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CLS > Cancer > Flashcards

Cancer Flashcards

1
Q

What is the definition of Neoplasia?

A

Abnormal mass of tissue. Growth exceeds and uncoordinated with that of normal tissue. Growth persists excessively after stimuli evoked.

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2
Q

Define hyperplasia?

A

An abnormal increase in the number of normal cells in normal arrangement in an organ or tissue which stops growing when the stimuli is taken away.

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3
Q

If a tumour is well differentiated is that good or bad for the prognosis?

A

Cells of tumour closely relate to the cell of origin. Better prognosis.

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4
Q

Describe 5 features of a benign tumour.

A

Do not infiltrate other tissues.
Stay at site of origin.
Grow by expansion, evenly and in path of outgrowths.
Compress adjacent tissue. Growth can lead to compression of nearby structures.
Not always harmless.

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5
Q

What are 4 features of a malignant tumour?

A

Potentially fatal.
Infiltrate, compress and invade adjacent tissues and can spread to form metastases.
Grow by expansion and infiltration, irregular outline with indistinct edges.

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6
Q

What are the criteria for a malignant tumour?

A 
Increased mitotic count.
Pleomorphism.
Nuclear hyperchromatism.
Increased nuclear cytoplasm ratio.
Abnormal mitoses.
Poor differentiation.
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7
Q

What is a carcinoma in-situ?

A

Dysplasia in an epithelium without invasion across epithelial basement membrane = precursor form of cancer.

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8
Q

Name 5 ways a tumour is diagnosed.

A

Biopsy, clinical history, physical examination, tumour markers and imaging.

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9
Q

Needle biopsy is used for what tissues?

A

Breast, lung and pleura, liver, kidney, lymph nodes, brain eye, thyroid.

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10
Q

Endoscopic biopsy is used for what tissues?

A

Respiratory tract: trachea, bronchus lung. Alimentary tract: oesophagus, stomach, small intestine.

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11
Q

What are the two main assessments made after biopsy taken?

A

Analysis of the degree of differentiation and growth pattern of tumour.
Evaluation of how far tumour has spread.

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12
Q

What are other biopsies that can be done?

A

Transvascular, direct excision and curettage biopsy.

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13
Q

Name 3 tumour markers and what they indicate.

A

HCG - human chorionic gonadotrophin, from tumours with trophoblast elements.
AFP - Alpha fetoprotein. Liver cancer, germ cell tumours.
PSA- Prostate specific antigen from prostate carcinomas.

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14
Q

Where are tumour markers liberated?

A

In blood, urine and CSF.

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15
Q

What is the difference between a low and high grade tumour

A

Low grade = slow growing and better prognosis.

High grade = fast growing and have poor prognosis.

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16
Q

How is the stage of a tumour defined?

A

Size of primary tumour, degree to which it has locally invaded, extent to which it has spread by distant metastasis.

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17
Q

How is Duke’s staging of colorectal cancer characterised?

A

Stage A - Within muscle.
Stage B - Through muscle.
Stage C - With nodes involved.

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18
Q

Give one example of a tumour with excellent, moderate and very poor prognosis.

A

Excellent - thyroid.
Moderate - Kidney, prostate, cervix, breast.
Very poor prognosis - pancreas, brain, oesophagus.

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19
Q

During differentiation, what alters adult and fetal growth?

A

Control genes.

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20
Q

What are the roles of the control genes?

A

To make control proteins and mRNA. These proteins have to switch off fetal genes needed for growth and switch on adult genes needed for mature cells.

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21
Q

What are the genes switched off called?

A

Oncogenes.

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22
Q

Genes switched on are known as what?

A

Tumour supressor genes or anti-oncogenes.

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23
Q

What are the 5 common characteristics of cancer?

A
  1. New growth
  2. Development of cellular pleomorphism: Anaplasia - loss of differentiation.
  3. Disturbance of cellular arrangements - can lead to pain.
  4. Invasion of adjacent tissues.
  5. Cell heterotopia - displacement/misplacement of parts, presence of a tissue in an abnormal location.
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24
Q

What are the 4 types of RNA viruses? How can you tell between?

