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J Term 2 mix > Cancer > Flashcards

Cancer Flashcards

1
Q

The 6 Hallmarks of cancer

AIRSAM

A
  1. apoptosis-resistant
  2. Indefinite growing
  3. Resistant to anti-growth signals
  4. self-sufficient growth signals
  5. angiogenesis
  6. metastasis - altered e-cadherin expression
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2
Q

What is dysplasia

A

abnormal maturation of cells, premalignant

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3
Q

3 characteristics of benign and malignant tumour

A

Benign: differentiated, compressing on surrounding tissue, low mitotic count

malignant: undifferentiated, irregular outline as it’s broken through surrounding BM, low-high mitotic count

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4
Q

What is a benign epithelial transitional neoplasm called

A

transitional cell papilloma

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5
Q

What is a benign epithelial cell cancer called

A

papilloma

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6
Q

What is a malignant epithelial cell cancer called

A

carcinoma

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7
Q

What do carcinomas commonly invade into

A

lymphatics

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8
Q

What would you call a benign glandular epithelial neoplasm and give an example

A

adenoma, ex; polyp of the colon

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9
Q

Where would you find a basal cell carcinoma

A

the skin

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10
Q

How would you describe a malignant epithelial cancer of the stomach

A

adenocarcinoma

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11
Q

Give the cancerous word for a … neoplasm
Benign: fibrous tissue, nerve, glial cell
Malignant: bone, cartilage, fat, nerve sheath, glial cell

A

Benign: fibroma, neurofibroma, glioma
Malignant: osteosarcoma, chondrosarcoma, liposarcoma, neurilemmosarcoma, malignant glioma

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12
Q

Name two types of lymphoid neoplasms

A

Hodgkin’s and non hodgkin’s

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13
Q

Name two types of hematopoietic neoplasms

A

Acute and chronic leukemia

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14
Q

What is a myeloma and what’s a consequence?

A

A malignant neoplasm of the plasma cells in the bone marrow, destroys adjacent tissue

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15
Q

What is a cancer of all cell types called, where can it form and when is it malignant or benign?

A

Teratoma, testis - malignant, ovaries - benign

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16
Q

What is a seminoma

A

Malignant neoplasm of seminiferous tubules (sperm)

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17
Q

Name the 5 mechanisms that facilitate invasion and metastasis

A
  1. altered cell adhesion
  2. altered enzyme synthesis and interaction
  3. angiogenesis
  4. lymphatics
  5. vascular
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18
Q

What changes in altered cell adhesion?

A

Cadherins - link cell to cell, alteration allows cells to move apart from each other

Integrins - links cell to the stroma, alteration allows cell movement

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19
Q

How does the alteration of enzyme synthesis and interaction occur?

A

Metastatic cells release matrix metalloproteinases that destroy cartilage and the ECM, allowing them to move through and metastasize

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20
Q

When does a metastatic cell do angiogenesis, how and what 2 things does it allow?

A

When it has grown to 1-2mm cubed and run out of nutrients, in response to a hypoxic environment it secretes proangiogenesis factors such as angiopoietin and VEGF
This allows for; 1. continued growth, 2. opportunities for metastasis

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21
Q

What type of cancer commonly spreads to lymphatics

A

carcinoma

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22
Q

What are 4 common sites cancers can spread to vascularly

A

bone, brain, lung and liver

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23
Q

What two things can happen if cancer spreads to the bone

A
  1. pathological fractures

2. Osteosclerosis: production of dense bone when bone loses flexibility and becomes weaker

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24
Q

Local complications of benign and malignant neoplasms (3 shared ones!)

A

Benign:
partial or complete obstruction, ulceration, space occupying lesion, compression

Malignant: partial or complete obstruction, ulceration, space-occupying lesion, infiltration into surrounding nerves vessels and lymphatics, destroy surrounding tissue

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25
Q

Name 3 components of Hematological systemic effects

A
  1. anemia
  2. low WC and platelet count
  3. thrombosis
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26
Q

Two types of endocrine systemic effects

A
  1. excessive hormone secretion - corticosteroids, parathyroid hormone
  2. ectopic hormone secretion - ACTH by small cell carcinoma of bronchus
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27
Q

What could occur as a result of a neuromuscular systemic effect

A

balance problems, sensory and motorsensor neuropathies, myopathy that can progress to muscle weakness, progressive multifocal leucenopathy

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28
Q

How does Hep B induce a neoplasm, is it direct or indirect?

A

Infects the hepatocytes by injecting viral DNA into the host cell genome, causes chronic damage to hepatocytes leading to regeneration and risk of mutation
Indirect.

