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MCD Cancer > Revision > Flashcards

Revision Flashcards

1
Q

reversible change in which one adult cell type is replaced by another adult cell type

A

metaplasia

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2
Q

examples of metaplasia

A
  • Barret’s Oesophagus from squamous epithelium to columnar

- In the cervix from columnar to squamous epithelium

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3
Q

abnormal pattern of growth with some morphological features of malignancy present

A

dysplasia

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4
Q

what are the features of dysplasia?

A
  • pre-invasive stage
  • basement membrane still intact
  • Loss of orientation
  • Loss of uniformity
  • Hyperchromatic and enlarged nuclei
  • Mitotic figures in abundance but in abnormal places

these determine whether the dysplasia is high or low grade

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5
Q

what are some common causes of dysplasia?

A
  • HPV infection in the cervix
  • Smoking in the bronchus
  • Ulcerative colitis in the colon
  • Pernicious anaemia in the stomach
  • Acid reflux in the oesophagus –> Barrett’s
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6
Q

A new abnormal proliferation of cells that are unresponsive to normal growth mechanisms

A

Neoplasia

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7
Q

what is malignancy?

A

An abnormal autonomous proliferation of cells unresponsive to normal growth control mechanisms

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8
Q

what is metastasis?

A

Discontinuous growing colony of tumour cells at a distance from the primary cancer site

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9
Q

what types of draining are important to determine the metastasis risk?

A

lymph and vascular drainage

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10
Q

benign epithelial tumour types

A

surface

glandular

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11
Q

surface epithelium

A

papilloma

skin, bladder

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12
Q

glandular epithelium

A

adenoma

stomach, thyroid, kidney, pancreas

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13
Q

malignant epithelial tumour types

A

Squamous cell
Adenocarcinoma
Transitional Cell
Basal Cell

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14
Q

where do sarcomas arises from

A

connective tissue types
(soft tissue/ mesenchymal tissue)

e.g.osteosarcoma, chondrosarcoma

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15
Q

what is leukaemia?

A

Malignant tumour of bone marrow derived cells that circulate in the blood

Myeloid or lymphoid lineage

myeloid: RBCs, platelets, granulocytes
lymphoid: B and T lymphocytes, NK cells

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16
Q

what is lymphoma?

A

Malignant tumour of lymphocytes usually within the lymph nodes (otherwise just the lymphatic system)

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17
Q

what is a teratoma?

A

Tumour derived from germ cells

  • from 1 to all 3 layers (ectoderm, mesoderm, endoderm)
  • found ectopically
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18
Q

how do male gonadal teratomas differ to female gonadal teratomas differ?

A

Male gonadal teratomas are malignant

Female gonadal teratomas often benign

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19
Q

what is a hamartoma?

A

Localised overgrowth of cells/tissue native to the organ that are disorganised but are histologically normal

key: disorganised structure , normal histology

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20
Q

features of benign tumours

A
  • encapsulated
  • well differentiated
  • slow growing
  • normal mitoses
  • do not invade
  • do not metastasise
21
Q

feature of malignant tumours

A
  • no capsule
  • poorly differentiated often
  • fast growing
  • abnormal mitoses
  • invades surrounding tissue
  • metastasises
22
Q

what features of a tumour can help grade the tumour i.e. degree of differentiation?

A
  • a large nucleus
  • irregular shape and size
  • nucleoli prominent
  • scarce cytoplasm
  • cytoplasm intensely coloured or pale
  • lack of normal function
23
Q

what features of a tumour help you stage the tumour i.e. the spread of the tumour?

A

this is more important for diagnosis
indicated whether the lymph nodes are involved –> if so, poorer prognosis

TNM:

  • tumour size
  • node involvement
  • metastasis
24
Q

which staging system is used for colorectal cancer?

A

Duke’s

based on invasion the basement membrane

25
Q

what is a proto-oncogene?

A

A piece of genetic material that codes for normal and essential proteins needed for controlled cell growth, division and differentiation

26
Q

examples of proto-oncogenes

A
  • Growth Factor
  • Growth factor receptor
  • signalling proteins
  • intracellular receptors
  • cell cycle regulatory proteins
  • cell death regulators
27
Q

what is an oncogene?

A

A piece of genetic material that codes proteins promoting uncontrolled cellular proliferation

28
Q

how are oncogenes expressed in cancer?

A
  • abnormally
  • excessively
  • hyperactively
29
Q

examples of oncogenes with the potential to cause cancer

A
  • Ras protein
  • c-Myc
  • Raf protein
30
Q

how are oncogenes activated (from proto-oncogene) ?

A
  • mutation in coding sequence
  • gene amplification (overproduction)
  • chromosomal translocation e.g. Philly (bcr-abl–> CML)
  • insertional mutagenesis (e.g. viral integration)
31
Q

what will a mutant Ras protein do?

A

Does not allow the GAP proteins to function and dephosphorylate the GTP to GDP
therefore Ras DOES NOT DEACTIVATE
and will be constantly active

32
Q

what is the effect of a constantly active Ras protein?

A
  • Abnormal growth
  • Abnormal proliferation
  • Abnormal differentiation
33
Q

Knudson’s two-hit hypothesis

A

two mutations are required for the TSG to lose control of its regulatory function

one mutation may be inherited whilst the other is acquired

34
Q

example of TSG function

A
  • regulate cell proliferation
  • maintain cellular integrity
  • regulate cellular growth
  • regulate the cell cycle
  • nuclear TFs
  • DNA repair proteins
  • cell adhesion molecules
  • cell death regulators
35
Q

example of TSG

A
  • p53

- APC (in Familial Adenomatous Polyposis)

36
Q

what is unique about p53 as a TSG

A

only 1 copy is needed to be mutated/lost for there to be functional dysregulation.

37
Q

what effect does an Adenomatous Polyposis Coli gene mutation have?

A

uncontrolled growth–> polyps

each polyp increases the chance of cancer

38
Q

what is beta catenin?

A

involved in regulation and coordination of cell–cell adhesion and gene transcription.

normally bound to cadherin in adheren junctions

39
Q

what pathway is APC involved in?

A 
Wnt pathway (part of a destruction complex)
--> controlling beta-catenin degradation
40
Q

what will happen when beta catenin is not being degraded by APC?

A

LEF-1 will create a transcription complex with beta catenin to alter gene expression and proliferation

41
Q

how is beta catenin expressed in Familial Adenomatous Polyposis?

A

high levels of beta catenin due to ineffective APC mutation (no degradation)

therefore increased transcription and proliferation via LEF-1 pathway

42
Q

when does colon cancer develop in normal epithelium?

A

when there is an APC mutation

43
Q

when does colon cancer develop in hyperproliferative epithelium?

A

when there is a k-ras mutation

44
Q

when does colon cancer develop when there is an adenoma?

A

when there is a p53 mutation

45
Q

what are the features of oncogenes?

A
  • active in tumour
  • translocations/point mutations
  • not often inherited
  • dominant: one mutation enough
  • e.g. leukaemia, lymphomas
46
Q

what are the features of TSGs?

A
  • inactive in tumour
  • deletions/mutation
  • inheritable mutations
  • recessive: 2 hit
  • solid tumours especially
47
Q

responses by p53

A
  • cell arrest
  • DNA repair
  • apoptosis
  • senescence
48
Q

what are the main two tests for prostate cancer?

A

1) Direct Rectal Exam (but does not detect microscopic tumour)
2) Prostate Specific Antigen

MCD Cancer (17 decks)

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