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Anatomy > Neoplasia 2 > Flashcards

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
Q

What type of carcinogen is UV light

A

Physical carcinogen

26
Q

What are viral carcinogens

A
  • DNA viruses
  • RNA viruses
27
Q

What are the two main factors in carcinogenesis

A
  • genetic
  • enviromental
28
Q

Name some important genes in carcinogenesis

A
  • oncogenes
  • tumour suppressor genes
  • DNA repair genes
  • MiRNAs
  • chromosomal aberrations
  • epidemic mutations
29
Q

What are oncogenes

A

Proto-oncogenes are normal genes which regulate cell division

Abnormal variants are oncogenes
They produce oncoproteins

30
Q

What is the effect of oncogenes

A
  • mutation
  • excess normal product
  • enhanced transcription
31
Q

What is the function of tumour suppressor genes

A

Brakes

They act to inhibit cell division and suppress growth
Act as anti oncogenes
- all require loss of both alleles
- retinoblastoma gene

32
Q

How many genes need to be knocked out/mutated for tumour suppressor genes and oncogenes

A

Oncogenes - 1 gene

Tumour suppressor - 2 genes

33
Q

What is P53

A

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
Q

What are the 2 ways p53 responds to damaged DNA

A

Stops and allows DNA repair
Apoptosis

35
Q

What is the action of HPV

A

Blocks p53 therefore mutated genes are carried on

36
Q

Describe inherited cancer synodromes

A
  • single mutant genes, often tumour suppressor genes
  • retinoblastoma, some colon cancers
37
Q

Describe familial cancer

A
  • family clusters
  • genes and pattern of inheritance not clear
  • breast, ovary and colon
38
Q

What is defective DNA repair

A
  • increased sensitivity to carcinogens and general increased cancer risk
  • xeroderma pigmentosum
39
Q

What are the hallmarks of cancer

A

Ability to evade anti growth signals
Provide their own growth signals
Evading apoptosis
Tissue invasion and metastatsis
Limitless replicative potential
Sustained antiogenesis

40
Q

What are some modes of spreading for malignant tumours

A
  • local spread
  • lymphatic spread
  • blood spread (haematogenous)
  • transcoelomic spread
  • intraepithelial spread
41
Q

What is metasis

A

Spread of the malignant cells to distant organs for morning secondary tumours

42
Q

What is the pattern of spread for carcinomas

A
  • lympathic
  • blood (often later)
43
Q

What is the pattern of spread for sarcomas

A
  • blood (lymphatic spread rare)
44
Q

Explain some predictable patterns of spread

A
  • lung to local nodes, liver, bone and brain
  • tongue to neck nodes, later lung and spine
45
Q

Explain the grade of the tumour

A

Biological nature of the tumor
Histolopathology

46
Q

Explain stage in tumours

A

Extent of the spread (clinical)

47
Q

What does cancer staging provide

A

Describes the extent or severity of a persons cancer, knowing the stage helps for planning treatment and prognosis

48
Q

Describe the clinical staging of oral cancer

A

TNM system is used for oral cancer
T - tumour size
N - lymph node involvement
M - metastases

49
Q

Immunotherapy

A

• • •
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
Q

Escape

A

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
Q

Elimination

A

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
Q

How does the immune system recognise tumour cells

A

Tumour associated antigens (TAAs); neoantigens
• Products of mutated genes
• Overexpressed proteins (tyrosinase)
• Viral proteins (HPV,EBV)
• Oncofetal antigens (carcinoembryonic antigen)
• Others

53
Q

Grading involves histological assessment of

A

• 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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