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CMP > Cancer > Flashcards

Cancer Flashcards

0
Q

What are the genes associated with breast cancer?

A

BRAC1, BRAC2, 60-80% risk.

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1
Q

Why has there been an increase in cancer incidences?

A

Breast cancer - delays in childbirth.
People are living longer.
Increase in environmental carcinogens eg. Smoking.

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2
Q

What is the gene associated with bowel cancer?

A

Familial adenomatous polyposis coli (APC) gene. Tumour suppressor gene.

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3
Q

What is “cancer”?

A

Breakdown of control of cell differentiation, proliferation and cell death.

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4
Q

What is required for cancer development?

A

Increased cell growth, decreased cell death.

Mutation of tumour suppressor genes and oncogenes.

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5
Q

What are the three stages of colorectal cancer?

A
  1. Early adenoma.
  2. Late adenoma.
  3. Carcinoma.
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6
Q

Why are 90% of cancers of epithelial origin?

A

Proliferating tissues - exposed - higher rate of mutation in proliferating cells.
Non-proliferating tissues - mutation less likely in non-growing cells.

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7
Q

What are the 6 hallmarks of cancer?

A
  1. Evading apoptosis.
  2. Self sufficiency in growth signal.
  3. Insensitivity to anti-growth signals.
  4. Tissue invasion and metastasis.
  5. Limitless replicative potential (immortal).
  6. Sustained angiogenesis.
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8
Q

Define genomic instability.

A

Acquired or inherited DNA repair defects resulting in a high mutation frequency.

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9
Q

How can chemical carcinogens cause cancer?

A

Mutation of growth control genes such as proto-oncogenes (ras) and tumour suppressor genes (p53) and alteration of gene expression.

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10
Q

What is a proto-oncogene?

A

A normal gene involved in normal growth control and differentiation.
Often involved in controlling the cell cycle.
E.g. C-rad or C-myc.

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11
Q

What is an oncogene?

A

A gene who’s product (protein) can act in a dominant fashion to help make a normal cell cancerous. Typically a mutant form of a proto-oncogene. Some tumour viruses encode oncogenes as part of their viral genome.

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12
Q

What is a complete carcinogen?

A

Produces tumours without the addition of tumour promoters.

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13
Q

What are incomplete carcinogens?

A

Initiating agents that cannot produce tumours without exposure of the treated cells (initiated cells) to tumour promoting agents.

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14
Q

Describe the action of initiating chemicals.

A

Almost always genotoxic (DNA damaging) and mutagenic.

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15
Q

What do tumour promotors do?

A

They are not mutagenic, instead they cause irritation and inflammation, alter gene expression and inhibit metabolic cooperation. They promote clonal expansion of initiated cells.

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16
Q

Give an example of a mutagenic initiating agent.

A

B(a)P found in tobacco

Benzo(a) Pyrene

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17
Q

Give an example of a non-mutagenic tumour promoting agent.

A

TPA - a phorbol ester that causes inflammation and activates the protein kinase c signalling pathway.

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18
Q

Give an example of an indirect carcinogen.

A

B(a)P once activated. Binds to guanine causing codon 12 mutations in c-H-ras oncogene.

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19
Q

Give an example of a direct carcinogen and how it works.

A

7,8-Diol-9,10-Epoxide. Bonds directly to guanine in DNA causing mutations.

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20
Q

What are oncogenic viruses?

A

10-20% of human cancers can have viral involvement.
Viruses capable either alone or in cooperation with other agents of converting normal cells to tumour cells OR pushing abnormal cells further along the pathway to cancer.

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21
Q

How can viral cancer incidence be reduced?

A

Vaccine production.
Identification and avoidance of infection risks. (Eg. Prostitutes)
Screening high risk patients. (Eg. Drug addicts)

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22
Q

Give an example of a changing trend in cancer incidence caused by viruses.

A

Cervical cancer caused by HPV virus. Sexually transmitted.

