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Neoplasia 2 Flashcards

1
Q

What are the two components of tumours

A

Neoplastic cells that constitute the tumour parenchyma

Reactive stoma made up of connective tissue, blood vessels and cells of the adaptive innate immune system

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2
Q

What is a benign tumour that originates from squamous epithelium called

A

Papilloma

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3
Q

What is a benign tumour called that originates from glandular epithelium (salivary)

A

Adenoma

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4
Q

What is a malignant tumour that originates from the glandular epithelium called

A

Adenocarcinoma

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5
Q

What do epithelial tumours names end in

A

Oma or carcinoma

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6
Q

What do tumours of connective tissues names end in

A

Sarcoma

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7
Q

What is a malignant tumour from a lymphoid tissue called

A

Lymphoma

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8
Q

What is a malignant tumour from haemopoietic tissue called

A

Leukaemia

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9
Q

What is leukoplaskia

A

White patch that cannot be rubbed off or attributed to any other cause

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10
Q

Benign tumours have the potential to…

A

Become malignant

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11
Q

How do you find out if a benign tumour has the potential to become malignant

A

Take a biopsy and pathology labs can look for dysplasia

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12
Q

What can dysplasia effect

A

Various epithelial tissues

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13
Q

What is dysplasia identified by

A

Identified by changes in cells -
- appearance
- arrangement

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14
Q

Name some risks of oral cancer

A
  • tobacco
  • chewing habits
  • alcohol
  • diet and nutrition
  • oral hygiene
  • viruses
  • immunodeficiency
  • socioeconomic factors
  • GORD (acid reflux)
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15
Q

What viruses are associated with cervical cancer and oral cancer

A

HPV 16 and 18

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16
Q

What is carcinogens

A
  • benign tumours
  • malignant tumours - chemical agents, physical agents, viruses, may affect tissue directly or indirect effect on other tissues
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17
Q

What are the three stages for carcinogenesis

A
  • initiation
  • promotion
  • progression
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18
Q

Describe the initiation phase

A
  • when a carcinogen induces a genetic change resulting in neoplastic potential
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19
Q

What is promotion

A

Another factor stimulates the initiated cell for division (clonal proliferation) does not act on non-initiated cells for division

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20
Q

What is progression

A

Additional mutations resulting in malignancy

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21
Q

What are some chemical carcinogens

A
  • smoking polycyclic hydrocarbons including tars
  • diet, drugs and alcohol
  • asbestos
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22
Q

What are physical carcinogens

A
  • ionising radiation (damages DNA, causing mutations)
  • radioactive metals and gases
    Radium - bone and marrow tumours
23
Q

What is the least sensitive to radiation sensitivity

A

Muscle tissue and nerve tissue

24
Q

What is the most sensitive tissue to radiation

A
  • embryonic tissues
  • spleen, bone marrow
25
What type of carcinogen is UV light
Physical carcinogen
26
What are viral carcinogens
- DNA viruses - RNA viruses
27
What are the two main factors in carcinogenesis
- genetic - enviromental
28
Name some important genes in carcinogenesis
- oncogenes - tumour suppressor genes - DNA repair genes - MiRNAs - chromosomal aberrations - epidemic mutations
29
What are oncogenes
Proto-oncogenes are normal genes which regulate cell division Abnormal variants are oncogenes They produce oncoproteins
30
What is the effect of oncogenes
- mutation - excess normal product - enhanced transcription
31
What is the function of tumour suppressor genes
Brakes They act to inhibit cell division and suppress growth Act as anti oncogenes - all require loss of both alleles - retinoblastoma gene
32
How many genes need to be knocked out/mutated for tumour suppressor genes and oncogenes
Oncogenes - 1 gene Tumour suppressor - 2 genes
33
What is P53
The guardian of the genome Acts just before the restriction point (cell cycle) 2 main functions in response to damaged DNA Often inactivated in cancer
34
What are the 2 ways p53 responds to damaged DNA
Stops and allows DNA repair Apoptosis
35
What is the action of HPV
Blocks p53 therefore mutated genes are carried on
36
Describe inherited cancer synodromes
- single mutant genes, often tumour suppressor genes - retinoblastoma, some colon cancers
37
Describe familial cancer
- family clusters - genes and pattern of inheritance not clear - breast, ovary and colon
38
What is defective DNA repair
- increased sensitivity to carcinogens and general increased cancer risk - xeroderma pigmentosum
39
What are the hallmarks of cancer
Ability to evade anti growth signals Provide their own growth signals Evading apoptosis Tissue invasion and metastatsis Limitless replicative potential Sustained antiogenesis
40
What are some modes of spreading for malignant tumours
- local spread - lymphatic spread - blood spread (haematogenous) - transcoelomic spread - intraepithelial spread
41
What is metasis
Spread of the malignant cells to distant organs for morning secondary tumours
42
What is the pattern of spread for carcinomas
- lympathic - blood (often later)
43
What is the pattern of spread for sarcomas
- blood (lymphatic spread rare)
44
Explain some predictable patterns of spread
- lung to local nodes, liver, bone and brain - tongue to neck nodes, later lung and spine
45
Explain the grade of the tumour
Biological nature of the tumor Histolopathology
46
Explain stage in tumours
Extent of the spread (clinical)
47
What does cancer staging provide
Describes the extent or severity of a persons cancer, knowing the stage helps for planning treatment and prognosis
48
Describe the clinical staging of oral cancer
TNM system is used for oral cancer T - tumour size N - lymph node involvement M - metastases
49
Immunotherapy
• • • Active immunisation.(HPV, Hep B) Reversal of immunosuppression Adopted cell transfer (ACT) Tumour- infiltrating lymphocytes (TILs) CAR T-cell therapy- haematological malignancies • Strengthening natural immune responses-research still needed.
50
Escape
Cells may acquire molecular changes such as: • Alter tumour antigen expression . Lack of T-cell recognition • Activation of immunoregulatory pathways leading to T-cell unresponsiveness and apoptosis. • Immunosuppressive factors eg. cytokines (TGF-β). Inhibit T-cell response
51
Elimination
Cell mediated immune response • Cytotoxic T-lymphocytes (CD8+) • Natural killer cells. First line of defence against tumour cells. • Macrophages. Mechanisms similar to anti-microbial killing. Immunodeficiency states can lead to an increased incidence of malignant tumours Elimination quickly moves to escape
52
How does the immune system recognise tumour cells
Tumour associated antigens (TAAs); neoantigens • Products of mutated genes • Overexpressed proteins (tyrosinase) • Viral proteins (HPV,EBV) • Oncofetal antigens (carcinoembryonic antigen) • Others
53
Grading involves histological assessment of
• Invasion into underlying tissue • Cellular atypia : abnormal mitotic activity, nuclear pleomorphism, differentiation, necrosis • Various methods – numerical grades (1,2,3 etc) – low, intermediate, high – degree of differentiation (squamous cell carcinoma)

Anatomy (13 decks)

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