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Biology of Cancer > Hallmarks of Cancer > Flashcards

Hallmarks of Cancer Flashcards

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1
Q

what does the T mean in the TNM naming system?

A

describes the size of the tumour, and how far is has spread into nearby tissue

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2
Q

what does the N mean in the TNM naming system?

A

describes if there is any cancer cells in the lymph nodes

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3
Q

what does the M mean in the TNM naming system?

A

describes if the cancer has spread to another part of the body

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4
Q

what are the biomedical cancer risk factors?

A

genetic susceptibility and hormonal factors in females

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5
Q

what are the lifestyle risk factors for cancer?

A

smoking, alcohol, obesity, physical inactivity, chronic infections and poor diet

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6
Q

what are the environmental risk factors of cancer?

A

sunlight, radiation, occupational exposure, pollution

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7
Q

what is stage 0 cancer?

A

very small and benign

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8
Q

what is stage 1?

A

small and contained within the organ of origin

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9
Q

what is stage 2?

A

tumour larger than stage 1, but not spread into surrounding tissues, may have spread into closely lymph nodes depending on cancer

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10
Q

what is stage 3?

A

cancer is larger, may have spread into surrounding tissues and there are cancer cells in lymph nodes nearby

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11
Q

what is stage 4?

A

means the cancer has spread from where it originated, such as the liver or lung, is also called secondary/metastatic cancer

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12
Q

in what 2 ways is cancer classified?

A

by the type of tissue in which it originated and the location where it developed

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13
Q

what is carcinoma?

A

malignant neoplasm of epithelial origin in internal or external lining of the body

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14
Q

what is adenocarcinoma?

A

a carcinoma that developed in an organ or gland

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15
Q

what is squamous cell carcinoma?

A

develops in a squamous cell

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16
Q

what is sarcoma?

A

cancer that originates in supportive and connective tissue such as bones, tendons, cartilage muscle and fat

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17
Q

what are the features of sarcoma?

A

generally occur in young adults and resemble the tissue in which they grow

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18
Q

what is myeloma?

A

originates in the plasma cells of the bone marrow

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19
Q

what is leukaemia?

A

cancers of the bone marrow

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20
Q

why is a person with leukaemia prone to infection?

A

overproduction of white blood cells that do not perform as they should so cannot fight infection

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21
Q

what is lymphoma?

A

cancer that develops in glands or nodes of lymphatic system, blood vessels and organs that purify bodily fluids

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22
Q

what is lymphoma classified as?

A

hodgkin or non-hodgkin

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23
Q

what are the hallmarks of cancer?

A

sustaining proliferative signalling, evading growth suppressors, activating invasion and metastasis, enabling replicative immortality, inducing angiogenesis and resisting cell death

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24
Q

what is growth signal autonomy?

A

normal cells need external signals in order to divide, cancer cells circumvent this leading to uncontrolled growth, and can also create their own growth factors

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25
Q

how can cancer cells cause hyper responsiveness to growth signals?

A

they have the ability to synthesise and secrete their own growth factors and can have mutations in the GF receptors that increase the amount present on cell surface

26
Q

how can cancer cell GF receptors be permanently switched on?

A

the receptor can become structurally altered causing a lack of regulatory regions

27
Q

what is Ras?

A

a key signalling pathway protein

28
Q

what is an oncogene?

A

genes that promote automomous growth in cancer cells

29
Q

how do oncogenes cause unregulated growth?

A

they produce oncoprotein which do not have important regulatory elements and their production in the transformed cells does not depend on growth factors or other external signals

30
Q

why is retinoblastoma classified as a tumour suppressor protein?

A

because at the molecular level, all antigrowth signals are fuelled through the retinoblastoma protein

31
Q

how does retinoblastoma prevent cell growth?

A

binds to E2F so that it is not free to then bind to transcribe DNA

32
Q

how is the intrinsic pathway of apoptosis activated?

A

by stress or damage to the cell

33
Q

what proteins are activated by intrinsic apoptosis?

A

BH3-only proteins

34
Q

how are BAX and BAK activated?

A

by pro-apoptotic BH3-only proteins

35
Q

what do BAX and BAK do?

A

cause mitochondrial outer membrane permeability which is a point of no return for apoptosis allowing cytochrome C init the cytoplasm

36
Q

what is the role of cytochrome C in apoptosis?

A

acts as a signalling molecule in cytoplasm which prompts formation of apoptosome

37
Q

what follows formation of apoptosome in apoptosis?

A

apoptosome turns pro-capsase-9 into capsase-9 which actives capsase -3 and -7

38
Q

what role do -3 and -7 have in apoptosis?

A

they begin the breakdown of cellular materials and -3 condenses and breaks down cellular DNA

39
Q

what is p53 responsible for?

A

detecting DNA damage, chromosome abnormalities and arresting cell cycle to initiate repair

40
Q

how does p53 induce apoptosis?

A

increases production of apoptotic protein BAX

41
Q

how can cancer cells compromise the activity of p53?

A

increasing inhibitors of p53 or silencing the activators of p53 which reduces apoptosis

42
Q

how does increased telomerase in cancer cells increase replication capability?

A

telomerase maintains the length of the telomere and so cancer cells are able to divide more times as they do not have a Hayflick limit

43
Q

what is angiogenesis?

A

process through which new blood vessels form from pre-existing blood vessels

44
Q

how can tumours gain their own blood supply?

A

release chemical signals that stimulate angiogenesis

45
Q

what are the immune evasion strategies of cancer cells?

A

release of immunosuppressive factors, T cell checkpoint dysregulation, recruitment of immunosuppressive cells, ineffective presentation of tumour antigens, tumour microenvironment

46
Q

what is the Warburg effect?

A

altered cellular energetics, where cancer cells have an increased glucose uptake and lactate production which allows them to survive in hypoxic conditions

47
Q

how are tumours and inflammation linked?

A

by NFkB and TAMs

48
Q

what is NFkB?

A

transcription factor that is key in inflammation responses

49
Q

how does NFkB become free to enter a nucleus?

A

IkB kinase phosphorylates IkBa which means it can no longer hold NFkB in an inactive state and therefore it is free to enter

50
Q

what does NFkB do once it enters the nucleus?

A

activates genres that promote cell growth, survival, migration and the formation of new blood vessels

51
Q

how is a positive feedback loop of NFkB form?

A

activation of NFkB in immune cells causes production of molecules that activate NFkB in cancer cells, which in turn induce molecules that attract more immune cells

52
Q

what does a NFkB feedback loop cause?

A

uncontrolled growth with immune cells actively enhancing hallmark capabilities of cancer cells

53
Q

what do TAMs do to encourage tumour growth?

A

supplies growth factors

54
Q

what do TAMs produce?

A

EGF, FGF and small molecules such as cytokine, primary IL-6 and TNF

55
Q

what growth factors are used by a tumour to carry out angiogenesis?

A

vascular endothelial growth factor and platelet derived growth factor

56
Q

how can oxygen derived conditions be beneficial to TAMs?

A

because they can activate angiogenesis through the hypoxia response pathway

57
Q

how can VEGF create a feedback loop?

A

attracts TAMs to a tumour which causes more VEGF to be produced

58
Q

how can TAMs and matrix degrading enzymes help metastasis?

A

they help to degrade the ECM of a cell which aids in the invasion and spread of cancer cells

59
Q

what is an example of a matrix degrading enzyme?

A

metalloproteases

60
Q

how do TAMs suppress the immune system?

A

produce immunosuppressive molecules, allowing the tumour to evade the immune system, and release cytokines that attract other immune cells

Biology of Cancer (1 decks)

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