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CLS > Cancer > Flashcards

Cancer Flashcards

1
Q

Define neoplasia

A

Abnormal mass of tissue, growth exceeds that of normal tissue, which persists in same excessive manner after the cessation of the stimulus which has evoked the change

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2
Q

Describe hyperplasia

A

Abnormal increase in no of normal cells in normal arrangement of tissue/organ which stops growing when the stimulus is removed

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3
Q

Define anaplasia/undifferentiation

A

Loss of differentiation of cells so cells of origin are unknown

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4
Q

Define tumour differentiation

A

Description of how alike cancer cells are to normal cells- helpful in predicting how tumour will behave
Cells well diff and resemble tissue of organ- better prognosis

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5
Q

Histogenesis

A

Identification by cell or tissue of origin

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6
Q

Describe benign tumours

A

Don’t infiltrate other tissues

Not always harmless- brain- increase intra cranial pressure

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7
Q

Describe malignant tumoura

A

Tumours can infiltrate and invade adjacent tissue and spread (via lymph and blood) to distant sites forming separate metastases-invasive and destructive behaviour
Potentially fatal

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8
Q

Describe epithelial tumours

A

Epi tumours- common due to high turnover rate and exposure to outside environment- GI, resp tract cells

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9
Q

Define adenomas

A

Tumour of glandular epithelium eg colonic/thyroid

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10
Q

Define papillomas

A

Tumour of squamous and transitional epi eg

squamous cell, transitional cell

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11
Q

List the main mesenchymal tissues

clue: suffix- osarcoma

A 
Osteoma- bone
Lipoma- adipose tissue
Chondrosarcoma- cartilage
Leiomyosarcoma- smooth muscle
Rhabdomyosarcoma- striated muscle
Fibroma- fibroblasts
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12
Q

List tumours that don’t follow rules

A 
Germ cell tumours- from germ cells in ovaries and testes
Teratomas- from germ
cells- 3 germ layers
Lymphoma
Glioma
Melanoma- melanocytes
Embryonal tumours
Leukemia- haemopoeitic cells in bm
Neuroendocrine tumours
Hodgkin's
Kaposi's 
Wilm's
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13
Q

Define cellular pleomorphism

A

Variation in size/shape of tumour cell

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14
Q

Define nuclear pleomorphism

A

Variation in size/shape of nuclei of tumour cells

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15
Q

Define nuclear hyperchromatism

A

Dark staining nuclei due to an increase in nuclear DNA

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16
Q

Define high mitotic count

A

Increase of no cells in mitosis, including abnormal mitotic forms

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17
Q

Define dysplasia

A

Abnormal cell structure due to the above

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18
Q

Define carcinoma in situ

A

Dysplasia in an epithelium without invasion across the epi basement membrane

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19
Q

List 6 criteria of a malignant tumour

A 
High mitotic count
High nucleus to cytoplasm ratio
Nuclear hyperchromatism
nuclear/cellular pleomorphism
Abnormal mitoses
Diff varies
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20
Q

Outline the role of dysplasia and carcinoma in situ in malignancy

A

Dysplasia in tumour cells- invasive behaviour
Dysplasia in epi without invasion- CIS
CIS assoc with hi grade dyplasia and many forms of invasive carcinoma originate from CIS
cancer precursor

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21
Q

List the main routes of metastatic spread in malignant tumours

A

Blood stream
Lymphatics
Serosal surfaces

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22
Q

Describe lymphatic spread of malignant tumours

A

MT invades lumen of lymph vessel, bits break off and pass to LN draining the area
Become trapped in subscapular sinus, tumours prolif until whole LN is replaced by tumour

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23
Q

Describe the bloodstream spread of malignant tumours

A

Tumour invades wall of small vessel-caps and small veins
Clumps of tumour cells break off, move in circ until meet vessel too small to pass through
Grow- distant metastases
Common sites- liver, brain, CSF, lungs, adrenals and bone
ALSO SEROSAL SURFACES

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24
Q

Bad effects of benign tumours

A
  • bleeding eg gut, bladder
  • pressure on adjacent vital structures eg in brain
  • obstruction eg in brain, bronchus
  • hormone secretion eg pituitary adenoma
  • conversion to a malignant tumour
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25
Q

