancer cells to utilise aerobic glycolysis?

A

Cancer cells are frequently hypoxic
Lack oxygen for oxidative phosphorylation
Process of glycolysis also generates intermediates for biosynthetic pathways such as growth

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

The immune system can recognise and eliminate cancer cells i.e. immune surveillance
T cells are key immune cells in cell killing
Name some T cells

A

cytotoxic T cells

Includes CD4, CD8, Natural Killer cells

24
Q

Cytotoxic T cells can kill target cells by triggering apoptosis
How?

A

Injecting granzymes into the target cell – directly cleave and activate effector caspases
Initiating the extrinsic route of apoptosis by activating death receptors

25
Q

How do cancer cells evade the immune system?

A

Loss of tumour antigens
Downregulation of antigen-presenting molecules (APCs)
Over-expression of immune checkpoint proteins and anti-apoptotic proteins

26
Q

What is an embryonic stem cell?

A

from inner mass of early embryo that can differentiate into different cell types during development

27
Q

What is an adult stem cell?

A

in regenerative tissue, replaces cells that mature and die

28
Q

What are CSCs?

A

Cancer stem cells

29
Q

Describe CSCs

A

Are are subpopulations within a tumour that are thought to initiate and maintain the cancer
May be responsible for:
Heterogeneity of tumours
Tumour plasticity
Migratory abilities
Can be identified (and isolated) through various and/or tissue specific stem cell markers e.g. CD44 (breast and pancreas), CD133 (colon, prostate, brain)
More likely to survive anti-cancer treatments
May arise from deregulation of self-renewal pathways e.g. Wnt and Hedgehog

30
Q

What is a driver and passenger mutation?

A

Driver mutation: confers growth/survival advantage

Passenger mutation: does not confer any advantage!

31
Q

What are some Carcinogenic agents and cancer risk?

A 
Radiation
Chemicals
Infectious pathogen
Endogenous reactions
Mutations arise due to both DNA damage caused by carcinogens and additionally, errors/malfunctions in DNA repair mechanisms
32
Q

Describe direct and indirect DNA damage

A

Direct DNA damage
Ionisation of atoms comprising DNA

Indirect DNA damage
Radiolysis of H2O and ROS generation
Hydroxyl radical 
H2O2
Superoxide radical
33
Q

Describe UV radiation

eg wavelengths

A

UVA - (wavelength 320-380 nm)
UVB - (wavelength 290-320 nm) * most effective carcinogen
UVC - (wavelength 200- 290 nm)

34
Q

Describe UVB

A

Most effective carcinogen
Mutations induced cause bends in the DNA which are misread by DNA polymerase
Causes 80% of skin cancers - squamous and basal cell carcinomas (some melanoma)
p53 tumour suppressor commonly affected

Risk factors – over exposure to the sun i.e. sunburn, sunbeds

35
Q

What is the general mechanism of action for a chemical carcinogen?

A

An electrophilic (or electron deficient) form reacts with the nucleophilic sites (sites that can donate electrons) in the purine and pyrimidine rings of nucleic acids.
Direct acting carcinogens (uncommon)
Indirect acting carcinogens (common)

36
Q

Describe Direct acting carcinogens (uncommon)

A

Reactive electrophiles
Interact with nitrogen and oxygen atoms in DNA
Examples include dimethyl sulphate and nitrogen mustards

37
Q

Describe Indirect acting carcinogens (common):

A

Unreactive and water soluble
Electrophilic centre produced by enzyme modification e.g. via processing by cytochrome p450 enzymes
Interact with bases in DNA forming adducts
Examples include polycyclic aromatic hydrocarbons (PAHs) (cigarette smoke) & aromatic or heterocyclic amines (cooked meats)

Risk: smoking, diet high in cooked or processed meat, preservatives in processed food

38
Q

What is an oncogenic virus?

A

A virus that can cause cancer
DNA tumour viruses
RNA tumour viruses (retroviruses)

39
Q

Describe DNA tumour viruses

A

Encode viral proteins that block tumour suppressor action
Example: Human papillomavirus (HPV) degrades RB tumour suppressor leading to constitutive activation of the cell cycle

oncogenic virus

40
Q

RNA tumour viruses (retroviruses)

A

Encode mutated forms of normal genes
Example: Human T-cell lymphotropic virus (HTLV-1) (only virus known to be linked with human leukaemia)

oncogenic virus

41
Q

Describe bacteria as an infectious agent

A

Cause chronic inflammation that helps promote cancer e.g. Helicobacter pylori infection can initiate gastric cancer
Bacterial proteins affect cell signalling proteins that regulate cell proliferation, survival and invasion

42
Q

What are Proto-oncogenes?

