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Molecular Basis of Disease > Lung cancer > Flashcards

Lung cancer Flashcards

1
Q

What percentage of lung cancers are caused by smoking?

A

71%

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2
Q

Why are survival rates of lung cancer so low?

A

Very few symptoms early on, only present in later stages

Rapid progression

Less funding so fewer advances in treatment options

Social stigma

Tumour resistance

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3
Q

What are the two main reasons for tumour resistance in lung cancer?

A

Intratumour heterogeneity

Lack of biomarkers

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4
Q

Which are 3 features we can use to categorize lung cancer?

A

Histology

Molecular mutations

Staging

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5
Q

Which histological features are used to categorize lung cancers?

A

Small cell/neuroendocrine

Non small cell

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6
Q

Which molecular mutations are commonly found to cause lung cancer?

A

EGFR

ROS

ALK

PD-L1

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7
Q

Which 3 features do we look at to stage non small cell cancer?

A

T - primary cancer

N - regional lymph node

M - distal metastasis

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8
Q

What is ECOG?

A

Scale used to assess a patients fitness to undergo treatment

0-5 scale

0 = fully active
5 = dead
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9
Q

What is the importance of mutations in cancer cells?

A

Trigger signalling pathways which confer survival advantage to cells compared to somatic cells

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10
Q

Which signalling pathways confer survival advantages to cancer cells?

A

Block oncogene pathways

Decrease apoptosis of cancer cells

Increase mutations of cells leading to relapse

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11
Q

What are the three main treatments of lung cancer?

A

Chemotherapy

Radiotherapy

Molecular therapy

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12
Q

Which chemotherapy is used in lung cancer?

A

Dual agent chemotherapy (platinum + another)

Docetaxel monotherapy

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13
Q

When do we use Docetaxel instead of dual agent chemotherapy?

A

Used for patients who do not respond to dual agent chemotherapy and are fit enough

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14
Q

What are the 3 types of radiotherapy?

A

Curative

Adjuvant

Palliative

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15
Q

What does molecular therapy target?

A

Protein mutations

Tyrosine kinase

Immune checkpoints

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16
Q

How does molecular therapy target tyrosine kinase?

A

Via tyrosine kinase inhibitors

Blocks signalling pathways preventing the tyrosine kinase from signalling to the nucleus

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17
Q

What is an example of a checkpoint inhibitor?

A

PD-1 and PD-L1 blockade

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18
Q

How does the checkpoint inhibitor Pembrolizumab act?

A

Blocks either the PD-1 on T-cells or PD-L1 on the tumour cells

Prevents the tumour cell from binding to the T cell and inhibiting it

Therefore the active T cell kills the tumour cells by cytotoxic killing

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19
Q

Why are MSCs immune priviledged?

A

Do not elicit an immune reaction

20
Q

What is the role of MSCs in stromal tissue cells?

A

Precursors of stromal tissue cells

21
Q

Where are MSCs found in the body?

A

Bone marrow

Umbilical cords

22
Q

How often do MSCs divide?

A

They show 5 population doublings per week

23
Q

What important fact was discovered about MSCs?

A

They home to tumors

24
Q

Why do MSCs home to tumors?

A

Microenvironment created by tumour cells releasing cytokine and matrix protein

Recognised by the conjugate receptors on MSCs

25
Q

Which cytokines released from tumours are MSCs especially attracted to?

A

MIF

Activates ERK and JNK through CXCR4

26
Q

How was the importance of MIF in homing MSCs to cancer cells discovered?

A

Study that knocked down the MIF signalling from cancer cells

Knockout of MIF lead to no MSCs homing to cancer cells

27
Q

What is the TRAIL pathway?

A

TNF-related apoptosis inducing ligand

Induces the extrinsic pathway of apoptosis by binding to its receptor (TRAI)

28
Q

How are tumour cells related to the TRAIL pathway?

A

Tumour cells express TRAI

So if we can activate its apoptosis by expressing TRAIL we can specifically target cancer cells

29
Q

Which apoptotic pathways do chemotherapy and radiation elicit?

A

Intrinsic apoptotic pathway

More of a destructive mechanism for killing mutated cells

30
Q

Why can’t we use TRAIL injections to kill cancer cells?

A

Very short half-life

Leads to cytotoxicity due to continuous dosages needed to provide effective treatment

31
Q

What is used to inject TRAIL into the host organism?

A

Modify MSCs to express TRAIL ligand and trigger the extrinsic apoptotic pathway

32
Q

What were the steps taken to ensure MSCs modified to express TRAIL were an effective therapy against lung cancer?

A

Construction of the TRAIL lentivirus

Prove that MSCTRAIL was effective at killing cancer cells

Prove that MSCTRAIL homed toward the tumour

Prove that MSCTRAIL effectively reduced tumour growth

33
Q

How was the TRAIL lentivirus constructed?

A

Lentivirus conjugated with doxycycline

Doxycycline could turn on or off the expression of TRAIL in the MSCs

Marked TRAIL with luminescent biomarker to be able to spot MSCs

34
Q

How was it shown that dox effectively turned the production of TRAIL on?

A

Measured the concentration of TRAIL produced by the lentiviruses

Lentiviruses without dox did not produce TRAIL

Lentiviruses with dox produced TRAIL

35
Q

What was used to show that MSCs homed towards tumour cells?

A

DiL labelled MSCs

36
Q

What is TRAIL synergy?

A

When MSCTRAIL therapy works together with other therapies to heighten their therapeutic effects

37
Q

What are mechanisms of TRAIL synergy?

A

Radiotherapy increases TRAIL receptors

Radiotherapy increases MSC homing

Chemotherapy increases TRAIL induced caspase cleavage

Chemotherapy downregulates inhibitors of apoptosis

38
Q

What was observed in the homing of MSCTRAIL in the lungs?

A

DiL-labelled MSCs showed that clusters wedge into the capillaries at first pass (90%)

Ideal for treating lung cancer

39
Q

Describe the extrinsic pathway of apoptosis

A

TRAIL L binds to the trimerised receptor

Activates FADD protein that connect the Casp8 to the receptor

Activation of FADD leads to activation of Casp8

40
Q

How was it proven that the extrinsic pathway was activated upon binding of MSCs to tumour cells?

A

Dominant negative construct of FAD was inserted into the tumor cells

Cancer cells were no longer apoptosed

41
Q

What is a dominant negative FAD construct?

A

Protein that no longer connect the Casp8 to the TRAIL receptor

42
Q

Which ECOG patients are eligible for chemo?

A

0-2 stage

43
Q

How many lung cancer patients survive after 10 years

A

5%

44
Q

How common is lung cancer death?

A

most common cancer DEATH - 1/5 cancer deaths

45
Q

Lung cancer prognosis has improved a lot since the 70s

TRUE or FALSE

A

False

46
Q

What are the types of curative radiotherapy?

A

SABR (stereotactic body radiation therapy)
EBRT (external beam radiation therapy)
- with Surgery (may take wedge, lobe or lung)

Molecular Basis of Disease (28 decks)

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