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Immunity and Pathology 1 > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

What is a neoplasm?

A

An abnormal mass of tissue

Growth is unco-ordinated and exceeds that of normal tissues

Persists after removal of the stimuli that initiated the change

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2
Q

What is oncology?

A

study of malignant tumours

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3
Q

What kind of disorder is neoplasm?

A

genetic disorder of cell growth by acquired/inherited mutations affecting a single cell and its clonal progeny

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4
Q

What are the two clinical classifications of neoplasm?

A

benign
malignant

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5
Q

What are the histological classifications of neoplasm?

A

Growth can occur in

Epithelial – lining/covering/glandular tissue
Connective tissue
Other tissues

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6
Q

What is the growth pattern of benign tumours vs malignant tumours?

A

benign tumours expand, may be encapsulated and are localised

malignant tumours invade, have no capsule and metastasis

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7
Q

What is metastasis?

A

to travel to other organs and other sites in the body and form tumours there

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8
Q

What is the growth rate of benign vs malignant tumours?

A

benign = slow
malignant = fast but variable

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9
Q

What is the microscopic appearance of benign vs malignant tumours?

A

benign
resembles tissue of origin in differentiation
uniform cell/nuclear shape and size
few mitoses (dividing cells)

malignant
variable resemblance to tissue of origin
nuclear and cellular pleomorphism
many abnormal mitoses

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10
Q

What are the clinical presentations of benign vs malignant tumours?

A

benign
lump/pressure/obstruction depending on site and size
+/-hormone secretion
treat by local excision

malignant
local pressure
infiltration and destruction
distant metastases
+/-hormone secretion
local excision and chemotherapy or radiation if metastases present

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11
Q

What are the effects of benign tumours dependant on?

A

Depend on site, size and tumour

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12
Q

What happens if the tumour is in endocrine gland?

A

it can increase or decrease hormone dosage

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13
Q

What are the effects of benign tumours?

A

Palpable lump
Pressure
Obstruction
Function – esp hormone secretion

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14
Q

What is an example of a benign tumour?

A

Benign salivary gland tumour
pleomorphic adenoma

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15
Q

What is an example of a malignant tumour?

A

squamous cell carcinoma

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16
Q

What are the two components tumours are composed of?

A

neoplastic cells that make the parenchyma

stroma (connective tissue, blood vessels, lymphatic vessels, and nerves.)

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17
Q

What is a malignant type of squamous and glandular epithelium tumour?

A

squamous = squamous cell carcinoma
glandular = adenocarcinoma

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18
Q

What added to the end of a connective tissue word usually indicates if the tumour is malignant or benign

A

saroma = malignant
oma = benign

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19
Q

What are tissues that cannot form benign tumours usually?

A

lymphoid
haemopoietic (fluid blood)

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20
Q

What is a teratoma?

A

germ cell tumour (usually found benign in the ovaries)

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21
Q

What is a potentially malignant disorder found in the oral mucosa?

A

leukoplakia - white patch that cannot be rubbed off or attributed to any other cause

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22
Q

If the dysplasia occurs in epithelium, what usually occurs?

A

does not extend to underlying connective tissue such as lamina propria and submucosa

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23
Q

What is a type of glandular dysplasia?

A

barrets oesophagus

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24
Q

What are the causes of oral cancer?

A

tobacco
betal quid chewing
alcohol
diet + nutrition
oral hygiene
viruses (HPV)
immunodeficiency
socioeconmic factors
GORD

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25
Q

What types of hpv cause cancer?

A

HPV-16 + HPV-18

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26
Q

What types of cancer do HPV cause?

A

oropharyngeal
cervical

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27
Q

What carcinogens cause malignant tumours?

A

chemical
physical
viruses

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28
Q

What are the steps of the multi-step theory of carcinogenesis?

A

intiation
promotion
progression

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29
Q

What does each step include?

A

Initiation: When a carcinogen induces a genetic change resulting in a neoplastic potential.

Promotion: Another factor stimulates the initiated cell for division. (clonal proliferation). Does not act on non-initiated cells.

Progression; Additional mutations resulting in malignancy.

30
Q

What are driver mutations?

A

genes that build up during development of cancer and induce characteristics that are necessary for cancer cell development

31
Q

What are examples of chemical carcinogens?

A

smoking polycyclic hydrocarbons (tar)
diet, drugs, alcohol
asbestos

32
Q

What are physical carcinogens?

A

ionising radiation
UV light (natural, sunbeds)

33
Q

What does ionising radiation cause and what are types?

A

– damages DNA, causing mutations
– radioactive metals and gases

34
Q

What tumours can radium cause?

A

bone and bone marrow tumours

35
Q

What are the most sensitive tissues and what are the least sensistive tissues?

A

Most - embryonic tissues, haematopoietic organs (spleen, bone marrow)

Least - connective tissue, muscle tissue and nerve tissue

36
Q

What does UV light cause?

A

damage to DNA

37
Q

What are the viruse types that can cause cancer?

A
  • DNA viruses
    – more common
    – viral DNA inserted into host DNA
  • RNA viruses
    – reverse transcribed and then inserted
38
Q

What cancer does epistein-barr virus cause?

