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Principles of dizzees > Tumour pathology > Flashcards

Tumour pathology Flashcards

1
Q

What is a tumour?

A

Abnormal growing mass of tissue, who’s growth is uncoordinated with the surrounding normal tissue

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2
Q

What is a neoplasm?

A

A tumour

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3
Q

What are the 2 types of tumours?

A

Benign and Malignant

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4
Q

Which type of tumour more harmful?

A

Malignant (cancer)

Benign is only really ever harmful if it grows in a key physiological structure

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5
Q

What is metastasis?

A

Spreading of cancer to other sites within the body

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6
Q

What are the 5 most common types of cancer (in the UK)?

A 
Breast
Lung
Prostate
Colon 
Melanoma
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7
Q

Which common form of cancer is most dangerous?

has lowest 5 year survival percentage

A

Lung cancer

10%

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8
Q

Tumours are classified depending on their type and where they are.

What is different between classifications of tumours?

A

Behaviour

Treatment route

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9
Q

What is the most common site (tissue) of origin for tumours to form?

A

Epithelial tissues

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10
Q

What is the name given to a malignant tumour in epithelial tissue?

A

Carcinoma

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11
Q

What type of tumour is an adenoma?

A

Benign tumour in the glandular epithelium

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12
Q

What is the name given to a malignant tumour in connective tissue?

What would one in fat be called?

A

Sarcoma

Lipo-sarcoma

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13
Q

What is the name given to a benign tumour in bone?

A

Osteoma

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14
Q

What is the name given to a benign tumour in white blood cells?

A

Prankd

Does not exist

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15
Q

Classify leukaemia as a type of tumour.

A

Malignant

White blood cells

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16
Q

Classify lymphoma as a type of tumour.

A

Malignant

Lymphoid tissue

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17
Q

What are Naevi?

A

Benign

Melanocytes

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18
Q

What is the name given to a malignant tumour of the melanocytes?

A

Melanoma

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19
Q

Give 2 examples of malignant tumours that originate in neural tissues.

A

Astrocytoma:

  • Astrocytes
  • CNS

Schwannomia:

  • Schwann cells
  • PNS
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20
Q

Describe what teratomas are, and the differences in them, based on gender.

A

Tumour of germ cells

In males (testes), they are usually malignant + can easily migrate to other areas/metastasise

In females (ovaries), they are (usually) benign

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21
Q

Describe the features of benign tumours in terms of:

  • Growth pattern
  • Encapsulation
  • Invasion
  • Metastases
  • Differentiation
  • Function
  • Behaviour
A
  • Non-invasive
  • Usually encapsulated
  • Non-invasive
  • No metastasis
  • Well-differentiated
  • Function similar to normal tissue
  • Rarely cause death
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22
Q

Describe the features of malignant tumours, considering:

  • Growth
  • Encapsulation
  • Metastasis
  • Differentiation
  • Function
  • Behaviour
A
  • Invasive growth
  • No capsule or capsule breached by tumour cells
  • Poorly differentiated
  • Abnormal appearance
  • Loss of normal function
  • Usually metastasises
  • Frequently causes death
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23
Q

What are the local effects of benign tumours?

A

Pressure

Obstruction

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24
Q

What are the local effects of malignant tumours

A

Pressure

Obstruction

Tissue destruction - ulceration/infection

Bleeding - anaemia/haemorrhage

Pain - pressure/infiltration of nerves/pathological fractures of bone

Effects of treatment

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25
Q

What are systemic effects of malignant tumours

A

Weight loss (cancer cachexia)

Hormone secretion*

Paraneoplastic syndromes

Effects of treatment

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26
Q

Describe the different types of hormone production by tumours*

A

Can be ‘normal’, when the tumour is of an endocrine organ. This normally produces the hormone, but will have abnormal control of hormone production

Abnormal/Inappropriate - when hormones are produced by a tumour in an organ that does not normally produce hormones

27
Q

What is a paraneoplastic syndrome?

A

A syndrome that is the consequence of cancer in the body but is not due to the local presence of cancer cells

(ie - it is not due to the pressing of the tumour on something)

28
Q

What is dysplasia?

A

A pre-malignant change/abnormality in cells

Cells with this change can progress to cancer

Earliest stage of progression to malignancy that can be identified

29
Q

What are the features of dysplasia, that can be identified when microscopically viewed?

A

Increased nuclear size

Increased mitotic activity

Abnormal mitoses

General disorganisation of cells

30
Q

What is the difference between high grade dysplasia, and low grade dysplasia

A

High grade = close to malignancy - more worrying

31
Q

Describe the cell cycle of a cell that divides by mitosis

A

G1 - synthesis of components for DNA synthesis

S - DNA synthesis

G2 - preparation for mitosis

M - mitosis

(+ G0)

32
Q

What factors control the cell cycle?

A

External factors - hormones, growth factors, cytokines and stroma

Intrinsic factors - revolve around checkpoints

33
Q

What is the restriction point?

