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Integrated Medical Sciences > L41 and L42 Aetiology of Cancer and Neoplasms 1 & 2 > Flashcards

L41 and L42 Aetiology of Cancer and Neoplasms 1 & 2 Flashcards

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USMLE® Step 1 flashcards
1
Q

Sarcomas originate __?__

A

in connective tissue

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2
Q

Papillomas originate __?__

A

on epithelial surfaces

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3
Q

Polyps are benign neoplasms that originate __?__

A

in mucous surfaces

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4
Q

Generally, benign neoplasm names end with the suffix __?__

A

-oma

Exceptions: melanoma and lymphoma are malignant

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5
Q

Malignant tumour names end with the suffix __?__

A
  • sarcoma, if derived from mesenchyme
  • carcinoma, if derived from epithelia
    (e. g. fibrous tissue - fibrosarcoma, cartilage - chondrosarcoma; epidermis - squamous cell carcinoma, glands - adenocarcinoma)

Exceptions: melanoma and lymphoma are also malignant.

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6
Q

What damage can tumours do?

A

Local tissue destruction

Obstruction and compression

Hormonal malregulation

(ultimately, death)

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7
Q

How are tumours classified?

A

Grade: how closely the tumour histology resembles the tissue of origin

Stage: how far the tumour cells have spread from the site of origin

TMN staging system:
Tumour (size)
Nodes (number of)
Metastasis (yes or no)

Staged according to chances of 5-year survival.

(1=>80%, 4=<20%)

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8
Q

Bloom and Richardson’s classification is used for what type of cancer?

A

Breast carcinoma

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9
Q

Dukes’ classification is used for what type of cancer?

A

Colorectal carcinoma

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10
Q

Ann Arbour’s classification is used for what type of cancer?

A

Lymphoma

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11
Q

Breslow/Clarke’s classification is used for which type of cancer?

A

Melanoma

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12
Q

Levels of cyclins and MPF peak at the beginning of which phase of the cell cycle?

A

Mitosis

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13
Q

Cdk 2, Cdk 4, and Cdk 6 are important factors in which stage of the cell cycle?

A

Entry from G1 into S phase.

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14
Q

Which cyclin is associated with Cdk 2?

A

Cyclin E

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15
Q

Which cyclin is associated with Cdk 4 and 6?

A

Cyclin D

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16
Q

How does retinoblastoma protein (pRb) regulate DNA synthesis?

A

Growth factors initiate production of cyclin D.

Cyclin D activates Cdk 4, which phosphorylates pRb and prevents it from inhibiting E2F-1.

E2F-1 binds with enhancer sequences and activates transcription and DNA synthesis.

Once S-phase begins, cyclin D is destroyed, inactivating Cdk 4. and pRb is dephosphorylated to prevent further DNA replication.

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17
Q

Where do you find control points for cell division?

A

G1/S

G2/M

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18
Q

What occurs if Wee1 function is lost in a cell?

A

The daughter cells will be smaller because division occurred prematurely.

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19
Q

What is the role of Wee1 at the G2/M control point?

A

Inactivates Cdk1 by phosphrylating it. This prevents entry into mitosis.

In normal cells, only when the cell is ready for mitosis will Wee1 be inactivated and the cell will progress to M stage.

Mutants with unphosphorylated Cdk1 will divide too early.

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20
Q

Which Cdk1 binding sites are phosphorylated by Wee1?

A

Threonine-14 and Tyrosine-15.

Prevents ATP binding.

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21
Q

In non-dividing cells, how is transcription factor E2F-1 inhibited?

A

It is bound to retinoblastoma protein (pRb)

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22
Q

What is the role of E2F-1?

A

Codes for special proteins only used by dividing cells.

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23
Q

What 3 signals lead to the arrest of cell growth (cell quiescence)?

A

Mitogen withdrawal

Loss of adhesion

Contact inhibition

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24
Q

How does contact inhibition arrest cell growth?

A

Dividing cells that come into contact with neighbouring cells stop dividing because cadherins cause production of Cdk-inhibitors: p16^INK4a and p27KIP1.

These inhibit G1 Cdks and prevent DNA synthesis.

Loss of this function is one of the first changes seen in the transformation of normal cells into cancer cells.

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25
Q

What gene is known as ‘Guardian of the Genome’?

A

p53

A tumour suppressor gene found on chr. 17.

Determines:

  • cell cycle arrest
  • DNA repair
  • block angiogenesis
  • apoptosis
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26
Q

How does p53 work?

A

When DNA is damaged, p53 lysis halts and concentrations increase. As this happens, more p21^CIP1 is produced and this inhibits G1 Cdks, preventing replication of defective DNA.

If DNA cannot be repaired within a few hours, the cell self-destructs by apoptosis.

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27
Q

What events can activate apoptosis?

A

1) Instructed death (death domain receptors signal apoptosis in response to viral infection)
2) Default death (absence of growth factors and phosphate kinase B activates bcl2 -associated death promoter (BAD))

3) Stress activated:
- direct activation of mitochondria
- p53 activation of BAX protein
- Protein kinase p38 (p38 MAPK)

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28
Q

What mechanisms can drive senescence (irreversible cell cycle arrest)?

