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Cell Pathology > 3 - Cancer > Flashcards

3 - Cancer Flashcards

1
Q

Why is cancer important?

A
  • Socioeconomic problem

- A significant cause of morbidity and mortality worldwide

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2
Q

What is a tumour?

A

swelling, originally for inflammation

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3
Q

What is a neoplasm?

A

New growth - 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 the cessation of the stimuli which may have evoked the change

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4
Q

What are the 2 basic components of tumours?

A
  1. Proliferating neoplastic cells parenchyma

2. Supportive stroma

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5
Q

Naming tumours:

BENIGN

A

given suffix -oma to cell of origin

eg. Adenoma (epithelial derivative) Fibroma (mesenchymal derivative)

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6
Q

Naming tumours:

MALIGNANT

A
  • of epithelial origin are called carcinomas

- of mesenchymal origin are called sarcomas

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7
Q

What does dysplasia mean?

A

Literally – disordered growth, limited to epithelium

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8
Q

Features of dysplasia?

A
  • Loss of uniformity of individual cells
  • Loss of their architectural orientation
  • Mild to moderate dysplasia may revert to normal
  • Severe dysplasia aka carcinoma in situ
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9
Q

What does metaplasia mean?

A

Substitution of one mature cell type for another mature cell type more suited to the environment
The result of a chronic stimulus, when withdrawn may resolve to normal
Is adaptive, not premalignant
e.g. Smoking causes metaplasia of glandular bronchial epithelium to squamous epithelium

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10
Q

What does neoplasia mean?

A

the presence or formation of new, abnormal growth of tissue.

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11
Q

What are the 4 factors distinguishing benign and malignant tumours?

A
  1. differentiation and anaplasia
  2. rate of growth
  3. local invasion
  4. metastasis
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12
Q
  1. Differentiation and anaplasia
A

Refers to the extent to which the parenchymal cells resemble there normal counterparts

  • Benign tumours are well differentiated
  • Malignant tumours show various levels of differentiation (well, moderately, poorly)
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13
Q
  1. Differentiation and anaplasia (cont.)

What does anaplasia mean?

A

Lack of differentiation.
Characterised by marked pleomorphism, hyperchromasia, large nuclei, nucleolation, irregularity of nuclear membrane, mitotic activity (the cytological features of malignant cells)

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14
Q
  1. Rate of growth
A

Generally the rate of growth of tumours correlates with the level of differentiation

  • Benign tumours grow slowly
  • Malignant tumours grow more rapidly
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15
Q
  1. Local invasion
A
  • Most benign tumours grow as cohesive expansile masses that remain localised to their site of origin (encapsulated)
  • Malignant tumours infiltrate and destroy the surrounding tissue, poorly demarcated
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16
Q
  1. Metastasis
A
  • Unequivocal evidence of malignancy
  • Formation of discontinuous tumour implants at a distance from the main tumour mass
  • With 2 exceptions, all malignant tumours can metastasise (gliomas and basal cell carcinomas)
  • Approximately 30% patients present with metastasis
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17
Q

What are the 3 pathways of spread?

A
  1. Direct seeding of body cavities and surfaces (peritoneal, pleural, pericardial, subarachnoid, joint).
  2. Lymphatic spread (most common route for carcinomas initially) along natural lymphatic drainage
  3. Hematogenous (typical of sarcomas also by carcinomas later)
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18
Q
  1. Seeding of body cavities
A

Most commonly from ovarian carcinomas which may cake the peritoneal surface.

Also spread of lung carcinoma into pleural cavity

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19
Q
  1. Lymphatic spread
A
  • Regional nodes drain tumours (i.e.. axillary then infraclavicular and supraclavicular from UOQ breast carcinomas)
  • Nodes may contain the spread locally
  • Evoke an immune response which causes nodal hyperplasia
  • Not every enlarged node in the region of a tumour contains metastatic spread
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20
Q
  1. Hematogenous spread
A
  • Veins penetrated more frequently than arteries due to thickness of walls
  • Liver and lungs are most common sites due to venous drainage
  • Renal cell carcinoma can grow within the renal vein to the IVC and into the right atrium
21
Q

How does the staging of cancer work??

A 
CLINICAL e.g. TNM stage but also FIGO for ovarian cancer and Ann Arbour for Hodgkins lymphoma
based on 3 factors:
-Size of the primary lesion
-Spread to regional lymph nodes
-Presence of metastases
22
Q

What is the TNM phase?

A

T – Primary Tumour size (T1-T4)
N – Nodal status (N0 or N1, 2, 3)
M – Presence of Metastasis (M0 or M1, 2)

23
Q

How does the grading of cancer work?

A

Histological
Based on the degree of differentiation and on the numbers of mitoses
Less useful than staging

24
Q

Cancer epidemiology factors…

A

AGE - Incidence of cancer increasing overall as the world’s population lives longer. In general, the incidence rises > 55 years
GEOGRAPHY - stomach cancer higher in Japan ct USA, melanoma higher in NZ ct Iceland

25
Q

Environmental agents…

A

UV light, occupational agents, diet and weight, alcohol, smoking, infections notably viruses (HPV)

26
Q

Genetic factors…

A

For a large number of cancers there exist some hereditary predispositions (e.g. lung cancer mortality four times higher in non-smoking relatives of lung cancer patients ct controls)

27
Q

What are the 3 forms of hereditary cancer?

