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Year 3 SBOM > Cancer Lectures > Flashcards

Cancer Lectures Flashcards

1
Q

Which are the most common cancers?

A

Breast
Lung
Colon and rectum

Cancer deaths however:
Lung
Colon and rectum
Liver

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2
Q

What is a gene?

A

Section of DNA that codes for a protein

Strands of DNA that contain many genes = chromosomes

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3
Q

How are proteins made?

A

Via transcription and translation

Gene is copied into RNA (transcription). This is translated from mRNA to build a protein molecule (translation)

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4
Q

What are Introns and Exons on DNA?

A

Introns = non-coding DNA
Exons = coding sequences of DNA

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5
Q

What is the difference beween germline and acquired mutations?

A

Germline mutations - mutations to the germ cells - which means they can be inherited from parent to offspring.

Acquired mutations occur to somatic cells - are not inherited.

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6
Q

What is a mutation?

A

A change to DNA that ultimately changes the resultant protein - can impact on its structure and/or its function.

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7
Q

How can we test for mutations?

A

Gene panel testing - tests for a single gene mutation

Whole exome testing - tests the entire specific coding area

Entire coding sequence - exome plus junk DNA

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8
Q

What is the difference between a synonymous and a non-synonymous change to DNA

A

Synonymous changes to DNA don’t cause a corresponding change to an amino acid produced

Non-synonymous changes - do cause an AA change

Occurence of these can reflect the incidence of natural selection.

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9
Q

What are silent mutations?

A

Mutations that don’t cause disease and are therefore tolerated.

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10
Q

What are pseudogenes?

A

Segments of DNA that resemble a gene but are not actually capable of coding for a protein - often derived from genes that have lost their coding ability over the process of evolution.

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11
Q

Mutations in which genes can cause a predisposition to cancer?

A

Mutations in proto-oncogenes and tumour suppressor genes.

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12
Q

What are
- Proto-oncogenes
- Tumour Suppressor Genes

A

Proto-oncogenes control cell growth - gas pedal - if mutated they make the cell divide uncontrollably (become oncogenes)

Tumour suppressor genes - have a negative effect on cell growth - they turn cell growth off. If mutated they stop working, and therefore cell growth isn’t turned off.

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13
Q

What are SNPs?

A

Single nucleotide polymorphisms

Ie. genetic variation of a single nucleotide.

Can act as biological markers - can relate to genes associated with disease (inc cancer).
Can also be synonymous or benign (i.e. tolerated)

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14
Q

Which are the most commonly inherited cancers?

A

Retinoblastoma
Phaeochromocytoma
Ovarian cancer

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15
Q

What are Cancer Predisposition Genes?

A

Germline gene mutations which inc risk of cancer.

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16
Q

Which inherited mutation of an oncogene is strongly linked to medullary thyroid cancer?

A

Multiple Endocrine Neoplasia Type 2 (MEN2A)

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17
Q

When should you suspect MEN2A mutation?
What type of gene is mutated in MEN2A?

A

When 2 or + endocrine tumours occur together
A proto-oncogene calle RET (tyrosine kinase receptor)

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18
Q

What is a clinical example of a mutation to a tumour suppressor gene?

A

Retinoblastoma

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19
Q

How can you identify retinoblastoma clinically?

A

White reflex replaces the red reflex of the eye.

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20
Q

What is the two hit theory of cancer causation?

A

That you need two mutations (one to each allele of a gene) in order for a cell to become cancerous. In normal cells = this requires two “hits”/damage before this occurs.

In cells with an inherited disease that has damaged one of the alleles - you only need one hit to get disease - therefore makes it much more likely.

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21
Q

Name any tumour suppressor genes that you know.

A

TP53 (somatic mutation)
BRCA 1 &2 (germline)
MLH1 (somatic or germline) - mismatch repair gene

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22
Q

What can a mutation in BRCA1 or 2 lead to increased risk of?

A

F - inc risk of breast and ovarian cancer

M - inc risk of prostate and male breast cancer

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23
Q

What is Li Fraumeni Syndrome?

A

AD mutation of TP53 - tumour suppressor gene

Linked to high rates of osteosarcoma, soft tissue sarcoma, acute leukaemia, breast, brain and adrenal tumours

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24
Q

What is epigenetics used for?

A

Is the process of how cells control gene activity without changing the DNA sequence. Modifies the DNA chain by methylation, histone proteins modification, chromatin remodelling and mRNA mechanisms.