How do malignant tumours cause death

A

Non metastatic effects

Cachexia

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26
Q

List the main techniques used in the investigation and diagnosis of tumours

A

S&S- clinical history, exam
Imaging- CT, MRI, Xray
Tumour markers- Substances liberated by tumours detected in body fluids
Biopsy- fix in Formalin- histology staining and immunucytochemistry
Glutaraldehyde- electron microscopy
Send fresh for cytogenetics or tumour genetics
Smear- diagnostic cytology, exam of cell in tissue fluid/exfoliated from surface

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27
Q

Define tumour stage

A

Description how much cancer has spread
takes into account size, degree of local penetration, regional lymphatics, spread by distant metastases
Important indicator of prognosis and treatment

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28
Q

Two clinical examples of tumour stage

A

Breast cancer- TMN- tumour, node metastases
Duke’s staging for colorectal cancer
A- in muscles more than 90% survival for 5 years
B through muscles 70%
C nodes involved 30%

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29
Q

Define the tumour grade and outline how this is determined in practice

A

Degree of differentiation of tumour cells, relative to normal tissue of origin
Assessed by mitotic indiex and plemorphism

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30
Q

Give 3 examples of tumour markers

A

HCG- tumours with trophoblast elements
AFP- liver, cell tumours
PSA- prostate specific antigen- prostate carcinomas

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31
Q

List the main modes of therapy for tumours

A

Radiotherapy
Chemotherapy
Surgery
Multimodal therapy

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32
Q

Outline the main cellular targets for tumour therapy

A

EGF receptors

Herceptin targets these receptors in breast cancer

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33
Q

Give examples of tumours with good prognosis

A

Thyroid

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34
Q

Give examples of tumours with moderate prognosis

A

Kidney, prostate, cervix, breast

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35
Q

Give examples of tumours with poor prognosis

A

Pancreas, brain, oesophagus

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36
Q

What is cancer?

A

Disease caused by uncontrollable division of abnormal cells in a part of the body

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37
Q

What sort of mutations cause cancer?

A

Somatic

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38
Q

What are familial syndromes?

A

Pts inherit predisposition to cancer

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39
Q

Describe the features that define a cancer cell

A 
Proliferation- grow w/o signals
Immortality- avoid senescence/telomere shortening
Avoid cell death- apoptosis
Angiogenesis- must be fed
Metastasis- many activities needed
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40
Q

Describe the prinicipal of a multi hit, multi step cancer progression

A

Sequential mutations give cell clones a growth advantage

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41
Q

Define passenger and driver mutations

A

Passenger- not relevant to cancer

Driver- reg prolif, apop etc

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42
Q

List cell cycle checkpoints

A

Regulate progression through cell cycle

  1. Restriction point in G1
  2. DNA damage checkpoints in G1 and 2
  3. Metaphase checkpoint in M
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43
Q

Describe the phenomena of senescence and apoptosis

A

Limit no of times cell can divide
Senescence- cells in G0 don’t prolif
Apoptosis- programmed cell death in response to DNA damage, cell damage, stress
Restrict tumour growth, overcome in cancer

44
Q

Describe senescence

A

Metabolically active, irreversible inability to enter cell cycle
Normal cells reach Hayflick limit of proliferative capacity, stop dividing– senescnece
Cancers avoid this
Telomeres undergo shortening
Cells bypass if p53 is inactivated
Telomeres lost, chromose instability, sis chromatids fuse, torn apart at anaphase
Cells undergo apoptosis

45
Q

Describe TERT

A

In cancer, rare cell reactivates TERT to become cancerous

Most cancers have activating mutations in the TERT gene promoter

46
Q

Describe how cancer cells evade senescence

A

50 cell divisions, telomeres too short, p53 fails, continue shortening, chromosomes rearranged, TERT reactivated, cells continue to proliferate with severely damaged chromosomes

47
Q

Describe apoptosis

A

Avoids inflam using caspases
Triggered by cell damage/DNA stress/oncogene activation
p53 and RB control prolif, sen and apop

