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CLS > Cancer > Flashcards

Cancer Flashcards

1
Q

A definition of cancer

A

Cancer is a term used for diseases in which abnormal cells divide without control and are able to invade other tissues. Cancer cells can spread to other parts of the body

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2
Q

Kinds of benign neoplasias

A

Hyperplasia

Metaplasia

Dysplasia

Adenomas/polyps/warts

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3
Q

Hyperplasia

A

Over proliferation of cells that appear otherwise normal

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4
Q

Metaplasia

A

Normal in appearnace but in the wrong place, usual from an adjacent tissue

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5
Q

Dysplasia

A

Cells that appear abnormal; often increased nuclear to cytoplasmic ratio

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6
Q

Adenomas/polyps/warts

A

Larger growths of dysplastic cells

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7
Q

Driver mutations vs Passenger mutations

A

driver mutations do affect function of genes that reegulate proliferation, apoptosis, immortality

Passenger mutations are ones not relevant to promotion of cancer

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8
Q

Function of proto-oncogenes

A

Promote cell proliferation

Gain of function mutations in cancer

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9
Q

Function of tumour supressor genes

A

Inhibit events leading to cancer

Loss of function mutations in cancer

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10
Q

Main characteristics of cancer

A

Proliferation: grow independantly of signals

Immortality: Avoid senescene/telomere shortening

Avoid cell death: Avoid apoptosis

Angiogenesis: They must be fed

Metastasis

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11
Q

At which cell cycle checkpoint do oncogenes work

A

Restriction point

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12
Q

Which two processes normally limit life of cell

A

Senescence: Cells in G0, dont proliferate

Apoptosis: programmed cell death

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13
Q

Define senescence

A
  • Metabolically active, irreversibly lost ability to re-enter cell cycle, stay in G0
  • Normal cells have finite proliferative capcity (Hayflick limit)
  • Cancers must avoid senscence to continue growing
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14
Q

Role of P53 in Telomeres/cancer

A

P53 normally warns about short ends and initiates senescence

Excess telomere shortening leads to crisis and apoptosis

Crisis

  • Normall cells will undergo apoptosis
  • In cancer cells TERT is reactivated; repairs broken ends, but creates faulty chormosomes
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15
Q

Which factor induces angiogenesis

A

Hypoxia-inducible factor 1-alpha is a hypoxia induced factor

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16
Q

Different word for tumour

A

Neoplasia

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17
Q

Define neoplasia

A

An abnormal mass of tissue, the growth which exceeds, and is uncoordinated with, that of normal tissue, and which presents in the same excessive manner after the cessation of the stimulus which has evoked the change

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18
Q

Cancer is colloqial speak for

A

A malignant tumour

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19
Q

Meaning of differntiation in tumours

A

Described how close in appearance the cells of a tumour are to the cell type from which they are derived. Important in predicting likely behaviour of a tumour

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20
Q

Different tumour types based on differentiation

A

Well-differentiated

  • Composed of cells which very closely resemble the cell of origin

Poorly differentiated

  • Bear little resemblance to the cell of origin, but just enought for original cell type to be indentified

Undifferntiated/Anaplastic tumour

  • Composed of cells which are so undifferntiated that cell of origin is unknown
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21
Q

Benign vs Malignant tumours

A

Benign

  • Grow by expansion
  • Compress adjacent tissue
  • DO NOT infiltrate/spread

Malignant

  • Grow by expansion AND INFILTRATION
  • Compress and invade adjacent tissue
  • INFILTRATE
  • Can spread to different sites = metastasis
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22
Q

Define Adenomas

A

Tumour of glandular epithelium

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23
Q

Define Papilloma

A

Tumour of squamous and transitional epithelium

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24
Q

Define Carcinoma

A

A malignant epithelial tumour

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25
Q

Suffix for benign mesenchymal tumuors

A
  • OMA
    e. g. osteoma, lipoma
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26
Q

Suffix for malignant mesenchymal tumours

A
  • OSARCOMA
    e. g. osteosarcoma

Liposarcoma

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27
Q

Define Teratomas

A

Tumours derived from ferm cells, containin representatives from all 3 germ layers

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28
Q

Difference in benign tumour growth in solid organs vs epithleium

A

Solid organs

Expand, compress adjacent tissue. Look circumscribed and give a spherical mass

Epithelial surfaces

Form papillary outgrowths in directino of least resistance=papilomas

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29
Q

Cytological characteristics of malignancy

A
  • High nucleus to cytoplasm ratio
  • Pleomorphism
  • Nuclear hyperchromatism
  • High mitotic count
  • Abnormal mitoses
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30
Q