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25
Q

What factors might modify epigenetic patterns?

A

Diet
Obesity
Physical activity
Smoking
Alcohol
Environmental pollutants
Stress
Night shift patterns

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26
Q

What do the following do:

  • Activated Epigenetic Modifiers
  • Suppressive Epigenetic Modifiers
A
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27
Q

Which viruses are thought to be potentially carcinogenic?

A

Epstein Barr
Hepatitis B
HPV

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28
Q

What is the difference between a
- direct carcinogen
- procarcinogen
- cocarcinogen

A
  • Directly cause cancer
  • Cause cancer due to changing during metabolism
  • Cause cancer by acting with another chemical
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29
Q

How do reactive oxygen species damage DNA?

A

Can cause oxidised DNA bases -> misfiring of bases -> mutations.

ROSs can also stimulate signal transduction pathways and activate key transcription factors - with altered gene expression can lead to carcinogenesis.

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30
Q

What are skip metastases?

A

Infiltration by the tumour of distant nodes, but without tumour involvement in the nodes adjacent to it.

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31
Q

What percentage of disseminated cancer cells successfully develop into a distant met?

A

<0.1%

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32
Q

Why can mets develop some time after the initial cancer?

A

Cells (micromets) can remain undetectable (in cell cycle or due to a balance between proliferation and apoptosis) before eventually developing into a detectable macro met.

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33
Q

Cancer cells can move individually or collectively - what is this facilitated by??

A

A change in cell plasticity - esp from epithelial to mesenchyme transition (EMT)

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34
Q

Which cytokine stimulates epithelial to mesenchymal transition and plays an important role in tumourigenesis?

A

TGF-β
(Transforming Growth Factor β)

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35
Q

Which cytokine stimulates tumour angiogenesis?

A

VGEF
Vascular Endothelial Growth Factors

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36
Q

What are immunohistochemical tests used for in cancer diagnosis?

A

Diagnosing the cancer type including subtypes - allows a prediction of response to therapy and helps guide treatment options.

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37
Q

What is the difference between TX (or NX or MX) and T0 (or N0 or M0)

A

X = cannot be measure
0 = not found

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38
Q

What is the grading of stages of T, N and M

A

T 0 - 4
N 0 - 3
M 0 - 1

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39
Q

How do we stage cancer?

A

We look at the TN&M of a cancer and assign whether it is Stage 1 (isolated cancer) to Stage 4 (spread to the limit of assessment measures)

40
Q

What is cytogenetic analysis used for?

A

To diagnose the type of cancer - plan Tx or predict how well Tx will work.

41
Q

What is immunophenotyping?

A

Method of uses antibodies to identify cells based on the types of antigens or markers on the surface of the cells. Used to identify haematopoetic cancers - such as leukaemia, lymphoma, myelodysplastic syndromes and myleoproliferative disorders.

42
Q

What are tumour marker tests used for?

A

They are substances produced by cancer cells (and normal cells - but in much higher quantities by cancer cells). They help diagnose the cancer, decide treatment, measure what worked etc.

43
Q

Which staging system is used for lymphoma?

A

Ann Arbor staging system

44
Q

How do bone mets develop?

A

Tumours - form new vessels - then invade the vessels and travel around until then arrive in capillary beds in bones - where they adhere to the vessel walls, break through them and start proliferating inside the bone.

45
Q

What are the three types of bone mets?

A

Lytic (osteoclastic)
Sclerotic (osteblastic)
Mixed

46
Q

How can you differentiate between metastasis in bones and benign bone pathology?

A

Depends on the pattern of distribution and the location of the lesions.

47
Q

What is the Warburg effect? What can it be used for?

A

That cancer cells metabolise glucose in a different manner from normal cells - means that you can use radioisotopes attached to glucose (FDG - Fludeoxyglucose) and where these are taken up in vast quantities you know there is a malignancy.

FDG-PET scan used for this.

48
Q

What are theranostics?

A

A combination of the terms therapeutics and diagnostics. Theranostics is the term used to describe the combination of using one radioactive drug to identify (diagnose) and a second radioactive drug to deliver therapy to treat the main tumor and any metastatic tumors

49
Q

How is a sentinel node identified?

A

Dye / tracer is injected in / around the tumour. The radioactive nodes are then identified on the surgical table, excised and sent to pathology for instant evaluation to see whether any signs of malignancy are present.

50
Q

Why is it difficult to treat and cure cancer?