48
Q

Describe renewed angiogenesis

A

O2 and nutrients needed for survival
Tumours promote angiogenesis
- Hypoxia induced factor 1 alpha
- cancers produce VEGF- new vessel growth and endo precursor cells in bone marrow, travel to tumour
- Disorganised vasculature, imbalance of factors
- Leaky due to impaired cell/cell junctions

49
Q

Describe the main stages of tumour metastasis

A 
Cells grow as benign tumour in epi
Break through basal lamina
Invade capillary (1/1000 survive when travelling in bs)
Adhere to bv in liver
Escape from bv-extravasion
Proliferation-metastasis in liver

Invasion of leaky bv
Activated of endogenous metalloproteinases

50
Q

What causes loss of adhesion?

A

E cadherin

51
Q

List the two main ways that cell growth occurs

A

Individual level- change in mass/vol

Proliferation- increased cell no (population) via clonal generation, exponential binary fission

52
Q

List the main stages of the cell cycle

A

G1- increase in cell mass
S- 7.5 hours, semi conservative rep of DNA
G2- prolif- 3.5-4 hrs
Mitosis- 1 hour- genome sep into 2 groups for daughter cells
G1- continued prolif and decision to exit cell cycle- 10hrs
G0- quiescence, cell decides whether to go to cell cycle or not

53
Q

Describe the M checkpoint

A

Cell monitors spindle formation and kinetochore attachment

54
Q

Describe the G2/M checkpoint

A

Cell monitors size and correct copy of DNA

55
Q

Why do cells enter G0?

A

To differentiate and specialise into non proliferative cell types eg skeletal, SM, cardiac
- If limited resources
exponential growth- no competition, unlimited resources
sigmoid curve- stabilised by available resources and competition

56
Q

List the three stages of resuming the cell cycle

A

Competency
Re entry
Progression

57
Q

Describe a cell’s re entry back into the cell cycle

A 
PDGF and FGF stimulate TFs c-cos c-jun and c-myc. These are all competency factors and immediate early genes. (G1a)
TFs transcribe proteins CYCLIN D and EZE which stimulate the cell to go into re entry. 
(delayed response) (G1b)
progression factors (eg insulin) finally cause the cell to reenter G1
58
Q

Which cyclins are expressed where in the cell cycle

A

DE in G1 cdk 6 and 4
A in S cdk2
B in M and G2 cdk1

59
Q

What is the role of CDK1

What does its activity depend on

A

Regulate entry into mitosis

Association with cyclin B

60
Q

How is cdk1 destroyed?

A

By proteolysis (ubiquitination) during cell cycle, stops cell activity, allowing cell to exit mitosis and enter G1

61
Q

How is cdk1 regulated

A
  • By inhibitory phosphorylation of tyrosines 14 and 15 by wee1
  • And by partial activatory phosphorylation by CAK
  • Activity of CKI (cyclin dependent kinase inhibitors)
62
Q

Define oncogenes

A

Promote tumour formation, +ve reg of cell cycle
Many needed for normal progression and are proto oncogenes when normal
When no longer need signal to become activated- become oncogenic

63
Q

List some proto oncogenes and their viral version

A

c- Jun, c-myc, c-fos

V-fos, v-jun, v-myc

64
Q

What are the activators of oncogenes?

A

Mutation
Gene amplification
Translocation

65
Q

Define tumour supressor genes

A

Negative regulators of cell cycle, prevent progression

Usually TFs or regulators of TF eg pRB

66
Q

Where was pRB first identified?

What occurs to pRB in tumours?

A

Childhood cancer, initial changes occur in the retina- retinoblastoma
Mutated in nearly all cancers, inactivated/absent in more than half

67
Q

list the three checkpoints where the integrity of the genome is monitored?

A

G2/M- p53 activated- arrest. G1/S- environment favourable?
Metaphase/Anaphase- are all chroms central and attached to spindle
Trigger anaphase and proceed to cytokinesis

68
Q

Describe the meaning of proto oncogenes and tumour suppressor genes

A

Proto oncogenes- promote events leading to cancer reg prolif

Tumour suppressor- inhibit events events leading to cancer, reg prolif, immortality, apoptosis

69
Q

What type of mutations are associated with TS and PO?