Cellular vs nuclear pleomorphism

A

Variation in size/shape of tumour cells

vs

Variation in size/shape of nuclei in tumour cells

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31
Q

What is a high mitotic count

A

Increasednumbers of cells in mitosis, including abnormal mitotic forms

Indicative of malignancy

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32
Q

Define Dysplasia and its causes

A

Abornam cell structure, due to:

  • Loss of differntiation
  • Pleomorphism
  • Nuclerar hyperchromatism
  • High nucleus/cytoplasm ratio
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33
Q

Carcinoma in-situ

A

A dysplastic epithelium showing cytological characteristics of malignancy but no evidence of invasion

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34
Q

Modes od spreak for malignant tumours

A

Lymphatics, transported to node, can proliferate within nodes

Blood stream, Clumps break off and enter circulation, can cause tumour embolisms and procue a distant metastasis

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35
Q

Effects/problems from benign tumours

A

Not alway harmless, can cause illnes and death by:

  • Bleeding e.g. gut, bladder
  • Pressure on adjacent vital structures e.g. in brain
  • Obstruction e.g. in brain, bronchus
  • Hormone secretion e.g. pituitary adenoma
  • Conversion to malignant tumour
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36
Q

3 Tumour markers

A

HCG

AFP

PSA

37
Q

What is the tumour marker HCG indicative of

A

From tumour cells with trophoblast elements

38
Q

What is the tumour marker alpha feotprotein idicative of?

A

Liver cancer, germ cell tumours

39
Q

What is tumour marker PSA indicative of

A

Prostate-specific antigen from carcinoma of prostate

40
Q

How are tumours graded?

A
  • The degree of differntiation of tumour cells realtive to normal tissue of origin
  • Cariation in size and shape of constituent cells of the tumour (pleomrophism)
  • The proportion of cells containing mitotic figures (mitotic index)
41
Q

What is considered in TNM staging

A

Tumour Nodes Metasteses

  • Based upon extent of local tumour spread, regional lymph node involvment and presence of distant metasteces
42
Q

Which staging system is used in colorectal cancers?

A

Dukes staging for colorectal cancers

43
Q

Describe stages in Dukes staging

A

A: Any tumour which does not extend beyond muscularis propria. no nodal ivolvment

B: Tumour extends beyond muscle. no nodal involvment

C: Any dpeth of tumour, present in nodes

44
Q

Tumours with excellent prognosis

45
Q

Tumours with moderate prognosis

A

Kidney, prostate, cervix, breast

46
Q

Tumours with poor prognosis

A

Pancreas, brain, oesophagus

47
Q

Define Generation time

A

Time it takes for acell to double its contents(population doubles in size)

48
Q

Components involves in control of cell cycle/proliferation

A
  • CDKs
  • Checkpoints
  • Intrinsic proteins
  • Tumour supressors
49
Q

Role of CDKs in cell cycle

A

Have to be bound to cycline for active kinase effect

Activation causes progression in cell cycle

50
Q

Role of Intrisic proteins in cell-cycle control

A
  1. Normal: proto-Oncogenes
    • Positive regulators of cell cycle
    • Promote growth
  2. Abnormal: oncogenes
    • ​​mutated/upregulated
    • No longer wait fro activating signal
51
Q

Role of tumour supressors in contorlling cell cycle/proliferation

A

Normal: Prevent progression of cell cycle if there are problems with DNA

52
Q

Mode of action fro Tumour supressor pRB

A

Workst at START checkpoint

53
Q

Mode of action for tumour supressor p53

A
  • Works at p53
    • START checkpoint
    • G/M checkpoint
      • Detects DNA damage
      • Perharps repariable(separate pthway)
      • Extenseive damage; Bax stimulated; apoptosis
  • Only active if theres a fault
  • Transient, removed once repair completed
54
Q

Pathway activated if repairable damge recognised by P53 in G/M checkpoint

A
  1. Stimulates p21 CKI
  2. Inhibits cyclin E/cdk2
  3. Cells arrests at G1/S or G2
  4. Gives cell an opportunity to repair DNA/progress to apoptosis
55
Q

What causes Cells to stay in G0

A

Proliferation inhibited

Maintained by TGF-b

56
Q

How do G0 cells re-enter cell cycle

A
  • Need growth factors e.g. PDGF or fibroblast growth factors

In 3 stages

  1. Competency: Immediate early genes
    • C-jun
    • C-fos/C-myc: Increase cyclin D1 expression, and decrease degredation
  2. Re-entry: Delayed response genes
    • E2F
    • Cyclin D-CDK4/CDK6, allows progression past START
  3. Progression
57
Q

What is monitored at G1/S

A

Size

DNA integrity

58
Q

What is monitored at START/restriction point

A

Favourable enviroment?