A
  • Telomere shortening
  • Genotoxic stress
  • Mitogens
  • Inflammatory cytokines

(ultimately culminate in the activation of p53 tumour suppressor and/or the Cdk-inhibitor p16)

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29
Q

What is ‘replicative senescence’?

A

Telomere dysfunction/erosion or reaching Hayflick’s limit (number of allowed divisions - around 50) leads to irreversible cell cycle arrest by p53-p21

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30
Q

What is ‘stress-induced premature senescence’?

A

DNA damage or reactive oxidation species lead to production of p16, which leads to irreversible cell cycle arrest.

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31
Q

What is ‘oncogene-induced senescence’?

A

Activation of oncogene leads to irreversible cell cycle arrest by p53.

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32
Q

What is the role of a telomere?

A

A repeated nucleotide sequence (TTAGGG) that prevents the ends of chromosomes being seen as DNA breaks, stops ligase linking the ends of DNA strands together.

Also prevents shortening of the lagging strand of DNA by allowing telomerase to add an extra sequence that can allow the formation of a primer site so that a DNA polymerase-alpha can complete the lagging strand.

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33
Q

How do tumours obtain their own blood supply?

A

The tumour cells secrete angiogenic factors that promote sprouting of new capillaries from existing vessels.

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34
Q

What happens if a tumour fails to obtain a blood supply?

A

hyperplasia (division of cells) is curtailed and the tumour remains as a carcinoma in situ.

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35
Q

What are the activators of angiogenesis?

A

VEGF-A, B, C

FGFs

36
Q

What are the inhibitors of angiogenesis?

A

Throbospondin-1 and 2

Interferon alpha and beta

Angiostatin

Endostatin

Collagen IV fragments

37
Q

True or false: Angiogenesis is determined by a balance of activators and inhibitors. If there are more activators present, angiogenesis will occur. If there are more inhibitors, it will not.

A

True

38
Q

True or false: Tumours secrete signals that work by either switching on angiogenic factors (VEGFR, bFGF) or by switching off expression of anti-angiogenic factors (DLL4).

A

True

39
Q

Thalidomide and avastin are used in what therapy?

A

Anti-angiogenic cancer therapy

40
Q

What term means ‘the process of inducing cancer’?

A

Carcinogenesis

41
Q

What is carcinogenesis?

A

A multistep process in which a normal cell progressively acquires cancer hallmarks (properties) via a series of molecular changes in its DNA (mutations).

42
Q

What are the hallmarks of cancer?

A

A small number of traits shared by all cancers that govern the transformation of normal cells into cancerous ones.

1) Sustaining proliferative signalling
2) Evading growth suppressors
3) Activating invasion and metastasis
4) Enabling replicative immortality
5) Inducing angiogenesis
6) Resisting cell death
7) Genome instability and mutation
8) Tumour-promoting inflammation
9) Avoiding immune destruction
10) Deregulating cellular energetics

43
Q

What does the Ras oncoprotein gene have to do with cancer?

A

A mutation in Ras oncoprotein disrupts the normal negative feedback mechanisms that dampen a signalling pathway when a mitogenic signal is hyperactivated.

Allows sustained proliferative signalling in cancer cells.

44
Q

How can cancer cells evade apoptosis?

A

Dysregulation of anti-apoptopic family members results in increased BCL-2. This inhibits pro-apoptopic factors BAX and BAK and leads to cell survival.

45
Q

How do cancer cells enable replicative immortality?

A

Normal cells limited in how many times they can divide by the shortening telomere (gets shorter every division). This limit is known as the Hayflick limit.

Cancer cells maintain the length of their telomeres, preventing replicative senescence.

46
Q

What diameter of vessel is required for a tumour to grow?

A

~0.4mm

Hence the need for tumours to induce angiogenesis.

47
Q

What are the four modes of metastasis?

A

Local invasion

Lymphatic spread

Vascular spread

Transcoelomic (trans-
body cavity) spread

48
Q

Regarding epithelial mesenchymal transition, what are the epithelial markers?

A 
E-Cadherin
Claudins
Occludins
ZO-1
Desmoplakin
Cytokeratins
49
Q

Regarding epithelial mesenchymal transition, what are the mesenchymal markers?

A 
N-Cadherin
Fibronectin
Collagen I/III
Snail
alpha-SMA
Vimentin
50
Q

How can local chronic inflammation enable cancer?

A

Inflammatory cytokines, chemokines and proteases promote tumour growth, proliferation, survival and angiogenesis

51
Q

What do regulatoryh T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) have to do with tumours?

A

Cancer cells ‘recruit’ these immunosuppressive inflammatory cells to help them avoid detection and destruction by the immune system.

52
Q

Which melanoma-specific antigens are capable of eliciting an immune response?

A

MART
MAGE (testis)
RAGE (kidney)
Gp100

53
Q

Which breast and ovarian cancer-specific antigens are capable of eliciting an immune response?