A

Point in the cell cycle, prior to which, progress through G1 phase was controlled by external factors

After R, progress through cell cycle becomes autonomous, and is controlled by intrinsic factors (checkpoints)

34
Q

What is the G0 phase?

A

Quiescent phase

Resting phase - cell has left cycle and does not divide

35
Q

Checkpoints in the G1 phase will cause G1 arrest if…

A

If the cell lacks components needed for S phase

If the cell size is inadequate

If there is an inadequate nutrient supply

If essential external stimuli are lacking

If DNA damage is detected

36
Q

Checkpoints in S phase cause arrest if…

A

If DNA is not replicated

37
Q

Checkpoints will cause G2 arrest if…

A

If cell size is inadequate

If DNA damage is detected

38
Q

The checkpoint in M phase will cause arrest if…

A

If there is chromosome mis-alignment

ensures cell is ready to complete division

39
Q

What stage of mitosis is the M phase checkpoint in?

A

Metaphase

40
Q

What are the 2 main components of a checkpoint?

A

Cyclin-dependent kinases (CDKs) - catalytic subunits
+
Cyclins - regulatory subunits

These together form a CDK/cyclin complex, where the cyclins regulate the CDKs

41
Q

What is the basic function of CDK/cyclin complexes, when acting on target proteins?

A

Phosphorylate

This activates/inactivates the target substrate

The substrates regulate events of the next phase of the checkpoint cycle

42
Q

Aside from cyclins, what else regulates CDKs

A

CDK inhibitors (CKIs)

These bind to cyclin/CDK complexes and inhibit stuff

43
Q

What are the 2 families of CKIs

A

INK4A

CIP/KIP

44
Q

pRb is a phosphoprotein encoded by the retinoblastoma gene (an anti-oncogene)

pRb becomes active (Rb) when…

A

Hypophosphorylated

Inactive (pRb) when phosphorylated

45
Q

What is the effect of pRb when activated?

A

Active Rb stops cell cycle progression

Active Rb binds to E2F transcription factor

pRb (inactive) loses affinity for E2F - which becomes ‘free’

Free E2F transcription factor activates vital target genes - stimulating entry to/progression of the cell cycle

46
Q

What is carcinogenesis?

A

Initiation of cancer formation

47
Q

What are DNA adducts?

A

Products of reaction between chemical carcinogens and DNA

Adduct formation at particular chromosome sites causes cancer

48
Q

Why is a mutation in the retinoblastoma gene potentially dangerous?

A

Absent or non-functional/inactive pRb releases the cell cycles brake

= uncontrolled proliferation

49
Q

What is P53?

A

Type of cell cycle regulator

50
Q

Describe how P53 works

A

Damage to cell causes P53 levels to rise

High P53 levels either;

  • induces cell cycle arrest at G1
  • Triggers DNA repair
  • P53 induced apoptosis - severe damage
51
Q

Why is mutation in the P53 gene dangerous?

A

Cells with mutated p53 will not G1 arrest, repair DNA or undergo p53 induced apoptosis

52
Q

Describe the differences between the sporadic and inherited mutations of anti-oncogenes

A

Sporadic - two point mutations of anti-oncogene occur in a single cell

Inherited - In order to have an effect, must have one inherited mutated gene and one somatic point mutation

(both alleles of anti-oncogene must be mutated for cancer to arise)

53
Q

What is an oncogene

A

A gene which under certain circumstances can transform a cell into a cancer cell

This can occur for 2 reasons:

  • Alteration of proto-oncogene structure
  • Dysregulation of proto-oncogene expression
54
Q

What types of proteins are coded for by proto-oncogenes

A

Growth factors

Growth factor receptors

Signal transduction proteins

Nuclear regulatory proteins

Cell cycle regulators

55
Q

What DNA viruses are known viral carcinogens?

A

HPV
Hepatitis B
EBV

56
Q

How do chemical carcinogens cause cancer?

A

Chemical reacts with DNA and forms adducts

Adducts at particular chromosome sites lead to activation of oncogenes and suppression of anti-oncogenes

57
Q

What are the main types of tumour biomarkers?

A

Onco-fetal proteins
Oncogenes
Growth factors and receptors
Immune checkpoint inhibitors

58
Q

What are onco-fetal proteins?

A

Proteins normally present during fetal development but are found in adults with certain types of cancer

59
Q

What is the main onco-fetal protein, and what it is a biomarker of?

A

Alpha fetoprotein

Biomarker of:

  • teratoma in the testes
  • hepatocellular carcinoma
60
Q

What is Kras?

A

Predictive biomarker for colorectal cancer

61
Q

What is Braf?

A

Predictive biomarker for melanoma

62
Q

What is EGFR?

A

Predictive biomarker of lung cancer

63
Q

What is PD-L1?

A

Predictive biomarker of lung cancer

64
Q

What is Her2?

A

Predictive biomarker of Breast cancer and gastric cancer

Principles of dizzees (28 decks)

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