A 
A,B,C,D.
A - Intracellular only, no know role.
B - Have eccentric cores
C - Have centric cores - 90% of RNA viruses are C type. 
D - Bullet shaped cores.
25
Q

What are the stages involved when infected by an RNA virus?

A

Virus goes into cell and codes. RNA released and reverse transcribed by DNA polymerase which creates a proviral double stranded DNA copy of RNA. DNA has all the codes the virus has but has different ends. They become identical long terminal repeats, LTRs. Double stranded DNA passed into nucleus and integrates into cell chromosome, can stay there forever. The virus is a budding virus and doesn’t lyse the cell. The virus carries tRNA that the host has. It is incorporated into a new particle, acts as primer in the new cell they are infecting.

26
Q

How can the sarcoma virus and leukaemia virus act as oncogenes?

A

Sarcoma - due to the presence of that extra gene, ‘src’. The sarcoma gene contains an oncogene that will be expressed along with other viral genes due to the strong promotor region at the left end of the proviral gene.
Leukaemia - doesn’t contain an oncogene but can integrate next to a silent human proto-oncogene and due to the right-ward LTR containing a strong promotor, the proto-oncogene will be expressed and will produce similiar products with similiar effects.

27
Q

Name and describe the function of 4 oncogenes.

A

Hormones - viral products mimic hormones. Eg: PDGF - platelet derived growth factor - once infected, all cells in vicinity will grow.

G-protein - oncogene mutates GTP-ase so it becomes inactive and GTP does not dissociate from the G-protein.

Receptors - can mimic hormone receptors.

Transcription factors - switch on cell growth.

28
Q

DNA virus can undergo two different life cycles. Name and describe each.

A

Lytic life cycle - invades, kills, lyses and releases new particles. Cells which allow this to happen, viral growth, are called permissive cells. There are early and late phase reactions after injection. New virus particles are produced and released when host cell lyses.
Transforming life cycle - involves non-permissive cells. Do not allow virus to grow. Only early phase reactions - whole life cycle not expressed - no new virus released but host cell continues to divide causing cancer.

29
Q

List some organic and inorganic molecules that cause cancer.

A

Organinc: Polycyclic aromatic hydrocarbons - benzo(a)pyrene.
Azodyes.
Nitosamines.
Inorganic: Asbestos.

30
Q

How does the body behave to get rid of these chemicals?

A

Intracellular metabolism.
Phase 1 - reaction involves making the chemical more reactive.
Phase 2 - reaction involves coupling this more reactive chemical with a water soluble substance so body can excrete it.

31
Q

Why are unreactive compounds often more carcinogenic than reactive ones?

A

Because reactive chemical bind to a protein and are got rid of quickly and easily. An unreactive chemical will not and therefore will get into cells in higher concentrations before it is made reactive.

32
Q

How is benzo(a)pyrene metabolised?

A

Activated by AHH (aromatic hydrocarbon hydroxylase) and made water soluble in order to remove it from the body.

33
Q

What is bad about the metabolism of benzo(a)pyrene.

A

When it is metabolised a highly reactive ‘ultimate carcinogenic’ form of BP is produced. When AHH is induced it adds an oxygen to one of the benzene rings, making it more reactive. the cell hydrolyses that, using epoxide hydrolase and puts two diols on the benzene ring. Still not water soluble but more reactive. Remains in membrane and another AHH reaction occurs, a seconnd oxygen is added and it is this molecule benzo(a)pyrene diol epoxide which causes cancer.

34
Q

What are the two possible fates of the ultimate carcinogen?

A

Can be detoxified and excreted or it can be attacked by electron rich atoms in molecules like guanine in DNA.

35
Q

What is the cause when the electron rich atoms in molecules covalently bind to guanine?