A

TS- loss of function

PO- gain of function

70
Q

What are the main types of mutations associated with loss and gain of function?

A

Loss- point, deletion, frameshift, loss of allele
Gain- amplification, regulatory regions change
Point mutations, fusions, non silent changes in aa sequence
Fusions- telomere shortening- hybrid gene

71
Q

Name three familial syndromes and describe one in detail

2 hit hypothesis

A

Retinoblastoma- rare childhood tumour, thickening of optic nerve due to tumour extension
Tumour arises in precursors of photoreceptors
Treat by radiotherapy and surgery
Colon cancer
Breast cancer

Phenotype of mutant Rb id dominant at level of whole organism
Recessive at cellular level
Characteristic of TS genes

72
Q

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

A

Highly unlikely that both genes copies inactivated by two successive mutational events
2nd mutation- diff process with higher frequency
eg mitotic recombination
- LOH for region containing the Rb gene
- Cells lacking functional Rb, advantage

73
Q

How do TS Rb and p53 act?

A

Rb- G1/S- require growth signals to pass

p53- G1/S, G2/M

74
Q

What is true about familial cancer and oncogene mutations?

A

Oncogone mutations rarely associated with familial cancer
Not tolerated in germ line- dominant
Disrupt normal embryonic development

75
Q

List the two main causes of cancer

A

Carcinogens

Infectious agents

76
Q

List infectious agents and the cancers they cause

A
  1. H Pylori- cure with antibiotics- stomach cancer
  2. HepB virus- inflammation and genes- acute- hepatitis, chronic- liver cancer
  3. HPV- oncogenes E6 and E7- cervical cancer
    EBV- oncogene- glandular fever, nasopharyngeal cancer (with malaria)
  4. HIV- immune suppression- Kaposi’s sarcoma
77
Q

Other mechanisms that cause cancer

A

Inflammation- viruses, asbestos
Immune suppression- HIV
Food, chemicals
Intrinsic causes- tissue growth- kids, hormones- breast, prostate

78
Q

What is caused by a mutation in p53, breast cancer

A

p53- Li Faraumini syndrome

BRCA1, BRCA2- breast cancer

79
Q

List the current cancer screening programmes

A
  • Breast- X ray based mammography- carcinogenic
  • Cervical- pap smear, liquid based cytology
  • Colon- faecal occult blood test- use colonscopy- detects 4-5 more polyps/virtual/sigmoidoscopy
80
Q

List the main cancer treatment therapies

A

Surgery, radiotherapy, chemo
Targeted therapies

  • Radio- hi energy radiation targets tumour- fractionated/brachytherapy
  • Conformational radiotherapy- beams matched to same shape as tumour
81
Q

Describe mitotic catastrophe

A

Dividing cells initially survive, continue to progress through cell cycle despite breaks in DNA
Genome more damaged until due
Free radicals gen during therapy can also damage other components eg cell membrane proteins- trigger apoptosis

82
Q

Describe the use of chemotherapy

A

Target cancers you can’t see
Mitomycin- streptomyces- cross link DNA
Bleomycin- streptomyces- break DNA strands
Etopside- Mayapple- topoisomerase inhibitor
Vincristine- bind tubulin subunit, block division

83
Q

List some targeted therapies

A
  • Antibodies- herceptin, EGFR, breast cancer
  • Small mol inhibitors- Abl, leukemia, BRAF, melanomas
    Synthetic lethality
    Angiogenesis inhibitors
84
Q

Describe cancer prevention

A

Immunisation- HPV/hepatitis
Lifestyle- smoking, UV, processed meat
Prenatal genetic diagnosis

85
Q

How do tumours develops?

A

Imbalance between rate of cell division and cell death

Growth control mechanisms regulate this

86
Q

What are growth control mechanisms?