A

Burkitt’s lymphoma nasopharyngeal carcinoma

39
Q

What cancer does hepatatis B/C cause?

A

hepatocellular carcinoma

40
Q

What are the important genes in carcinogenesis?

A
  • Oncogenes (“accelerators”)
  • tumour suppressor genes (“brakes”)
  • DNA repair genes
  • miRNAs
  • Chromosomal aberrations
  • Epigenetic mutations
41
Q

What are proto-oncogenes?

A

normal genes which regulate cell divison

42
Q

What do proto-oncogenes control?

A

– growth factors
– growth factor receptors
– signal transducers
– control of gene expression

43
Q

What are abnormal versions of protoco-oncogenes called?

A

oncogenes
produce Onco-proteins

44
Q

What do onco-genes cause?

A

– mutation
* increases activity of product

– excess normal product
* duplication of the gene
* viral product

– enhanced transcription
* translocation
* chromosome rearrangement

45
Q

What do tumour suppressor genes do?

A

Act to inhibit cell division and suppress growth

46
Q

What are tumour suppressor genes described as?

A

anti-oncogenes

47
Q

What tumour suppressor gene is usually lost and what must happen to cause retinoblastoma cancer?

A

retinoblastoma gene (RB)
both alleles must be lost (Knudson’s “two-hit” hypothesis)

48
Q

What are functions of tp53? and where does it act?

A

acts just before the Restriction Point (cell cycle)

in response to damaged DNA

– stops the cell cycle to allow DNA repair
– apoptosis (if repair not possible)

49
Q

What are genetic susceptibilites to cancer and what are cancer examples of each?

A
  • inherited cancer syndromes
    – single mutant genes, often tumour suppressor genes
    – retinoblastoma, some colon cancers.
  • familial cancer
    – family clusters
    – gene(s) and pattern of inheritance not clear
    – breast, ovary, colon
  • defective DNA repair
    – increased sensitivity to carcinogens and general increased cancer risk
    – Xeroderma pigmentosum
50
Q

What are the effects of cancer on other mechanisms?

A
  • other cell division controls
  • DNA repair mechanisms
  • apoptosis inhibited
  • stimulation of blood vessel formation
  • destructive enzymes activated
  • cell motility increased
51
Q

What are the hallmarks of cancer?

A

tissue invasion/ metastasis
evading apoptosis
sustained angiogenesis
insensitivity to anti-growth signals
limitless replicative potential
self-sufficieny in growth signals

52
Q

What are the modes of spread of malignant tumours?

A
  • local spread
  • lymphatic spread
  • blood spread (haematogenous)
  • transcoelomic spread (through cavity)
  • Intraepithelial spread ( Paget’s disease of the breast)
53
Q

What is the difference between sarcoma and carcinoma?

A

sarcomas are cancers of connective tissue (fat, blood vessels, nerves, bones, muscles, deep skin tissues and cartilage)

carcinomas are cancers of epithelial tissue

54
Q

How do carcinomas spread?

A

via lymphatics first and blood secondly

55
Q

How do sarcomas spread?

A

usually through blood mostly

56
Q

What are the predicatable patterns of spread?

A

– lung to local nodes, liver, bone and brain
– tongue to neck nodes, later lung and spine

57
Q

What is the grade and stage of a tumour?

A

grade -how normal or abnormal cancer cells look under a microscope. (histopathology)

stage - extent of spread (imaging)

58
Q

What is the grading meant to assess?

A
  • Invasion into underlying tissue
  • Cellular atypia : abnormal mitotic activity, nuclear pleomorphism, differentiation, necrosis
59
Q

What are the methods of grading?

A

– numerical grades (1,2,3 etc)
– low, intermediate, high
– degree of differentiation (squamous cell carcinoma)

60
Q

What are assessments used to determine the stage of cancer?

A

Physical exams, imaging procedures, laboratory tests, pathology and surgical reports

61
Q

What system is used to clinically stage oral cancers?

A
  • TNM system is used for oral cancer
  • Tumour size (T)
  • Lymph node involvement (N)
  • Presence of metastases (M)
62
Q

What antigens allow recognition of tumour cells?

A

tumour-associated antigens
(neoantigens)

63
Q

What are examples of tumour-associated antigens?

A
  • Products of mutated genes
  • Overexpressed proteins (tyrosinase)
  • Viral proteins (HPV,EBV)
  • Oncofetal antigens (carcinoembryonic antigen)
64
Q

What is the tumour immunology reaction?

A

Elimination-Equilibrium-Escape

65
Q

What is 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.

66
Q

What response is largely decreased in immuno-deficient individuals?

A

elimination

67
Q

How do tumour cells evade (escape) immune system?

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

68
Q

What is equilibrium in tumour cells?

A

involves the continuous elimination of tumor cells and the production of resistant variants

may last years

69
Q

What is immunotherapy?

A

Use the patient’s own immune response to control and destroy malignant cells

70
Q

What are examples of 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.

Immunity and Pathology 1 (13 decks)

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