A

They promote cell proliferation or cell survival
Examples: components of signalling pathways driving cell proliferation ; anti-apoptotic proteins

Effect of mutation – GAIN of function
Dominant mutation
Converts proto-oncogenes into oncogenes

43
Q

What are tumour suppressors?

A

Inhibit cell survival and/or negatively regulate cell proliferation
Examples: apoptosis promoting proteins; CDK inhibitors; cell cycle checkpoint regulators
Effect of mutation – LOSS of function
Recessive mutation

44
Q

What are some genetic events that can cause loss of function in tumour suppressor genes?

A

Loss of entire chromosome
Region containing normal gene is deleted
Mutation in coding sequence which results in non-functional protein
Chromosomal rearrangements – gene is disrupted
Gene activity silenced by epigenetic changes
Mutations in genes coding for chromatin-remodelling complexes e.g. SWI/SNF

45
Q

Describe what could happen if you inherit mutations in tumour suppressor genes

A 
Predisposition to develop cancer
Hereditary retinoblastoma (loss of RB TS gene results in childhood retinal tumours and other tumours later in life)
Familial adenomatous polyposis (FAP) (loss of APC gene – formation of colon polyps which if untreated could develop into malignant colon cancer
46
Q

What are caretaker genes?

A

Repair or prevent DNA damage
Examples: DNA repair enzymes

Effect of mutation – LOSS of function
Recessive mutation

Arise by deletion, point mutation or methylation
Repair mechanisms affected
DNA mismatch repair
Nucleotide excision repair
Double stranded DNA breaks

Can get inherited defects

47
Q

Passage through the cell cycle is regulated by cyclins and cyclin-dependent kinases (CDKs)
Describe cyclins and CDKs

A

The concentration of different cyclins varies in different stages of the cell cycle
Cyclin is the regulatory subunit of the CDK

Pairing of cyclins and CDKs is specific
Examples: Cyclin D /CDK 4/6

CDKs are serine threonine kinases

48
Q

Cyclins are divided into four classes defined by their activity in the cell cycle
What are these 4 classes?

A

G1 cyclins
G1/S cyclins
S phase cyclins
M phase cyclins

49
Q

What is CDK activity influenced by?

A

Cyclin binding
Phosphorylation & dephosphorylation
Binding to CDK inhibitors e.g. p15, p16, p21 and p27

50
Q

What is p53?

A 
Guardian of the genome
Transcription factor
Multi-functional TS that can promote:
Arrest in G1 and G2 phase
Via production of p21 and p27 cdk inhibitors
Apoptosis
DNA repair with respect to DNA damage
51
Q

True or false
Mutations in p53 promote the formation of the malignant phenotype and they are the most common mutations found in tumours

Nearly all p53 mutations are located in its DNA binding domain

A

True

52
Q

What are the two Mechanisms leading to abnormalities in EGFR signalling?

A
  1. Increased ligand production
    EGFR ligands particularly EGF are frequently over-expressed in cancer
    Occurs via autocrine stimulation
  2. Increased EGFR receptor levels
    Can occur due to:
    Gene amplification
    Defective gene promoter activity (binding of p53 proteins)
    Defective receptor downregulation (inability to bind c-Cbl)
53
Q

*****What is a mechanism leading to abnormalities in erbB signalling?

A

*****Mutations giving rise to constitutively active variant receptors

A variety of mutations are known to exist and can be found in all areas of the receptor i.e. both extracellular and intracellular

Example: EGFR variant III

Loss of most of the extracellular binding domain

Constitutively active (in absence of ligand)

Prominent in the very aggressive brain tumour glioblastoma

Strongly and persistently activates the PI3 kinase/Akt signalling pathway

Increased cell survival, proliferation and motility

Resistance to treatment

54
Q

Apoptosis can be triggered by two routes

What are these?

A

Intrinsic / mitochondrial route or extrinsic (death receptor mediated) route

Intrinsic route most commonly disrupted in cancer

55
Q

Whether the intrinsic pathway is activated depends upon the release of what?

A

cytochrome c from the mitochondria

Regulated by a balance between molecules that promote apoptosis and those which inhibit apoptosis

56
Q

Give examples of pro apoptotic and anti apoptotic molecules

A

pro - BAK, BAK, BAD

anti - BCL-2, BCL-XL = L is small

biology (41 decks)

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