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PHAY00011 > Understanding Cancer > Flashcards

Understanding Cancer Flashcards

1
Q

Risk of getting cancer at some point in life.

A

Men: 1 in 2

Women: 1 in 3

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2
Q

Most common cancers for men

A

Prostate cancers

Lung cancers

Bowel cancers

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3
Q

Most common cancers for women

A

Breast cancers

Lung cancers

Bowel cancers

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4
Q

What are the risk factors of cancer development?

A

Gender -> type of cancers too

Age

Gentic predisposition

Dietary status

Geography and climate

Smoking status (associated with lung cancer)

HPV infection (associated with cervical cancer)

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5
Q

What are the genes associated with breast cancer?

A

Mutation of BRCA1 and BRCA2 DNA repair genes

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6
Q

Why is the use of Selective Oestrogen Receptor Modulators like tamoxifen and raloxifen not always effective?

A

Type of cancer developed from mutations of BRAC1 and BRAC2 genes are not the type controlled by oestrogen receptor modulators

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7
Q

Why is cure rate NOT used to determine prognosis, only survival rate?

A

Cancer might relapse and appear that it has been treated -> not trivial to use

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8
Q

What cancer types have a better survival rates?

A

More accessible and noticeable ones like testicle cancer, breast cancer or skin cancer

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9
Q

Why brain, lung and pancreas cancers have low survival rate?

A

Hard to access

Can only be noticed until the last stages

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10
Q

What is the link between diagnosis and prognosis of cancer?

A

Early diagnosis increases the chance of positive prognosis

Still localised, yet to invade

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11
Q

Briefly describe the natural progresison of cancer tumour.

A

Genetic mutations -> cells grow in less controlled fashion

Additional mutations -> accummulate more defects -> benign cancer become malignant

Gain ability to invade neighbouring tissues -> reach blood and lymphatic vessels -> invade other organ -> grow tumour there

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12
Q

Progression and different stages of breast cancer

A

Stage 0: Carcinoma in situ - abnormal cells develop in specific tissues, non invasive

Stage 1: Tumour formed, cells invasive -> involved lymph node

Stage 2: Tumour grows, more cancer cells on other parts of lymphatic system

Stage 3: Tumour cont to grow + cancer cells invade neighbouring tissues

Stage 4: Matastasis

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13
Q

Why is early stage cancer easier to treat?

A

Surgery to remove the tumour can be done

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14
Q

What factors affect the clinical outcomes of the cancer treatment?

A

Tumour types

Tumour population

Molecular make-up of tumour cells

Metastasis status

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15
Q

What can be used to treat cancers?

A

Surgery

Radiotherapy - for locally advanced disease

Chemotherapy - attempt to manage metastasis and systemic forms of cancer

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16
Q

Definition of proliferation.

A

Continued cell division

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17
Q

Typical life of a cell include:

A

Cell growth

Cell division - can occur multiple time

Cell differentiation

Apoptosis - occur when there is problems that cannot be repaired.

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18
Q

What does it mean by ‘cell division is sequential’?

A

There are distinct phases in the process

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19
Q

What are the different phases in the cell division process?

A

Division (M phase - mitosis)

Synthesis (S phase)

Gap 1 (G1) and Gap 2 (G2 phase)

G0 phase (quinescene) - after mitosis

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20
Q

What happens after the cells enter G0 phase?

A

If have phenotype commitment -> differentiate and eventually senescent

If not, go back to G0 and enter cell cycle again

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21
Q

Purpose of G1 phase in cell division

A

Duplication of cellular content, except chromosomes

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22
Q

Purpose of S phase

A

Duplication of chromosomes

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23
Q

Purpose of G2 phase

A

Check for errors in duplicated cellular content

Make repairs

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24
Q

Are cells always cycling in cell cycle?

A

No, they can enter G0 stage

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25
Q

What is R point in cell division?

