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Cancer Biology > An introduction to Cancer (Pathology) > Flashcards

An introduction to Cancer (Pathology) Flashcards

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1
Q

How many people get some form of cancer?

A

1 in 3

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2
Q

What is the disease definition of cancer?

A

A group of diseases which share certain biological and pathological features

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3
Q

Define neoplasm

A

Abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissues, and persists in the same excessive manner after cessation of the stimuli that evoked the change

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4
Q

What are the signs of breast cancer?

A

Nipple is indrawn
Swelling under the nipple
Hard lump (due to the connective tissue in the tumour)

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5
Q

What does an CRC look like?

A

It arises from the lining of the colon

Big lesion which oozes blood

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6
Q

What does advanced colon cancer look like?

A

The muscle coat is destroyed
There is white tissue which is the invading tissue
Doesn’t go into the lumen, invades into the wall

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7
Q

What does oestosarcoma of the femur cause?

A

Destruction of the hard cortical bone and this leads into the thigh muscle

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8
Q

Phenotype of melanoma

A

melanocytes darken and are ~1cm

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9
Q

Issue with liposarcoma

A

They can grow for years before they show a phenotype and it is very reoccuring

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10
Q

What is atrophy?

A

Cell loss > cell growth

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11
Q

How do tumour cells overcome the inability for oxygen to disease into the cell when they get to big?

A

When they undergo hypoxia they release stress signals and this causes the production of further vascular formation so that they are able to receive oxygen

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12
Q

What is the structure of a normal cell wall?

A

Mucosa at the top
Smooth muscle in the middle
A muscle coat at the bottom

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13
Q

How does stomach cancer metastasise?

A

There are glands which invade from the stomach outwards and drop into the paritoneal cavity
This commonly forms gastric or ovarian cancer

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14
Q

How are daughter cells of cancer different from their parents?

A

They have 3 identical spindles instead of 2 so they are unable to be identical to their parent

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15
Q

How can you distinguish mitotically active nuclei of cells on histology?

A

Their size and shape vary

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16
Q

What is an aneuploid population?

A

A group of cells who all have a different number of chromosomes

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17
Q

What chromosomes are associated with B-cell lymphoma?

A

Chromosome 11 is translocated onto chromosome 14

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18
Q

What is an adenoma?

A

Improper proliferation of the epithelial cells - they do not invade outwit the epithelial

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19
Q

What is dysplasia?

A

A preinvasive stage in a developing cancer

20
Q

Process to develop an invasive tumour

A

Normal cell -> Initial event -> Early dysplasia -> Severe dysplasia -> Invasive malignancy

21
Q

Phenotype of dysplasia

A

The nuclei are bigger
The cells are bigger in general
The cells are crowded

22
Q

2 forms of single cell movement

A

Mesenchymal migration

Amboeboid movement

23
Q

What is mesenchymal migration?

A

Proteolysis/ traction

24
Q

What is amboeboid movement?

A

Propulsion/ utilise defects

25
Q

How do groups of cells migrate?

A
  • Require cell-cell adhesion and communication
  • Predominates in well differentiated carcinomas
  • Inner cells protected from immunological assault
  • High levels of autocrine pro-migratory factors and of proteolytic enzymes
  • Heterogeneous sets of cells invade together
26
Q

Mechanisms cancer cells use to invade

A

Autocrine
Paracrine
Chemotactic factors
Proteolytic factors - degrade the connective tissue
Adhesion molecules - can pull themselves through

27
Q

How can epigenetic factors effect cancer formation?

A

Histone modification and DNA methylation
Global hypomethylation
Tumour suppressors can be silenced by hypermethylation

28
Q

What carcinogen can induce head and neck cancer?

A

Human papilloma virus

29
Q

How does p53 regulate angiogenesis?

A

Represses VEGF and stimulates thrombospondin-1 expression

30
Q

How doe ras and myc influence angiogenesis?

A

Stimulates VEGF production -> increase angiogensis

31
Q

What is poor differentiation associated with?

A

A bad prognosis

32
Q

What is the grading scale for differentiation?

A

1 - well differentiation
2 - moderately differentiated
3 - poor differentiation

33
Q

How many doublings have to occur for a cancer to be clinically detectable?

A

30

34
Q

How many doubling have to occur for the cancer to turn into an advanced cancer?

A

40

35
Q

Where do primary CNS tumours spread to?

A

They stay within the CNS

36
Q

What route do carcinomas favour to metastasise?

A

The lymphatic route

37
Q

What route do sarcomas favour to metastasise?

A

haematogenous route

38
Q

What therapy targets Her2 in breast cancer?

A

Trastuzumab

39
Q

What is the issue with Her2 inhibitors?

A

Expensive

Only help a minority of patients

40
Q

What cancers are associated with Epstein Barr virus (EBV)?

A

Lymphoma - usually high grade B cell

41
Q

How do viral infections promote cancer?

A
  • Stimulates increased proliferation
  • Generates proteins which inhibit tumour suppressor function
  • Integration into viral DNA
42
Q

How do tumour cells evade the immune system?

A 
Selection for less antigenic clones 
Reduce expression of MHCI 
Reduce expression of co-stimulatory molecules 
Immunosuppression 
Antigen masking 
Expression of FasL
43
Q

How do tumour cells cause immunosuppression?

A

Oncogenic agents e.g. radiation and chemicals
Tumour products e.g. TGF-beta
Immune/ inflammatory responses e.g. IL-10 suppresses T cells

44
Q

How does tumour cells cause antigen masking?

A

They produce mucopolysaccharides

45
Q

How does FasL expression evade the immune system?

A

Will stimulate apoptosis in T cells which express Fas

Cancer Biology (13 decks)

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