A

Causes incorrect base pairing, point mutation, happens to an oncogene or TSG then cancer is initiates and in a similar way to UV light it can induce the SOS DNA repair system to remove the BP adducts and consequently insert mutations.

36
Q

How can genetic factors influence the process of chemical carcinogenesis?

A

High inducers produce more of the enzyme AHH and therefore more prone to the cancer.

37
Q

What is Xeroderma Pigmentosum?

A

A rare but autosomal recessive disease resulting in abnormal pigmentation.

38
Q

What is the difference between XP cells and normal cells?

A

XP cells do not get more damaged than normal cells, they are just unable to repair the damage caused.

39
Q

What effects does radiation have on DNA?

A

Direct - excitation and ionisation of electrons to produce ions. Dimerisation of pyrimidine nucleotides by UV.
Indirect - Free radical formation - XP.

40
Q

What are the 4 key features of familial cancer predisposition?

A

Early onset tumours, multiple tumours in close relatives, multiple tumours within an individual, clusters of different tumours in recognisable pattern.

41
Q

What is the two hit hypothesis of mutation?

A

1st mutation in gene is present in all cells of patient. This may arise as a new mutation (sporadic) or may be inherited (pre-disposed).
2nd mutation arises in a somatic cell in the organ in which the tumour develops - tumour only develops when the 2nd mutation occurs.

42
Q

Name a cancer predisposition.

A

VHL - Von Hippel - Lindau Syndrome. Birth incidence of 1:36,000. It’s autosomal dominant condition caused by mutation in VSL gene which is a TSG.

43
Q

To become malignant, what does the tumour need to acquire?

A

Limitless replication - insensitivity to antigrowth signals and self sufficiency in growth signals.
Angiogenesis - induction of new blood vessel growth by secreting vascular endothelial growth factors.
Invasion and metastasis - features acquired by disrupting gene function a.k.a by mutation.

44
Q

Mutation can arise in what ways?

A

Sequence change, gene amplification, gene deletion, gene silencing.

45
Q

Give and example of neoplasia involving upregulation of growth factor.

A

Increased secretion of IGF2 occurs in Wilm’s tumour.

46
Q

Give and example of neoplasia involving upregulation of GF receptor.

A

cErbB2 is upregulated in BRCA.

47
Q

Give and example of neoplasia involving permanent activation of GF receptor.

A

Mutation in tyrosine kinase domain of c-kit in GI stromal tumours (GISTs).

48
Q

Give and example of neoplasia involving down regulation of apoptosis.

A

Caspase 3 - downregulated in colorectal tumours.

49
Q

What is a lymphoma?

A

Neoplastic proliferation of lymphoid cells of various types.

50
Q

What can lymphoma’s be classified into?

A

Hodgkins and Non-Hodgkins disease.

51
Q

What can Hodgkins disease be split into?

A

Nodular lymphocyte-predominant Hodgkins and classical Hodgkins lymphoma.

52
Q

What is specific about classical Hodgkins lymphoma?

A

Lymphocyte rich, mixed cellularity, nodular sclerosing and lymphocyte depleting.

53
Q

Brain tumours are most commonly derived from glial cells such as what?

A

Astrocytes, oligodendrocytes and ependymal cells.

54
Q

What are the most common type of brain tumour? What is special about them?

A

Astrocytomas, they all behave in a malignant manner (local invasion) and do not metastasise.

55
Q

Embryonal tumours derive from where?

A

Embryonic remnants of primitive ‘blast’ tissue.

56
Q

Give four important characteristics of embryonal tumours.

A

Mainly in young children, highly malignant, spread early and widely by lymphatics and veins, sensitive to chemotherapy.

57
Q

Give two examples of embryonal tumours.

A

Nephroblastoma - Wilms tumour.

Neuroblastoma - in adrenal gland, derived from primitive adrenal medullary precursors.

58
Q

Teratomas derived from where?

A

Primitive germ cells - retain capacity o differentiate along all 3 primitive embryological lines, therefore contain representatives of ectoderm, mesoderm, endoderm.

CLS (6 decks)

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