A
  1. Inherited autosomal dominant cancer syndromes
  2. Familial cancers
  3. Autosomal recessive syndromes of defective DNA repair
28
Q
  1. Inherited autosomal dominant cancer syndromes

EXAMPLES

A 
Familial retinoblastoma
Familial adenomatous polyposis coli
MEN
NF 1 and 2
Von Hippel Lindau syndrome
29
Q
  1. Familial cancers

EXAMPLES

A

Breast cancer
Ovarian cancer
Colonic cancer

30
Q
  1. Autosomal recessive syndromes of defective DNA repair

EXAMPLES

A

Xeroderma pigmentosa
Ataxia telangectasia
Bloom syndrome
Fanconi anaemia

31
Q

Inherited cancer syndromes

A

Inheritance of a single mutant gene greatly increases the risk of developing cancer
Inherited retinoblastoma carriers have a 10,000 fold increased risk of developing retinoblastoma (usually bilateral)
FAP 100% get colonic carcinoma by age 50

32
Q

Molecular basis of cancer?

A

The genetic hypothesis of cancer implies that a tumour mass results from the monoclonal expansion of a single progenitor cell
Subsequently additional mutations allow progression and account for heterogeneity

33
Q

What are the targets of genetic damage?

A
  1. Growth promoting genes – Oncogenes
  2. Growth inhibiting (tumour suppressor) – Anti-oncogenes
  3. Genes regulating programmed cell death – Apoptosis
  4. DNA repair genes
34
Q

What are oncogenes?

A

Derived from proto-oncogenes, genes regulating normal cellular growth

35
Q

Examples of oncogenes associated with tumours?

A
  • myc Burkitt lymphoma
  • N-myc Neuroblastoma
  • cyclinD1 Mantle cell lymphoma
36
Q

What do cancer (tumour) suppressor genes do?

EXAMPLES

A

These genes usually regulate normal cell growth.
EXAMPLES
- Rb gene (13q)in genetically inherited retinoblastoma (40%) Development of this tumour requires “two hits” i.e. inheritance of a mutated copy of one Rb gene followed by acquisition of damage to the remaining copy, leading to cancer
- p53 (chromosome 17) 50% of all human tumours contain mutations in this gene. Its function is to prevent genetically damaged cells from replicating “housekeeper of the genome”
- BRCA-1 and BRCA-2 (chromosome 13q) 5-10% of breast cancer are familial and mutations in one of these genes is present in 80% of those cancers

37
Q

Genes regulating apoptosis?

A
  • bcl-2 prevents programmed cell death
  • over expression of bcl-2 and prevention of apoptosis results in indolent growth of lymphocytes found in many low grade lymphomas
38
Q

What is a carcinogen?

A

Agents that cause genetic damage and induce neoplastic transformation of cells

39
Q

3 categories of carcinogen?

A

Chemicals
Radiation
Microbial agents (mainly viruses)

40
Q

Chemical carcinogens - types

A

Carcinogenesis is a multistep process:
Some chemicals are inducers (permanent DNA damage)
Others are promoters (reversible DNA damage)
Neither step alone is sufficient to cause cancer

41
Q

Chemical carcinogens -

Direct Acting Agents

A

Do not require metabolism for activation

  • Dimethyl sulphate
  • Diepoxybutane
  • Cyclophosphamide, chlorambucil, nitrosoureas and other anticancer drugs
42
Q

Chemical carcinogens -

Procarcinogens

A

Require metabolism for activation

  • Beta napthylamine
  • Benzidine
  • Aflatoxin B1 (grains and peanuts)
  • Betel nuts
  • Vinyl chloride
  • Insecticides, fungicides
43
Q

Chemical carcinogens -

Promoters

A 
Hormones (e.g. oestrogen)
Drugs
Phenols
Bile salts
Fat in diet
44
Q

Radiation carcinogens

A
  • Ultraviolet (SCC, BCC, MM)
  • Ionising electromagnetic i.e. X-rays
  • Cause an increase in leukaemia and solid tumours
45
Q

Microbial carcinogens

A
  • DNA oncogenic viruses HPV, EBV, HBV and HHSV8
  • RNA viruses HTLV-1
  • Bacterial carcinogens; Helicobacter Pylori
46
Q

Cancer diagnosis -

Laboratory methods.

A 
Cytology FNA (freehand or USS guided)
Histology (core biopsy, incisional or excisional biopsy)
47
Q

Additional methods to diagnose cancer?

A 
Tumour typing
Immunocyto/histochemistry
Flow cytometry
Molecular methods (PCR, FISH)
48
Q

What are the clinical effects of tumours?

A

Both benign and malignant tumours affect the host
Anxiety (breast lumps)
General (pressure, ulceration, infection, bleeding, hormonal effects)
Metabolic cancer cachexia (increased BMR, reduced fat and muscle bulk) TNFα

Cell Pathology (5 decks)

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