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23
Q

How can a proto-oncogene become an oncogene?

A

A single base pair point mutation in the gene leading to mutant protein function.
Over expression of the normal (unmutated) gene leading to high levels of normal protein (eg c-myc). Epidermal growth factor receptor can be over expressed and/or mutated.

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24
Q

What is the product of the ras proto-oncogene?

A

P21 protein. Has reduced GTPase activity.

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25
Q

What does the ras oncogene do?

A

Functions as a G protein involved in signal transduction at the cell membrane.

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26
Q

What is the outcome of a ras mutation?

A

Ras in constitutively switched on to continuously signal for growth. The ras-proto-oncogene is regulated by growth factor binding to receptors. Mutant ras doesn’t require growth factor binding to be active. Mutant ras is dominant.

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27
Q

What are acute transforming viruses? Give three examples.

A

Viruses with oncogenes that transform cells quickly in culture, inducing tumours within 2-6 weeks. Eg. Avian erythroblastosis, simian sarcoma virus or Harvey ras virus.

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28
Q

Give an example of a slow transforming virus.

A

Avian leukosis virus - no oncogene.

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29
Q

What is a slow transforming virus?

A

Does not have an oncogene. Takes 3-14 months for tumours to appear, has specific integration sites in cellular DNA leading to viral promoter sequences causing over expression of c-myc.
Slowness due to the randomness of integration.

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30
Q

What are the three basic models for transporting growth factors to cells?

A

Endocrine, Paracrine and autocrine (EGF, FGF, TGF)

31
Q

What is autocrine secretion?

A

Tumour cells often respond to their own growth factors.

32
Q

What is the function of TGF-B?

A

Stimulates fibroblasts, inhibits epithelial cell growth.

33
Q

Describe the relationship between simian sarcoma virus and PDGF growth factor.

A

A region of 104 amino acids on the PDGF is almost identical to the predicted sequence of the p28sis oncogene. This suggests that Simian sarcoma virus has acquired cellular sequences which encode a growth factor identical or similar to PDGF and the expression of the protein mediates transformation by the virus.
V-sis is a mutated version of c-sis picked up by the simian sarcoma virus during infection of mammalian cells.

34
Q

What is PDGF?

A

Platelet derived growth factor. A growth factor found in blood serum, released from platelets at wounded sites and thought to be involved in wound healing. Major mitogen in serum for cells of mesenchymal origin.
PDGF receptors are found on fibroblasts, smooth muscle cells and glial cells bells but not epithelial, endothelial or lymphocytes.

35
Q

How can simian sarcoma virus lead to uncontrolled growth by tumour cells?

A

Secretion of the growth factor to interact with its PDGF receptors.
Direct intracellular effect bypassing the need for receptors.

36
Q

What is epidermal growth factor?

A

A single polypeptide chain that binds to epidermal growth factor receptors.
Binding EGF to its receptor triggers the induction of DNA synthesis as a result of phosphorylating tyrosine residues.
Has an important role in growth control.

37
Q

Where are EGFReceptors found?

A

Found on a wide range of cells including all germ layers; ectoderm, mesoderm and endoderm, epithelial and fibroblastic. Not restricted to the epidermis.

38
Q

Where is EGF produced in rats and mice?

A

Salivary glands.

39
Q

What is the relationship between EGF and avian erythroblastosis virus?

A

Close structural similarity between EGF receptor and V-erb B oncogene of avian erythroblastosis virus.

40
Q

How does the mutant EGF receptor stimulate DNA synthesis?

A

The growth factor binds to the receptor and activates the intrinsic tyrosine kinase activity associated with the inner cytoplasmic domain of the receptor.
This leads to autophosphorylation of the receptor and other cellular proteins, stimulating DNA synthesis.

41
Q

How can tumours grow in the absence of growth factors?

A

Mutant EGF receptors are activated even in the absence of the growth factor.

42
Q

Describe the process of autocrine secretion.