A

Restriction check point - where cell made decision to undergo division or not

Check the presence of mitogen growth factors

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26
Q

What does the cellular decision to undergo cell division depend on?

A

Sufficient concentration of growth factors.

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27
Q

Where is the R point in the cell cycle?

A

In between G1 phase

NOT before G1 or right after M phase

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28
Q

What does the entry at restriction point depends upon?

A

Presence of nutrients + growth signals

Absence of inhibitor signals + damage or problems

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29
Q

What are the main characteristics of the cell cycle?

A

Subsequent phase depends on previous phase

Checkpoints ensure completion of each phase

Not exit if commit to cycling

Apoptosis if repair attempt failed to correct issues affecting cycling

Not go back to previous phase

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30
Q

What are the 3 key elements control the cell cycle regulation?

A

Cyclins = Cyclin dependent kinase (CDKinase) and CDKI (CDKinase inhibitors)

Increase in cyclin level

Increase in CDKI activity

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31
Q

When in the cell cycle does the cyclin level increase?

A

At the start of each phase

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32
Q

Roles of cyclins and CDKI in cell cycle.

A

Cyclin = activate CDKs and allow phosphorylation -> trigger downstream of transcription programme -> initiate next phase

CDKI = inactivate CDK -> inhibit + stop cell cycle

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33
Q

What do CDKs need for activation?

A

Protein like CLN to form complex -> active form

Growth factors

Nutrients

Cyclins

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34
Q

What are the cyclins involved in the regulation of cell cycle?

A

A, B, D and E

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35
Q

What does oscillation of cyclins mean?

A

Concentration of different cyclins increase and decrease regularly through out different stage of the cell cycle

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36
Q

Describe the oscillation pattern of cyclins during cell cycle.

A

Cyclin A = peaks during G2 phase

Cyclin B = peaks and drop during M phase

Cyclin D = present through out the cycle

Cyclin E = present at the start of S phase

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37
Q

What CDKs do each cyclin controlling the cell cycle exert?

A

Cyclin A -> CDK 2

Cyclin B -> CDK 1

Cyclin D -> CDK 4

Cyclin E -> CDK 2

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38
Q

Taking regulation of G1 and G1/S transition as a example, what is the feedback loops mechanism of cyclin regulation.

A

RB (retinoblastoma) protein get phosphyrated to activate the production of Cyclin E

Cyclin E forms complex with CDK2 -> inactivate RB by further phosphorylated RB.

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39
Q

What are the potential drug targets specific to cell cycle specific?

A

Topoisomerase inhibitor - target DNA unwinding

Anti-metabolites - target build-up of DNA blocks

Spindle toxins

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40
Q

What is the potential drug target for non-cell cycle specific?

A

Interfere with regulation of cell cycle in general.

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41
Q

Which phases of cell cycle can cell death be triggered?

A

Any in G1, G2, S and M phase

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42
Q

What is mitogen signal and why is it a potential drug target?

A

Mitogen signals trigger growth and proliferation of cells

Interefer mitogen signal -> switching off the proliferation before R point

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43
Q

What are the mitogen signals from?

A

Different pathways with complex interactions between each pathways

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44
Q

What are growth factors? How are they related to cell cycle entry?

A

GFs are signalling molecules

Proteins and steroid hormones

Drive cellular functions: growth, proliferation and differentiation

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45
Q

What receptors do GFs bind to?

A

Human receptor tyrosine kinases (RTKs)

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46
Q

Structure of RKs.

A

Extracellular part = point outside -> allow GFs to bind + dimerise with other RTKs

Transmembrane part

Intracellular part = tyrosine kinases -> phosphorylate tyrosine -> activate molecules for downstreamign signalling -> trigger complex cascade -> epxression of target genes + change in cell response -> differentiation and proliferation

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47
Q

What are the outcomes of phosphorylated tyrosines upon GFs binding to RTKs?

