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IMS > Aetiology of Cancer and Neoplasms I > Flashcards

Aetiology of Cancer and Neoplasms I Flashcards

1
Q

What is one defining feature of Cancer?

A

Rapid creation of abnormal cells that grow beyond usual boundaries

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2
Q

What is the spreading of Cancer reffered to as?

A

Metastasis

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3
Q

What are Malignant Neoplasms?

A

Carcinoma in Situ and cancer

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4
Q

What is the difference with a Benign Tumour in terms of spreading?

A

Dont metastasize, remain encapsulated by connective tissue fibrous sheath

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5
Q

What are the 5 main groups of Cancer?

A 
Carcinoma - skin
Lymphoma - Lymph
Leukaemia - blood
Sarcomas- connective tissue
CNS tumours - brain and spinal cord
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6
Q

How do Benign tumours appear microscopically?

A

Innocent, tumour staying localised and remains encapsulated

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7
Q

What are Malignant tumours?

A

Referred to as cancer, can invade and destroy structures, migrate to sites as they metastasize

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8
Q

What type of Benign tumour would Glands have suffix of?

A

Adenoma

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9
Q

What type of Benign tumour would Surfaces have suffix of?

A

Papilloma

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10
Q

What type of Benign tumour would Mucous surfaces have suffix of?

A

Polyp

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11
Q

What type of Benign tumour would Hollow masses have suffix of?

A

Cysadenoma

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12
Q

Where are Sarcoma cells in malignant tumours derived from?

A

Mesenchyme

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13
Q

Where are Carcinoma cells in malignant tumours derived from?

A

Epithelia

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14
Q

What 2 Tumours are definitely malignant?

A

Melanoma and Lymphoma

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15
Q

Why are Cancers bad for us?

A

Local tissue destruction
Obstruction/compression
Hormonal malregulation

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16
Q

How are Cancers classified?

A

Based on grade - how close cells resemble tissue of origin

Stage - how far spread from nidus

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17
Q

What is TNM in the common staging system?

A

Tumour size
Nodes involves
Metastasis

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18
Q

Why is Staging import?

A

For treatment and to factor 5 year survival rate

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19
Q

What test is used to Specify Tumours?

A

PAP test

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20
Q

What is a Neoplasm?

A

A mass formed by autonomous proliferation of cells or new growth

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21
Q

What does Abnormal proliferation of cells result in?

A

Neoplasm or tumour

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22
Q

Are neoplasms malignant?

A

Not all e.g uterine fibroids

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23
Q

What is Cell division dependant on?

A

Signals and Sensors

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24
Q

What happens of signals or sensors become damaged?

A

Cell division is unregulated can result in tumour

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25
Q

What are the 3 Main types of Body cells during cell division?

A

Cells that never divide
Cells that retain ability to divide but dont
Cells that routinely divide and can alter rate of division

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26
Q

How do Cells duplicate in a Eukaryotic cell?

A

Meiosis

Mitosis

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27
Q

What are the 4 Phases of Cell cycle?

A

G1
S phase
G2
M phase

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28
Q

What happens in G1?

A

High rate metabolism, proteins synthesis, organelles duplicate and centriole replicates

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29
Q

What happens in S phase?

A

DNA replicated, synthesis of new histones and assembly of new chromatin

30
Q

What happens in G2 phase?

A

Synthesis of enzymes and proteins, replicate of centrioles done, transport

31
Q

What happens in M phase?

A

Mitosis and splitting of genome

32
Q

What are 2 critical points for dividing cell

A

G1/S boundary - dna synthesis

G2/m boundary - mitosis

33
Q

What happens to cells that fail to undergo mitosis?

A

Apoptosis

34
Q

What are the important factors that regulate entry of cell in S phase?

A

Cdk 2,4,6

35
Q

What allows proper functioning of Cdk 2?

A

Cyclin E

36
Q

What allows proper functioning of Cdk4,6?

A

Cyclin D

37
Q

What do growth factors activate and produce?

A

Cyclin D

38
Q

What does Cyclin D activate?

A

Cdk4

39
Q

What does Cdk 4 do?

A

Phosphorylates pRband prevents inactivation of E25-1

40
Q

What does E2F-1 do?

A

Binds with enhancer sequences activating transcription for dna synthesis

41
Q

What happens to these regulations once the S phase begins?

A

pRB is dephosphorylated to prevent further rounds of DNA replication Cyclin D destroyed

42
Q

In the G2/M phase what protein kinase is present?

A

Cdk 1 With Cyclin B

43
Q

What does Cyclin B do?

A

Cell switch - modifies proteins
Sets in motion a sequence of changes
Activated only at G2/M boundary for mitosis

44
Q

Post mitosis what happens to inactive heterodimer?

A

Phosphorylated at threonine 14, tyrosine 15

45
Q

At the G2/M phase what removes phosphates?

A

Cdc25

46
Q

What is Wee1?

A

Phosphorylation to ensure complete inactivation adding 2 phosphates to Cdk1 and thrty14,15

47
Q

What does WEE1 prevent binding of?

A

ATP to Cdk1 - first step of phosphorylation of other proteins

48
Q

What transcription factor activates gene coding?

A

E2F-1

49
Q

In non-dividing cells why is E2F-1 inhibited?

A

Bound to protein pRb

50
Q

What are 3 signals that lead to arrest of cell growth?

A

Mitogen withdrawal, Loss of adhesion, Contact inhibition

51
Q

What 2 CKI’s are inhibited to prevent DNA synthesis?

A

P16 ink4a P27kip1

52
Q

What is P53?

A

Tumour surpressor gene found on chr 17 involved with dna repair

53
Q

What does Increased conc of P53 activate?

A

DNA repair

54
Q

What inhibits G1 CDK’s?

A

p21 cipi1 to prevent replication of defective DNA

55
Q

What is Apoptosis?

A

Programmed cell death

56
Q

What is Apoptosis characterised by?

A

Cell shrinkage, Cell contents in blebs, Chopping up DNA, Secretion of cytokines

57
Q

What is the Extrinsic pathway?

A

Instructed death - viral infection

58
Q

What is the Intrinsic pathway?

A

Default death - absence of growth factors

59
Q

What is stress activated apoptosis?

A

Direct activation of mitochondria and protein kinase P38

60
Q

What is Senescence?

A

Irreversible cell cycle arrest

61
Q

Whatr is replicative senscence?

A

Telomere dysfunction

62
Q

What is stress induced senscence?

A

DNA damage p16

63
Q

What is oncogene induced senescene?

A

Oncogene activation p53

64
Q

What is replication stress induced senescence?

A

Haemophiatic stem cells

65
Q

What is developmental senescence?

A

Embryogensis p21

66
Q

What is cell-cell fusion?

A

Placental syncitiotrophoblast

67
Q

What are telomeres?

A

Chr capping function, prevents ends of chr from seen as double stranded breaks

68
Q

What is telomere shortening?

A

DNA polymerase cant lengthen terminal section

69
Q

What is angiogenesis?

A

Own blood vessels for blood supply to cancer growth

70
Q

What growth factors switch angiogenic factors on?

A

VEGFR , bFGF

71
Q

What factors switch of anti-angiogenic factors?

A

Delta like ligand 4

IMS (53 decks)

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