A

Mucin

54
Q

ErbB2 antigen is overexpressed in what type of cancer?

A

Ovarian and breast cancer

55
Q

CD10 antigen is overexpressed in what type of cancer?

A

Leukaemia

56
Q

Because of a point mutation caused by melanoma, what gene product is made?

A

Cdk 4

57
Q

Because of a point mutation caused by head/neck cancer, what gene product is made?

A

Caspase 8

58
Q

Tyrosine, PSA, and CEA are differentiation antigens. What does each one indicate?

A

Tyrosinase = Melanoma

PSA = Prostate

CEA = Colon

59
Q

How do cells deregulate cellular energetics?

A

Cancers use abnormal metabolic pathways to generate energy.

“The Warburg hypothesis”

Most cancer cells predominantly produce energy by a high rate of glycolysis followed by lactic acid fermentation in the cytosol.

Most normal cells have a low glycolysis rate followed by oxidation of pyruvate in mitochondria.

60
Q

Which cancer hallmark is targeted by cyclin-dependent kinase inhibitors?

A

Evading growth suppressors

61
Q

Which cancer hallmark is targeted by immune activating anti-CTLA4 mAb?

A

Avoiding immune destruction

62
Q

Which cancer hallmark is targeted by Telomerase inhibitors?

A

Enabling replicative immortality

63
Q

Which cancer hallmark is targeted by selective anti-inflammatory drugs?

A

Tumour-promoting inflammation

64
Q

Which cancer hallmark is targeted by inhibitors of HGF/c-Met?

A

Activating invasion and metastasis

65
Q

Which cancer hallmark is targeted by inhibitors of VEGF signalling?

A

Inducing angiogenesis

66
Q

Which cancer hallmark is targeted by PARP inhibitors?

A

Genome instability and mutation

67
Q

Which cancer hallmark is targeted by proapoptotic BH3 mimetics?

A

Resisting cell death

68
Q

Which cancer hallmark is targeted by aerobic glycolysis inhibitors?

A

Deregulating cellular energetics

69
Q

Which cancer hallmark is targeted by EGFR inhibitors?

A

Sustaining proliferative signalling

70
Q

What cells are involved in the tumour stroma?

A

Vascular elements - provide growth factors, blood supply, O2, nutrients

Fibroblasts - contibute matrix metalloproteinases (MMPs) for extracellular matrix degradation during cancer cell migration

Tumour-associated macrophages (TAMs) provide defense against immune system

71
Q

How do tumour-associated macrophages (TAMs) help tumours?

A

Secret EGF for growth and proliferation of cancer cells.

Secrete proteases to make space in the matrix for angiogenesis and liberate growth factors.

Secrete angiogenic factors to promote angiogenesis.

72
Q

An oncogene is associated with:

A. Tumour growth during tumourigenesis
B. Averting tumour cell growth
C. Preventing tumour cell apoptosis
D. Triggering cell transformation

A

D. Triggering cell transformation

73
Q

What is a procarcinogen?

A

A chemical that requires metabolic conversion before it has cancer-causing effects.

74
Q

What are some examples of carcinogenic microbes?

A

RNA viruses (HTLV1) - leukaemia

DNA viruses (HHV) - Kaposi’s sarcoma

Pathogenic species (H. Pylori) - gastric carcinoma and lymphoma

75
Q

What did Percival Pott discover in 1775?

A

Carcinogenic link between soot and squamous cell carcinoma of the scrotum.

Identified in chimney sweeps.

76
Q

True or false: Data shows that there is a 20-year lag between smoking and lung cancer

A

True.

Comparing the number of cigarettes smoked per person per year to the number of lung cancer deaths per 100,000 people suggests it takes 20 years for mutagenesis.

77
Q

Roughly what proportion of cancer deaths are related to preventable causes?

A

Two-thirds

78
Q

Imatinib is an ABL kinase inhibitor used to treat what?

A

Chronic myelogenous leukaemia (CML)

79
Q

Philadelphia chromosome (abnormality in chr. 22) is associated with which disease?

A

Chronic myelogenous leukaemia (CML)

80
Q

Cervical cancer is associated with which pathogen?

A

Human papilloma virus (HPV) types 16 and 18.

81
Q

How do the E6 and E7 oncogenes facilitate the development of cervical cancer?

A

E6 inactivates p53 via ubiquitination.

E7 competes for pRb binding, freeing E2F to transactivate targets and drive cell division

82
Q

What are gardasil and cervarix?

A

HPV vaccinations

83
Q

What are non-carcinogenic forms of HPV-induced neoplasia?

A

Warts, respiratory papillomatosis, epidermodysplasia verruciformis

84
Q

What factors increase your risk of breast cancer?

A

Female, older, lack of childbearing/breastfeeding, smoking, obesity, alcohol, diet, carcinogens, BRCA1 or 2

85
Q

What treatments are used for breast cancer?

A

Surgery, radio/chemotherapy, herceptin

Integrated Medical Sciences (51 decks)

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