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29
Q

How does Epstein Barr induce a neoplasm, what is associated with, is it direct or indirect?

A

Associated with the pathogenesis of Burkitt’s lymphoma, some Hodgkin’s lymphoma and Nasopharyngeal carcinoma
Infects epithelial cells, oropharynx and B cells, makes them proliferate more increasing the chance of mutation
Indirect.

30
Q

How does Human papilloma induce a neoplasm, is it direct or indirect?

A

HPV produces E6 and E7, E6 inhibits P53 (tumour suppressor gene) - the guardian of the genome, scavenges mutated cells and marks them for apoptosis
E7 inhibits PRB - the restriction point in the cell cycle, another tumour suppressor gene
Direct.

31
Q

What two things can asbestos result in and how? How is it related to cigarette smoke?

A

Asbestos has a long exposure time and is a complete carcinogen. It has thin fibres that can get into the lungs, causing inflammation that ciggy smoke can get stuck in
Malignant mesothelioma, lung cancer

32
Q

What are aflatoxins and what can they result in?

A

Aflatoxins are poisonous carcinogens produced in certain molds, hepatocelular carcinoma

33
Q

What can result from a Schistosoma?

A

It’s a parasite depositing in the bladder wall, leading to inflammation and mucosal squamous metaplasia - bladder cancer

34
Q

What can cause helicobacter pylori cause

A

Gastric inflammation, it is an indirect carcinogen

35
Q

What is ulcerative colitis? How can it predispose cancer?

A

A long term condition causing inflammation of the colon and rectum - leading to DNA damage and colorectal carcinoma

36
Q

What is liver cirrhosis? How can it predispose cancer?

A

Fibrosis of the liver, caused by chronic Hep B, alcohol use or alpha1antitrypsin deficiency - leading to hepatocellular carcinoma

37
Q

What kind of epithelial cancer can an adenoma (benign tumour of glands) cause ;)))))

A

adenocarcinoma

38
Q

Hereditary non-polyposis colon cancer

A

Autosomal dominant, it’s a germline mutation affecting one of several DNA mismatch repair genes - colon carcinoma associated

39
Q

What can retinitis xeroderma pigmentosum cause?

A

Mutation in DNA repair genes, increases risk of skin cancers when exposed to UV

40
Q

What can ataxia-telangiectasia cause?

A

Radiation damage can lead to profound susceptibility to lymphoid malignancies

41
Q

What is Fanconi’s anemia

A

Sensitivity to DNA cross-linking agents leads to BM hypofunction and multiple congenital abnormalities - predisposing cancer

42
Q

How can a proto-oncogene become an oncogene? What do oncogenes do?

A

Needs one allele to be mutated, oncogenes create oncoproteins that allow the cell to escape normal growth control - providing self-sufficiency

43
Q

How can a proto-oncogene become an oncogene? What do oncogenes do?

A

Needs one allele to be mutated, oncogenes create oncoproteins that allow the cell to escape normal growth control - providing self-sufficiency

44
Q

What is the theory behind mutating tumour suppressor genes and what does this lead to?

A

Tumour suppressor genes encode proteins that suppress growth, need both alleles to be mutated.
Knudson’s 2 hit hypothesis states that you can have 2 sporadic mutations or 1 inherited and 1 sporadic to mutate a TSG

45
Q

What is Ras and what is its role?

A

An oncogene.
Encodes a small G protein that pushes cell pas the R point - leading to continuous stimulation of cells
(colon and lung cancer)

46
Q

What is c-myc and what is its role? What can it cause?

What is an example of Burkitt’s lymphoma

A

stimulates proliferation and transcription factors in DNA, the defect becomes amplified. Causing neuroblastoma, breast cancer, and
BL: translocation 8-14

47
Q

What is Her-2 and its role?

What would you give?

A

Human epidermal GF receptor - an oncogene that encodes for GF receptor and is amplified - causing proliferation and gives 25% of breast cancers
Give herceptin, a competitive antagonist against the receptor

48
Q

How does PRB suppress tumour growth

A

When the cell is ready to divide, retinoblastoma (RB) phosphorylates into pRB, therefore inactivating itself so the cell can go through. Becomes permanently fucked in cancer

49
Q

How does p53 work?

A

Encodes for a nuclear protein that binds to and modulates the expression of genes important for cell-cycle arrest, DNA repair and apoptosis

50
Q

What’s an initiator?

