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MedST IB: Biology of Disease (BoD) > 7.0 Cancer > Flashcards

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
Q

What molecules are pro-apoptotic?

A

BAX<br></br>p53<br></br>Cytochrome C<br></br>Caspases

26
Q

What molecules are anti-apoptotic?

A

Bcl2

27
Q

What are the repeats in telomeres?

A

TTAGGG

28
Q

What can HPV do to Rb-1 and p53?

A

Bind to and inactivate

29
Q

What is the major barrier to metastasizing cells?

A

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
Q

Define initiator (with regards to cancer):

A

Initiator = chemicals that damage DNA directly

31
Q

Define promoter (with regards to cancer):

A

Promoter = Promote development of tumors without damaging DNA

32
Q

Mechanism for imantinib:

A

Inhibits BCR-ABL receptor tyrosine kinase<br></br><br></br>Used for CML

33
Q

How does resistance to imantinib occur?

A

Via point mutation (prevents imantinib from binding)

34
Q

Mechanism for Herceptin:

A

Monoclonal antibody to HER2 (RTK)

35
Q

Mechanism for Vemurafenib:

A

BRAF inhibitor

MedST IB: Biology of Disease (BoD) (9 decks)

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