A

activate molecules for downstreamign signalling -> trigger complex cascade
-> epxression of target genes + change in cell response -> differentiation and proliferation

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48
Q

Describe the relationships between HER2 receptors and breast, ovarian and stomach cancers.

A

Gene amplification and overexpression of HER2 receptors

High level of pro-growth signalling -> inappropriate cell proliferation

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49
Q

What are the differences between HER2 receptors and other HER/EGFR family members like HER1,3 and 4?

A

HER2 is orphan receptor -> not need ligand binding for dimerisation

Always open conformation

Heterodimerisation preferred

Homodimers are predictive of therapeutic response.

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50
Q

What are the 2 signalling pathways through HER2 receptors binding?

A

MAPK pathways = mitogen activated protein kinase pathways

PI3K/Akt pathways

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51
Q

Describe how the signals being relayed from the cytoplasmic side of membrane into cytoplasm.

A

Binding -> exposed SH2 binding sites -> docking of proteins

Docking -> adaptor proteins like GRB2 to recognise phosphorylated tyrosine residue -> binding to the residue

The adaptor protein also bind to protein SOS1 - a GNEF

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52
Q

What are the roles of Ras?

A

Proteins - switch for a number of signalling pathways including MAPK -> vital for proliferation

53
Q

What are the two factors involved in the Ras cycle?

A

GAP = GTPase activating protein -> accelerates inactivation of Ras-GTP into Ras-GDP

SOS1 -> release GDP from Ras-GDP to make binding site available for GTP to activate Ras

54
Q

Briefly describe the activation of MAPK pathways.

A

Ras activate MAP3K

MAP3K activate MAP2K

MAP2K activate MAPK

MAPK phosphorylate proteins on thretonin, tyrosin and serine residues -> activates transcription factors and specific gene expression

55
Q

In the case of HER2 receptors, briefly describe the activation of MAPK pathways

A

Ras activate Raf -> Raf is MAP3K

Raf activate Mek -> Mek is MAP2K

Mek activate Erk -> Erk is actual MAPK

Erk phosphorylate transcription facot like AP1 family member jun and fos -> bind to protein -> transcription of target gene for proliferation.

56
Q

What are the MAPK in HER2 receptors-induced MAPK pathways?

A

Raf is MAP3K

Mek is MAP2K

Erk is MAPK

57
Q

Briefly describe the PI3K/Akt pathways.

A

RTK phosphorylated -> PI3K bind to RTK

Binding of PI3K phosphorylate PIP2 to PIP3

PIP3 allows binding and co-localisation of PDK1 and Akt -> expose phosphyrylation site of Akt

Akt phosphyrated by PDK1 and PDK2 (also known as mTORC2) -> Akt-DP

Akt-DP involved in many cellular processes including proliferation

58
Q

What processes is Akt-DP involved in?

A

Proliferation

Survival

Angiogenesis

Growth and metabolism

59
Q

What substance control the PIK3/Akt process?

A

PTEN = inactivate PIP3 into PIP2

60
Q

Definition of oncogenes

A

Cancer-causing genes

61
Q

Definition of pro-oncogenes

A

Normal genes that oncogenes similar to

62
Q

Name some noticeable human oncogenes.

A

Ras = invovled in 20% of cancer, 95% of pancreatic cancer

Myc = involved in cervical, colon, lung and stomach cancers

Bcr-Abl = involved in chronic myeloid leukaemias (CML)

EGFR family = involved in breast and ovarian cancers

63
Q

How is Myc an oncogene?

A

c-myc, l-myc and n-myc code for TF -> downsteram expression regulation

Contituitive expression of Myc -> continued cell proliferation -> cancer

64
Q

What is Bcr-Abl? How is it an oncogene?

A

Philadelphia chromosomes - broken chromosomes 9 and 22 fuse together

Translocation -> Abl tyrosine kinase fused with Bcr region

Abl tyrosine kinase always active -> continue cell proliferation

65
Q

What drug is used for Bcr-Abl gene-associated CML?

