7.0 Cancer Flashcards

1
Q

What can the genetic changes in cancer be due to?

A

<b>1) Mutations</b><br></br>- Anything that alters DNA sequence<br></br><br></br><b>2) Epigenetics</b><br></br>- Methylation / histone modifications<br></br><br></br><b>3) Viruses</b><br></br>- Tumour viruses bring extra genes into cell

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2
Q

What normally precedes a colorectal malignant tumour?

A

Polyp/adenoma

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3
Q

Common sites for metastasis:

A

1) Brain<br></br>2) Liver<br></br>3) Bone marrow<br></br>4) Lung

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4
Q

Where does breast cancer normally metastasise?

A

Local lymph nodes and bone

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5
Q

Where does colorectal cancer normally metastasise?

A

Liver

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6
Q

Define lipoma:

A

Benign fat cell tumour

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7
Q

Define leiomyoma:

A

Benign smooth muscle tumour

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8
Q

Define Adenoma:

A

Benign tumour of glandular tissue

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9
Q

Define papilloma:

A

Wart

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10
Q

Define carcinoma:

A

Malignant epithelial tumour

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11
Q

Define adenocarcinoma:

A

Malignant epithelial tumour of glandular origin

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12
Q

Define liposarcoma:

A

Malignant fat cell tumour

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13
Q

Define leimyosarcoma:

A

Malignant smooth muscle tumour

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14
Q

Define osteosarcoma:

A

Malignant bone tumour

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15
Q

What are neuroblastomas / glioblastomas?

A

Both are <b>malignant</b> neural tumours

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16
Q

Difference between leukaemias and lymphomas:

A

Leukaemias = Liquid haematopoietic neoplasms<br></br><br></br>Lymphomas = Solid haematopoietic neoplasms (usually lymphocytic)

17
Q

Define the following terms with examples:<br></br><br></br>1) Neoplasia<br></br>2) Hyperplasia<br></br>3) Metaplasia<br></br>4) Dysplasia

A

“<div><img></img></div>”

18
Q

Define cachexia:

A

General systemic wasting<br></br><br></br>Exact mechanism unknown - ?competition for metabolic resources?

19
Q

Oncogenes vs tumour suppressor genes:

A

<b>Oncogene</b><br></br>- Overactivity mutations<br></br>- Dominant in the cell<br></br>- Only one copy needs to be mutated<br></br><br></br><b>Tumour suppressor genes</b><br></br>- Loss of function mutations<br></br>- Recessive in the cell<br></br>- Both copies need to be mutated

20
Q

What is the structure of p53?

A

Tetramer <br></br><br></br>This creates a unique form of mutation. It is a tumour supressor gene but only needs one copy of the gene to be mutated to have an effect. Losing both copies has a stronger effect

21
Q

What are the two types of genetic instability in colon cancer?

A

<b>1) Chromosomal instability (CIN)</b><br></br>- Rearranged chromosomes<br></br>- Due to loss of protective mechanisms against chromosome aberrations<br></br><br></br><b>2) Sequence instability</b><br></br>- Normal chromosomes<br></br>- <b>microsatellite instability</b><br></br>- Mainly due to DNA mismatch repair inactivation

22
Q

What are MLH1 + MSH2 needed for?

A

Mismatch repair<br></br><br></br>Defects seen in colon cancer

23
Q

What is BRCA2 needed for?

A

Single + double strand repair<br></br><br></br>Defects seen in breast cancer

24
Q

What are the hallmarks of cancer?

A

<b>Proliferation and survival changes</b><br></br>1) Independence of growth signals<br></br>2) Resistance to growth inhibitory signals<br></br>3) Resistance to apoptosis<br></br>4) Immortality<br></br>5) Differentiation block<br></br><br></br><b>Genetic instability</b><br></br>6) Metabolic changes<br></br>7) Angiogenesis<br></br>8) Metastasis

25
What molecules are pro-apoptotic?
BAX
p53
Cytochrome C
Caspases
26
What molecules are anti-apoptotic?
Bcl2
27
What are the repeats in telomeres?
TTAGGG
28
What can HPV do to Rb-1 and p53?
Bind to and inactivate
29
What is the major barrier to metastasizing cells?
Survival and growth in distant site (many cells can circulate body and exit circulation at different sites - most die because cannot survive and grow at this site)
30
Define initiator (with regards to cancer):
Initiator = chemicals that damage DNA directly
31
Define promoter (with regards to cancer):
Promoter = Promote development of tumors without damaging DNA
32
Mechanism for imantinib:
Inhibits BCR-ABL receptor tyrosine kinase

Used for CML
33
How does resistance to imantinib occur?
Via point mutation (prevents imantinib from binding)
34
Mechanism for Herceptin:
Monoclonal antibody to HER2 (RTK)
35
Mechanism for Vemurafenib:
BRAF inhibitor