A

Over expression of growth factors (PDGF).
Abnormal growth factor receptors (EGF receptor).
Over expression of normal growth factor receptors due to mutations in genes regulating the expression of growth factors. (EGF).
Ross sarcoma virus encodes protein activity and aberrant phosphorylation of signalling pathways.
Mutation of intracellular signalling pathways such as ras or over expression such as c-myc.

43
Q

What is the difference between a benign tumour and a cancerous one?

A

A tumour is malignant when it has invaded the basement membrane.

44
Q

What similarities are there between foetal cells, normal embryogenesis and cancer cells?

A

Cancer cells often hijack normal cellular processes.
Cancer cells often show retro-differentiation, can behave similarly to embryonic cells and express embryonic markers (eg become more motile and grow rapidly, angiogenesis and can be invasive).

45
Q

How do cancers spread?

A

A formerly benign tumour becomes malignant when it penetrates the basal lamina, and invades the capillaries below.
The metastatic cells then adhere to capillary walls and escape to surrounding tissues, where they proliferate.

46
Q

What are the pathological differences between benign and malignant tumours?

A

Benign:
Encapsulated. Non invasive. Highly differentiated (organised). Rare mitosis. Slow growth. Little or mild dysplasia (size, shape and organisation). Non metastatic. Often completely curable.
Malignant:
Non encapsulated. Invasive (destroys local tissue). Poorly differentiated. Mitosis relatively common. Rapid growth. Dysplasia. Metastatic. More difficult to treat due to metastasis and spread.

47
Q

What happens when a cell becomes dysplasic?

A

The tissue becomes disorganised, large nucler:cytoplasm ratio, the cells are abnormal.

48
Q

What is angiogenesis?

A

The process of generating new capillary blood vessels, resulting in neovascularisation.
Occurs during the growth of a progressive tumour.

49
Q

How is metastasis influenced by angiogenesis?

A

Before vascularisation tumours are generally unable to shed cells into the circulation. Hence prevascular tumours have a low probability of metastasising compared to their vascularised counterparts.

50
Q

How can angiogenesis factors be detected?

A

Cell culture of endothelial cells - induce DNA synthesis.

Implantation in the developing rabbit cornea - induce production of new blood vessels.

51
Q

Give some examples of angiogenesis factors.

A

Acidic and basic fibroblast growth factors.
TGF-B and a
Angiogenin
Heparin
Vascular endothelial growth factor (VEGF)

52
Q

How do tumours respond to hypoxia?

A

Reduction in oxygen levels within a tumour initiates a mostly transcriptional response mediated by the HIF-1 transcription factor (Hypoxia Inducible Factor).

53
Q

What is HIF-1?

A

A heterodimic transcription factor composed of two subunits.
Direct target of HIF-1 is VEGF which stimulates new blood vessel formation.

54
Q

What are two possible anti-angiogenesis factors?

A

Thrombospondin-1 and angiostatin. Both are expressed in normal cells and reduced in tumours.

55
Q

What is the three step hypothesis proposed to describe biochemical events during tumour invasion of the extracellular matrix?

A 
Attachment to the extracellular matrix. 
Local proteolysis (production of proteases to destro the basement membrane). 
Tumour cell locomotion into the region of matrix modified by proteolysis.
56
Q

What is epithelial mesenchymal transition?

A

EMT - cells become more motile.

Characterised by a loss of E Catherine expression (cell:cell adhesion molecule).

57
Q

What is anoikis?

A

A form of programmed cell death induced by anchorage-dependant cells detaching from the surrounding extracellular matrix.

58
Q

How are metastatic cells resistant to anoikis?

A

Increased expression of bcl-2 survival anti-apoptotic genes.

59
Q

What is the NM23 gene?

A

Expressed in non-metastatic tumours but not in metastatic tumours. It is a tumour suppressor gene. Present in benign tumours and normal cells.

60
Q

What prevents most metastatic cells from becoming tumours?