A

Gleevec

66
Q

What is the two-hit hypothesis?

A

Case of cancers developed from the recessive allele.

Patient’s gene become disfunctional when both alleles have mutations

67
Q

Definition of tumour suppression genes.

A

Anti-proliferative function

68
Q

Functions of protein coded by tumour suppression genes

A

Regression of cell cycle driving genes

Negative feedback in signalling pathways

DNA damage signalling

DNA damage repair

69
Q

What are the examples of tumour suppression genes?

A

RB (retinoblastoma)

BRCA1 - associated with breast cancer

APC - associated with colorectal cancer

70
Q

Is tumour suppressor genes and oncogenes recessive or dominant?

A

TSG = recessive, except TP53

Oncogenes = tend to be dominant

71
Q

Name some examples of the mutations in the RTK pathways that can result in cancer.

A

Dysfunction of GAP -> continued activation of Ras-GTP

Mutation of Ras -> constituitively active

72
Q

What mediators determine the effects of growth factors in tissue?

A

Concentration of GFs

Time and locations

73
Q

What factors in tissue environment can add to the modulation of GFs?

A

Components in extracellular matrix

Extracellular emzymes

74
Q

How is the proliferative signalling described in cancer?

A

Autonomous, unregulated and out of context

75
Q

What are the two types of disturbances of proliferative signallings?

A

Receptor-ligand dependent interactions = disregulation caused by modifications around interactions

Receptor-ligand independent interactions = disregulation associated with downstream elements

76
Q

What are the examples of receptor-ligand dependent interactions to cause disturbance?

A

Increased level of GFs due to autocrine loop or paracrine release with bystander stimulation

Increase receptor proteins

Alteration of receptor structure -> ligand-independent firing or hypersensitive

77
Q

What are the examples of receptor-ligand independent interactions to cause disturbance?

A

Somatic mutations -> constituitive activation of proteins like B-Raf, PI3k

Inactivation of negative feedback loop -> loss function of GAP and PTEN

78
Q

Why is molecular targeted therapy not always effective?

A

Only interfere with a particular path of signalling pathway

Signalling pathways complex = multiple branching and interconnections

There are alternative pathways -> overcome effects of drugs -> continue to drive sustained proliferation

79
Q

Definition of mutations

A

Changes to genomic nucleic acid sequence of organism

80
Q

Why is mutation an essential factor?

A

Driver of evolution

Introduction of genetic variation is important in development of immune system

81
Q

What are the two types of mutations?

A

Spontaneous mutations = changes occurs randomly at baseline level = due to many potential mechanisms including errors

Induced mutations = changes induced by external factors = due to various factors like chemicals, UV, tobacco smoke

82
Q

What are the levels of effect on DNA sequence and structure from mutations?

A

Nucleotide levels = only specific nucleic acid residue affected

Gene level = affect the whole sequence of nucleotides

Chromosome level = multiple genes are affected

83
Q

What factor explained the heritable element of cancer?

A

Cancer mutation can affect on chromosome level

84
Q

What are the effects of mutations dependent on?

A

Where they occur: coding? non-coding? or regulatory region?

85
Q

Is mutation associated with 100% change in function? Why?

A

No

Degenerate code at nucleotide level

86
Q

What are the effects of the changes of nucleiotides?

A

Silent (no change)

Non-sense (early stop codon)

Mis-sense (changed amino acid)

87
Q

Definition of epigenetics

A

Behaviors and environment can cause changes that affect the way genes work.

Reversible

Not change your DNA sequence, change how body reads a DNA sequence -> controlling gene expression

88
Q

What are the two mechanisms that determine active gene expression programme?

A

Covalently tagging specific DNA sections = DNA methylation

Modify how DNA is stored on the nucleosomes = Histone code modifications

89
Q

What is DNA methylation?

A

Covalent modification of the DNA regions - CpG islands, associated with gene promoters region

90
Q

Effects of DNA methylation.