A

Mutagen, exposing the cell to a dose is irreversible but cannot induce a tumour on its own

51
Q

What’s a promoter

A

Causes overproliferation of cells - increasing the chances of mutation and that mutation being mitosed

52
Q

What’s a complete carcinogen and what does that mean?

A

It’s an initiator and a promoter - cigarettes

53
Q

List 2 agents that can result in the development of tumours

A
  1. Radiation

2. Chemicals

54
Q

How does radiation cause a mutation, and what are the types?

A

A direct effect: causes single and double-strand breaks and base damage
Indirect: free radical production
If enough mutations occur in TSG and proto-oncogenes cancer can occur
-ionizing radiation, e.g; hiroshima
-UV radiation, skin cancers: squamous cell, basal cell carcinoma and malignant melanoma

55
Q

Name the 5 types of chemicals that can interact with DNA and how they work

A
  1. Polycyclic aromatic hydrocarbons: produced in the combustion of tobacco and fossil fuels - hydroxylated to active form
  2. Aromatic amines: e.g 2-nap thylamine
    Hydroxylated in the liver and conjugated with glucuronic acid in the urinary tract by glucuronidase - active form sits in the bladder causing bladder cancer
  3. alkylating agents: binds directly to DNA, causes alkylation which leads to DNA damage
  4. N-nitroso compounds
  5. Natural diverse products: aflatoxins and asbestos
56
Q

What do pro-carcinogens require to be converted to carcinogens

A

P450 enzymes in the liver

57
Q

How does TNM staging work?

A 
T= primary tumour size 1-2
N = lymphatics - 3
M = metastasis - 4
58
Q

What is Dukes staging used for? How does it work?

A

Colorectal carcinoma
A - still in the bowel wall
B - through the bowel wall
C - lymph node involvement (1-2) depending on the distance away

59
Q

What staging is used for Hodgkin’s disease

A

Ann Harbor Classification
1 - one node
2 - two nodes on the same side of diaphragm
3 - two nodes on both sides of diaphragm
4 - multiple foci

60
Q

What does grading tell you?

A

Based on the degree of differentiation of tumour cells

G1-G4 well - undifferentiated (malignant)

61
Q

What does anaplasia mean?

A

The most severe dysplasia, obviously undifferentiated

62
Q

What grading system is used for Breast Carcinoma and what 3 things does it measure? What does the grading system tell you?

A 
Scarff-Bloom-Richardson Grading System 
-Degree of Tubule formation
-the extent of nuclear variation
-number of mitoses 
Grade 1-3, decreases the % of 10-year survival rate
63
Q

What grading system is used for prostate cancer

A

Gleason Grading System

64
Q

How does radiotherapy help cancer?

A

Causes damage to DNA of rapidly dividing cells - if DNA damage becomes extensive this leads to apoptosis

65
Q

How does chemotherapy help cancer? Name 3 drugs and what they do

A

Drugs have effects at particular stages of cell cycle and on rapidly diving cells

  • Cyclophosphamide: acts on cells in G1, S and mitosis
  • Plant-based drugs: Vincristine: blocks cells entering cell cycle
  • Methotrexate: acts on S phase
66
Q

Name 2 types of hormone therapy and what they’re used for

A

Tamoxifen - 50-80% of breast cancers express estrogen receptors, therefore tamoxifen competes for binding to estrogen receptors

Herceptin: competes to bind to Her2 receptors which are overexposed in 20-30% of breast carcinomas
-side effects: cardiac/pulmonary toxicity which can be fatal

67
Q

What does treatment depend on for prostate cancer

A

The type of androgen

68
Q

Name 3 tumour markers

A

Carcinoembryonic antigen
Human Chorionic Gonadotrophin (HCG)
Alpha-fetoprotein (AFP)

69
Q

What does carcinoembryonic antigen do?

A

Normally only expressed in embryonic tissue but cancer cells express it again - useful to see if there’s residual disease leftover after removal of tumours

70
Q

When is HCG used?

A
  1. evaluates testicular masses (germ cell)
  2. indicates residual disease
  3. monitors response to therapy and prediction of recurrence
71
Q

When is AFP used?

A

normally synthesized early in fetal life by the yolk sac, fetal liver and fetal GIT
Raised plasma levels indicate cancer of the liver and yolk sac tumour of the testis/nonseminatous testicular tumours

72
Q

How is screening used? Name two examples

A

Aims to detect pre-malignant, non-invasive/early invasive cancers to improve prognosis
Cervical Intraepithelial neoplasia - CIN
Breast: identifying invasive cancers before they can be felt

J Term 2 mix (8 decks)

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