A

Is a disease of our own cells - hard for the immune system to recognise them and they can hide (immune evasion). Is also difficult to identify target that are present exclusively or predominantly in the tumour cells but not in the normal cells.

51
Q

What are tumour-specific characteristics?

A
52
Q

What do you need to get in order to definitely confirm a cancer diagnosis?

A

Histological confirmation

53
Q

What is the most common type of cancer histologically?

A

Carcinoma (from epithelial tissue)

Followed by sarcoma (from connective tissue)

54
Q

What are the 4 basic types of tissue in the body?

A

Connective tissue
Epithelial tissue
Nervous tissue
Muscle tissue

55
Q

What is the difference between somatic and germline mutations?

A

Somatic = the mutation is present only within the tumour cells.

Germline = the mutation is present in all cells and can therefore be inherited

56
Q

How do mutations to proto-oncogenes cause cancer?

A

Proto-oncogenes drive the cell cycle, which is the process cells go through before they can divide. Proto-oncogenes also control how fast cells grow, when cells divide and when cells die (apoptosis).
When a proto-oncogene mutates and becomes an oncogene, the gene never stops sending signals telling cells to grow and divide. Cells respond by multiplying faster than usual, eventually creating tumors.

57
Q

What are biomarkers and what are they used for?

A

Genes, proteins and other substances that can provide information about a specific cancer.

They can be use for prognostication - i.e. informing a patient about what their outcome is likely to be,

They can also be predictive - they inform about which treatment should be used in terms of what the cancer is more likely to respond to.

58
Q

What is the difference between oligometastatic and polymetastatic disease?

A

Oligometastatic = limited spread to one area

Polymetastatic = extensive metastatic disease

59
Q

What is the clinical behaviour of a tumour?

A

Whether it is indolent/slow growing or aggressive

60
Q

What is performance status of a patient?

A
61
Q

What side effect of chemotherapy can be life threatening?

A

Febrile neutropenia (high temp, low WCC)

62
Q

What are the side effects of chemotherapy?

A
63
Q

What is the difference between primary and secondary drug resistance?

A

Primary = resistance to the drug before exposure (innate)

Secondary = resistance to the drug following exposure

64
Q

How is personalised medicine playing a role in cancer treatment?

A

Tumours are analysed to identify druggable targets which can be attacked with drugs inc
- small molecules
- monoclonal antibodies
- immunotoxins

65
Q

What is synthetic lethality?

A

A means of attacking cancer cells whilst sparing the normal cells.

E.g. - cells have PARP and BRCA2 genes - both of which are meant to be responsible for repairing DNA damage. In certain cancer cells - BRCA2 is already mutated and doesn’t work. If the cells are then hit by a drug which disinhibits PARP as well - it means that the cancer cells cannot repair any cell damage and therefore they undergo apoptosis.

Olaparib is the dug which does this.

66
Q

How are monoclonal antibodies used in cancer treatment?

Give an example.

A

They interact with surface antigens on the CSM of cancer cells - blocking the transmission of intracellular signals and trigger an immune response against the cell.

E.g. Trastuzumab - HER2 and Breast Cancer

67
Q

What are immunotoxins?

A

Monoclonal antibodies conducted with drugs or radioactive molecules - bind to tumour cells and directly effect them.

68
Q

How is hormonal therapy used against cancer?

A

Hormone therapy is used to treat cancers that use hormones to grow, such as some prostate and breast cancers. Hormone therapy is a cancer treatment that slows or stops the growth of cancer that uses hormones to grow by blocking the hormones required.

69
Q

How is immunotherapy used against cancer?

A

Immunotherapy is a type of cancer treatment. It uses substances made by the body or in a laboratory to boost the immune system and help the body find and destroy cancer cells. Immunotherapy can treat many different types of cancer. It can be used alone or in combination with chemotherapy and/or other cancer treatments.

70
Q

What is the purpose of
- Phase 1
- Phase 2
- Phase 3
in a clinical trial of drug development?

A
71
Q

What is Olaparib?

A

PARP (poly ADP ribose polymerase) inhibitor = used in Rx ovarian, breast, pancreatic and prostate cancer.

Targets enzymes involved in DNA repair.

72
Q

Which of the following is not related to the pharmacokinetics of a drug?

1). The side effects
2). The bioavailability
3) The excretion
4). The diffusion through the bowel into the blood stream

A

The side effects

73
Q

What is the MTD?

A

The maximum tolerated dose

= The maximum dose level at which a drug has a therapeutic effect and acceptable toxicity in human studies

74
Q

What is the mechanism of mutagenesis?