A

Reduce access of TF -> reduce gene expression

Changes chemical structure of DNA, not the sequence

91
Q

The reactions occured in DNA methylation.

A

Cytosine -> 5-methyl cytosine

Enzyme: DNA methyl transferase

92
Q

How does cancer arise from inappropriate DNA methylation?

A

Increased gene expression -> oncogenes -> incude cancer

Reduced gene expression -> inactivating tumour suppression genes -> induce cancer

93
Q

What are the roles of histone code modifications?

A

Modultate the storage and accessibility of DNA in the nucleus

Nucleosomes = 8 histone subunits -> wrap around DNA -> chromosomes

Histone = regulate and coordinate gene expression through accessibility of DNA regions.

94
Q

How do histones regulate gene expression?

A

Covalent modification of specific residues of histones = methylation, acetylation, phosphorylation by specific set of enzymes

Provide tags for host machinery to transcribe which part of the DNA

95
Q

What are the enzymes invovled in histone tags?

A

Histone methyl transferase

Histone acetyl transferase

Histone deacetylase

96
Q

When are epigenetic mutations continuously active?

A

Cell terminal differentiation like during embryogenesis

Allow distince cell populations developed from initial omnipotent stem cells

97
Q

Do cancer develop from one mutation?

A

No

Cancer is the result of multi-step carcinogenesis = many mutations in each stage of cancer

98
Q

Are all the mutations in cancer equally effective?

A

No, not all are relavant as drivers of cancer progression

99
Q

With respect to cancer development, what are the two types of genes?

A

Driver genes = potential role in cancer progression

Passenger genes = no role in cancer

100
Q

How many potential driver genes are there?

A

120 genes potentially

50 oncogenes and 70 tumour suppression genes

101
Q

For some common forms of cancer, what are the least possible driver mutations require for the development?

A

At least 3 driver mutations for 3 phases:

Breathrough phase = affect growth-related pathway -> slow but abnormal proliferation

Expansion phase = further thriving, hyperproliferation

Invasive phase = invasion initiated, transform to maligant and allow metastasis

102
Q

What does it mean by somatic evolution?

A

Somatic cells constantly exposed to selective pressure -> DNA mutations, chrosomal changes and epigenetic modification

Cells with favourable phenotypes will survive and expand

Further exposed -> acquire more evoluntionarily advantagous characteristics

103
Q

What are the outcomes of somatic evolution in terms of cancer?

A

Longer somatic evolution -> higher variability

Higher chance of cancer cell clones to evolve -> able to resistant to drugs

This explain why early diagnosis and treatment is important

104
Q

Why are cancer patients normally treated with different agent?

A

To ensure kill all cancer cells

Not allow the scenario where resistant clines can proliferate

105
Q

What are tumour-initiating cells?

A

Also known as tumour-propagating cells or cancer stem cells.

Are cells with the ability to initiate and propagate tumour

106
Q

Are all cancer cells can induce tumour repeatedly?

A

No, only tumour-initiating cells can

107
Q

What are the ability to give rise to tumour dependent on?

A

Specifc lineage markers

Certain stage of differentiation

108
Q

What is self-renewal?

A

Ability of adult stem cells in the niche

Undergo indefinnite number of cell division while remain in a fully undifferentiated state

109
Q

What are the 2 types of cancer cells, with respect to ability to differentiate?

A

Progenitor-like cells = proliferate for a limited time but cannot recapitulate the complete tumour

Stem-cell like cancer cells = give rise to new tumours

110
Q

Describe the special traits of cancer stem cells (CSCs)

A

Have stem cell origin as mutation occurs to transform adult stem cell -> cancer stem cells

Can arise from more differentiated type cells as acquire mutations to give stem-cell like properties

Has long life-span

Being exposed to more multiple mutations

111
Q

Explain how can cancer stem cells associated with tumour heterogeneity.