A

Levels of secreted growth factors/inhibitors
Environmental growth inhibitory factors
Intrinsic programme of diff/apoptosis
Tumour immune response

87
Q

Give an example of increased growth factor secretion

A

IGF2 upreg in Wilm’s tumour

88
Q

Give an example of upreg of growth factor receptor

A

cErbB2 (EGFR fam) upreg in breast cancer

89
Q

Give an example of activation of gf receptors

A

Mutation in TK domain of c-kit in GISTs

90
Q

Give an example of upreg of anti apoptotic factors

A

Bcl2 upreg in follicular lymphomas

91
Q

Give an example of loss of function of pro apoptotic factors

A

TP53 mutated in colorectal tumours

92
Q

Give an example of down reg of pro apoptotic factors

A

Caspase 3 down reg in colorectal tumours

93
Q

How can knowledge of these factors be used in clinical practice

A
  • Identify mutations characteristic of tumour type, use in diagnostic test
  • Identify genetic subgroups with a morphologically uniform group of tumours
  • Identify new prognostic factors eg n-myc in neuroblastoma
  • Identify mutations which predict response to specific treatments
  • Identify therapeutic targets
94
Q

Define chemical causatives and list 3

A

Chemicals grouped depending on mechanism by which they stimulate neoplasia

  • Genotoxic
  • Mitogenic
  • Cytotoxic
95
Q

Outline genotoxic causatives

A

Cause direct damage to DNA
Form adducts, abnormal segment of DNA bound to cancer causing chemicals- start carcinogenesis
Prone to damage in replication, some resistant to normal DNA repair mechanisms

96
Q

Outline mitogenic causatives

A

Not direct damage to DNA
bind to receptors in/on cell, stim cell division
eg SKIN CARCINOGENESIS- agents bind to protein kinase C- sustained epidermal hyperplasia

97
Q

Outline cytotoxic causatives

A

Produce tissue damage- hyperplasia, cycles of tissue regen and damage
Cytokines generated in response

98
Q

Describe the difference between direct and indirect agents

A

Direct- directly cause neoplasia eg cyt p450

Initiating agents- exposure doesn’t directly cause neo,promoting agents cause increased cell division

99
Q

Describe the role of the following in human tumours:

  • Polycyclic hydrocarbons
  • Aromatic amines
  • Nitrosamines
  • Alkylating agents
  • Diet and exercise
  • Infection
A

1- from tars, cig smoke– lung cancer

  1. from dyes/rubber–urothelial carcinoma
  2. from dietary nitrates–stomach/GI tract cancer
  3. from environ, chemo– mutagenic
  4. Viral- Slow/acute transforming- viral oncogene
100
Q

List examples of pre-neoplasia

A

Endometrial hyperplasia/epi of breast lobules/ducts
Chronic gastritis/colonitis
Hepatic cirrhosis
Chronic autoimmune diseases

101
Q

Define lymphoma and give a simple classification

A

Neoplastic proliferation of lymphoid cells of various types

  • HL and non HL
102
Q

List the types of Hodgkin’s Lymphoma

A

Nodular lymphocyte- good prognosis
Lymphocyte rich Hodgkin’s (GOOD)
Mixed cellularity Hodgkin’s (IN BETWEEN)
Nodular sclerosing Hodgkin’s (IN BETWEEN)
Lymphocyte-depleted Hodgkin’s (BAD)

103
Q

List features of Non Hodgkins Lymphoma

and define myeloma

A

Majority are malignant
B most common in adults- poor diff, high grade
T cell lymphomas affect skin

Tumour of mature plasma cells. Presents with bone tumours, osteolytic, painful

104
Q

Name three glial cells and the one that most commonly gives rise tu tumours

A

ASTROCYTOMAS- malignant, don’t metastasise
oligodendrocytes
ependymal ce;;s

105
Q

Define embryonal tumours and give two examples

A

EMBRYONAL TUMOURS are derived from embryonic remnants of primitive “blast’ tissue.
Nephroblastoma-Wilm’s of kidney
- Neuroblastoma- adrenal gland

106
Q

Define teratoma and give 2 examples

A

are tumours derived from primitive germ cells which retain the capacity to differentiate along all 3 primitive embryological lines

  • OVARY- young women- benign, cystic, cont keratin, skin hair, bronchial
  • TESTIS- young men, swelling, MALIGNANT, spread early via bs, lung liver, chemo,

CLS (11 decks)

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