Mediated by: pRB & p53

59
Q

CDK complex involved in S phase

A

Cyclin A-CDK2

7.5hrs

60
Q

CDK complexes involved in G2

A

cyclin A-CDK1

cyclin B-CDK1

61
Q

What is monitored at G2/M point

A

DNA synthesis, succesful?

Meidated by P53

62
Q

CDK complexes involved in M phase

A

Cyclin A-CDK1

Cyclin B-CDK1

  • Peaks, then has to be completely eradicated to exit M phase
    • Degradede by proteolysis at M/A poin
63
Q

What is monitored at M/A checkpoint?

A

Spindle formation

65
Q

Which mutations cause gain of function

A
  • Overexpression: amplification/regulatory regions change
  • Point mutations/fusions
66
Q

Which mutations cause loss-of function

A

Point mutation, deletion(frameshift), loss of allele

67
Q

Difference between sporadic and familial retinoblastoma

A

Sporadic is unilateral

Familial is bilateral

68
Q

Inheritence pattern of retinoblastoma

A

Autosomal Dominant

69
Q

2-hit hypothesis

A
  • Familial tumours due to a single random somatic event
  • Sporadic tumors require two random somatic events
70
Q

2-hit hypothesis for retinoblastoma

A
  • Phenotype of Rb allele is dominant at the level of the whole organism, one hit
  • However - The phenotype of mutant allele is recessive at cellular level, requirst two hits
    • Characteristic of TS genes
71
Q

Explain how TS genes are associated with loss of heterozygosity in tumours

72
Q

How do the tumour supressors Rb and P53 act? Cell cycle checkpoints

73
Q

What happens in loss of TS function

A

Normal: TS porteins detect errors, mediate repair, inhibit replaication or initiate apoptosis

Cancer: Loss of TS function means errors not repaired but cell continues to proliferate

74
Q

Prevelance of oncogene mutations in familial cancers

A

Generally, mutant ocogenes cannot be tolerated in germ line - their action would be dominant

  • Disrupt normal embryonic development
75
Q

Eaxmple of a deletion oncogene mutation

A

ErbB: the EGFR with its external domain deleted

76
Q

Example of point mutation oncogene mutation

A

EGFR - Actiavte kinase activity in non-small cell lung cancer

77
Q

How do translocational oncogene mutations work?

78
Q

Example of oncogene mutation by translocation to an actively transcribing region

79
Q

How does an amplificiation mutation of oncogen work

A

Tumours end up containing many copies of said gene(100-150 copies)

e.g. Myc in neuroblastoma

80
Q

how do carcinogens cause mutations?

A
  • Reaction with free radicals
  • Mechanisms of mutation, adducts, cross links breaks etc
    • Increase rate of mutation, DNA breaks or base chnges
81
Q

Li-Fraumeni inheritance and mutation

A
  • Autosomal dominant inheritance
  • High suceptibility to cancers from early age
  • Mutations in TP53: Another tumout supressor gene that codes for P53
82
Q

Lifetime risk of breast cancer with BRCA1/BRCA1 genes

83
Q

Age groups screened for:

Breast

Colon

Prostate

Cervical

A

Breast: 47-73

Colon: 60-74

Prostate: 50+

Cervical: 25-65

84
Q

Different screening methods for bowel cancer

A
  • Foecal occult blood test
  • Colonospy, 4-5x more polyps detected than FOBT
85
Q

Mechanisms by which cancer therapies can exert their impact

86
Q

Ways by which chemotherapy work

87
Q

READ CLINICAL CANCER GENETIC LECTURE AND SELF STUDY ON CARCINOGENS

88
Q

Define lymphomas

A

Neoplastic proliferation of lymphoid cells of various types

89
Q

Two main categories of lymphomas

A

Hodgkin’s and

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