A

Can have repeated mutations -> clonal expansion -> fittest clones within cancer cell population

CSCs repopulate a lineage of cells at different stages of maturation

112
Q

What are the clinical consequences of CSCs?

<hint: 5 characteristics>

A

Longevity -> accummulation of mutations + prolonged clonal evolution -> various cancer hallmarks

Initiate tumour growth -> rise to metastasis

Ability to recapitulate different cell maturity stages -> rise to metastasis and faster development

High level of efflux pumps

Assymmetric division -> divide less frequently -> reduce sensitivity to chemotherapeutic agent

Can be the target of treatment.

113
Q

How can CSC be targetted to induce tumour regression

A

Impair self-renewal properties

Induce specific cell death

Induce differentiation

Target stem cell niches

114
Q

Definition of cancer hallmarks

A

Features of shared by all cancer cells

Integral to cancer progression but not equally important to normal cells

115
Q

Do cancer hallmark develop spontaneously?

A

No

Result of randome mutation and epimutation during somatic evolution -> fitness advantages

116
Q

Name the 10 cancer hallmarks

A
  1. Sustained proliferative signalling
  2. Evade growth suppressions
  3. Resisting cell death
  4. Inducing angiogenesis
  5. Activation of invasion and metastasis
  6. Enabling replicative immortability
  7. Avoiding immune system
  8. De-regulation of cellular energetics
  9. Genome instability and mutation
  10. Tumour promoting inflammation
117
Q

Is it possible to predict the sequence of hallmarks will be acquired?

A

No as it is not an active process

118
Q

What is tumour organ?

A

Cancer cells exist as a part of tissue

Compete with healthy cells for nutrients and environment

119
Q

What is angiogenic switch?

A

When tumour sites acquire the ability to induce growth of blood vessels

Tumour expand rapidly and able to metastasise from then

120
Q

What are the growth of blood vessels in tumour cells dependent on?

A

VEGF - activators

Endostatin - inhibitors

121
Q

Are tumour vasculature as functional as normal blood vessels?

A

No

122
Q

Clinical relevance of angiogenesis in tumour

A

Anti-angiogenic therapy

Avastin (bevacizumab) - bind to extracellular VEGF

Sunitinib (Suten) - inhibit tyrosine kinase, intefere with intracellular effects

123
Q

What are the limitations of anti-angiogenic therapy?

A

Ineffective as diagnosis typically happens after vasculaturation

Complex multi-node pathway -> development of resistance

Stop tumour growth, not kill all the cells

124
Q

What are the new functions achieved by cancer cells once they acquire invasion hallmarks?

A

Reduced adhesion with neighbouring cells

Producing degrading enzymes to disrupt surrounding extracellular matrix

Motility and migration ability

Disruption of endothelial cells to gain access to vessel (intravasation)

125
Q

The relationships between angiogenesis hallmarks and invasion hallmarks

A

Likely that inducing angiogenesis need to be acquired at the same time or early

As limitations to tumour growth are due to absence of blood vessels

126
Q

Is there any pattern of metastases?

A

Tend to occur in specific organs like liver

Due to nature of tissue, volume and access of blood flow of an organ

127
Q

Why are cancer metastasis analogous to the planting of seeds?

A

Once cancer cells are scattered in the blood, they only grow depending on the tissues environment they arrive on

128
Q

Differences between apoptosis and necrosis

A

Apoptosis - suicide, controlled by genes, safe shut down, no inflammatory response, associated with shrinkage, peptide and DNA cleavage before phagocytosis

Necrosis - murder, no control sequence, trigger inflammatory response.

129
Q

What factors regulate apoptosis?

A

Extrinsic pathway activated by binding of ligands like FAS, TNF-alpha

Intrinsic pathways induced by DNA damage, cell cycle problems, hyperactive oncoproteins

Balance of pro and anti-apoptotic signals

PHAY00011 (9 decks)

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