A

Too much cell growth or too little cell death = cells that have lost control of the cell cycle -> tumour / neoplasm

75
Q

What is the difference between a benign and malignant tumour?

A

Benign = unable to invade health surrounding tissue

Malignant = becomes progressively more invasive until it is metastatic

76
Q

Do cancers require a single mutation?

A

Rarely - there are very few cancers which require a single mutation, most cancers require several accumulations of DNA errors/mutations

Many mutations occur as random events in normal cells without generating malignant transformation

77
Q

What are gene sequences that encourage cancer growth and proliferation called?

A

Oncogenes

78
Q

What are genes called that discourage or inhibit cell growth and proliferation?

A

Tumour suppressor genes

79
Q

Which viruses can cause cancerous mutations?

A

Hep B Virus
EBV - in African children this can be seen as Burkitt’s lymphoma
Papillomavirus (HPV)

80
Q

The appearance of which cells in a tumour or lymph nodes suggests a good prognosis for cancer in humans?

A

CD8 Tumour Infiltrating Lymphocytes

81
Q

The presence of which cells in a tumour is a predictor of reduced survival in humans?

A

Treg cells

82
Q

How does the BCG virus being introduced to the bladder help in treating bladder cancer?

A

Bladder cancer cells alone internalise the BCG virus and present on their CSM - immune cells of the body are then recruited and they kill the cells which present.

83
Q

What are the two types of tumour antigens that have been identified on tumour cells?

A

TAAs - tumour associated antigens - may be present on normal cells but at low levels. Are over expressed in tumours.

TSAs - Tumour specific antigens - are unique to tumour cells and not present on normal body cells

84
Q

What is the innate response of the immune system to attack tumour cells?

A

Natural Killer cells - can directly kill
Macrophages - can infiltrate tumour masses (called Tumour Associated Macrophages) - can be pro-tumour growth or anti-tumour growth.

85
Q

What is the adaptive response of the immune system to attack tumour cells

A

CD8 cells
CD4 cells
B cells

86
Q

Why do tumours still develop in the body if the immune system has the ability to recognise them?

A

Tumours can outsmart the host immune system and escape from attack. They can also manipulate immune cells to help the survival and spread of cancer cells.

87
Q

What is the mass of cells, molecules and blood vessels that surround and feed tumour cells called?

A

The tumour microenviroment

88
Q

What is cancer immunoediting theory?

A

The immune system can kill cancer cells - but it can also induce changes in the tumour (by epigenetic changes or Darwinian selection) and thus further growth of the tumour mass

89
Q

What are the 3 Es of cancer immunoediting?

A

Elimination
Equilibrium
Escape

90
Q

What are the mechanisms of tumour escape from the immune system?

A

Reduced levels of absence of MHC I molecules so they are not recognised by CD8 cells

Cessation of expression of the antigens recognised by the immune system

Production of immunosuppressive factors by the tumour (e.g. TGF-β) PD-1 Ligand

Some tumour cells have an inherent defect in antigen processing and presentation

Blocking of receptors on T-cells by specific antigen antibodies complex (after shedding of tumor antigens) prevents them from recognizing and attacking tumor cells

Antigens on the surface of tumors may be masked by sialic acid-containing mucopolysaccharides

91
Q

How do modern immunotherapies target cancer cells?

A

They dont target one particular weakness - because cancer cells can find a way around. Usually try to attack on several fronts at once.

92
Q

What is immunotherapy?

A

Rx that stimulates the body’s immune system to fight the cancer

93
Q

How do antibody drugs work?

A

They contain a domain which is bound to a toxin. They bind to the tumour cell and induce a cytokine response.

94
Q

What is CAR-T?

A

Specifically engineered T-cells that trick the immune system to recognise the cancer. Tumour specific antigens from the cancer are harvested from the P - incorporated into non-viral vectors - engineers a functional T-cells specifically for that Ps cancer.
In the lab, they change the T cells. You might hear this called genetically engineering the T cell. The T cell is now a CAR T-cell. CAR stands for chimeric antigen receptor. These CAR T-cells are designed to recognise and target a specific protein on the cancer cells.

These changed T cells grow and multiply in the lab. Once there are enough cells you have a drip containing these cells back into your bloodstream. The aim is for the CAR T-cells to then recognise and attack the cancer cells.

95
Q

What are the limitations of immunotherapies?

A
96
Q
A
97
Q
A

Year 3 SBOM (6 decks)

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