A

Mechanical sheer forces.
Loss of attachment and spreading leads to cell death by anoikis.
Oxygen toxicity.
Destruction by host circulating natural killer cells.

61
Q

Why do primary tumours often metastasise to specific organs, eg. Colon cancer –> liver, breast cancer –> lung or prostate –> bone.

A

Easy access via circulation from primary tumour through blood or lymphatics.
Some tumours still require certain growth factors but not others eg hepatocyte growth factor receptors are over expressed on colon cancers so the cancerous cells will metastasise to the liver. Seed and soil hypothesis.

62
Q

When does a benign tumour become malignant with the ability to metastasise?

A

Accumulates further genetic changes - further proto-oncogenes mutated and deletion of more tumour suppressor genes. Reduced E Cadherin involved in cell-cell adhesion.
Develops new blood supply through production of angiogenesis factors, allows the tumour to grow.
Tumour becomes invasive.

63
Q

Outline the currently available cancer therapies.

A

Surgical removal of primary tumours.
Radiotherapy to shrink primary or secondary tumours.
Chemotherapy.

64
Q

What are the issues with surgical removal or radiotherapy in cancer treatments?

A

Radiotherapy in brain tumours can damage surrounding tissue, and neither can treat disseminated disease which has spread with the location of the cancer cells not known.

65
Q

What are the issues with chemotherapy?

A

Kills proliferating cells and normal cells, particularly in renewing tissue such as the bowel, skin and blood.
Toxic to bone marrow.
Drug resistance - relapse not uncommon.

66
Q

What is fluorouracil (5FU)?

A

Common chemotherapy drug used to treat various cancers.

Pyrimidine analogue, inhibits DNA synthesis in rapidly growing cells (including normal cells, hence side effects).

67
Q

How can monoclonal antibodies be used in cancer treatment and research?

A

Localisation of tumours - hunt for primary tumours and metastasis.

68
Q

What changes on the cell surface can be possible targets for monoclonal antibodies?

A

Altered carbohydrates.
Over expressed EGF receptor.
Virally coded protein.

69
Q

How can herceptin be used in breast cancer treatment?

A

HER2 (human epidermal growth factor receptor 2) is over expressed on a subset of breast cancers resulting in increased intrinsic HER2 kinase activity and growth.
Herceptin is a monoclonal antibody to the HER2 receptor and blocks its intrinsic kinase activity and is only effective in the minority of patients that over express HER2.

70
Q

What is tamoxifen?

A

An antagonist of the oestrogen receptor, blocking its activity by blocking oestrogen binding in breast cancer tissue. Standard endocrin therapy in hormone-positive early breast cancers.

71
Q

What is avastin?

A

Humanised monoclonal antibody. Angiogenesis inhibitor. Prevents the formation of new blood vessels by targeting and inhibiting the function of a natural protein called vascular endothelial growth factor that stimulates angiogenesis.

72
Q

What does ricin do?

A

Ricin toxins inhibit protein synthesis and induces cell death.

73
Q

How can ricin be used in cancer treatment?

A

If theB chain of ricin is replaced by other proteins, ie antibodies specific to tumour cells, should have a powerful cytotoxic effect against those cells.

74
Q

Describe the process of autologous bone marrow transplantation.

A

A sample of the patients bone marrow is removed before high dose therapy and later re implanted upon completion of the treatment.
With diseases such as leukaemia or lymphoma the marrow is infiltrated with malignant cells and so it is imperative to clear the marrow of these cells before it is returned to the patient.
No problems with rejection.

75
Q

What is allegeneic bone marrow transplantation?

A

The patient is given normal bone marrow from an uninfected individual.
The donor and recipient must be matched for histocompatability antigens in order to reduce the risk of provoking graft versus host disease (GVHD) a life threatening complication resulting from the attack of host cells by T lymphocytes in the allograft (donor tissue).

76
Q

What is the solution to GVHD?

A

Removal or killing of T lymphocytes in the marrow of the donor before it is infused into the patient.

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