CE L1 Introduciton Flashcards

1
Q

Why is cancer so hard to treat?

3

A

It’s self
Not diagnosed until late (few symptoms)
Need to eradicate every single cell

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2
Q

Cancer is cells growing ….. and …..

A

too fast and too much

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3
Q

Cancer is more common in what type of cells?

Why?

A

Cells with a high turnover

- most mutations are passed on during cell division

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4
Q

When do we actually want cells to divide and proliferate? (2)

A

Growth and repair

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5
Q

What is cancer?

A

Unregulated growth of abnormal cells, often at inappropriate locations

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6
Q

What is cancer caused by?

A

DNA damage - proteins controlling the function of cells are changed

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7
Q

Cancer cells appear ….

A

immature - therefore cannot carry out their function

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8
Q

What normally kills you in cancer?

A

Not the tumour itself but the lack of normal funciton

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9
Q

What is missing in cancer that would normally prevent cells from keeping growing once they are touching other cells?

A

Contact inhibition

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10
Q

Tumours are classified according to

A

tissue of origin

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11
Q
Sarcomas
Carcinomas
Leukaemias
Adenocarcinomas
arise from...
A

Sarcomas - connecting tissue/muscle
Carcinomas - epithlial cells
Leukaemia - blood cell
Adenocarcinomas - glandular tissue

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12
Q

Properties of benign tumour (4)

A
  • Resembles normal cells
  • Localized
  • Surrounded by fibrous capsule
  • Usually require little treatment (e.g. warts) - Surgical removal if apprprate
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13
Q

Genetic make-up can predispose you to environmental shock e.g.

A

smoking - some people don’t develop cancer even after many years

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14
Q

Properties of malignant tumours: (6)

A
  • less well differentiated
  • grow and divide rapidly
  • high nucleus to cytoplasm ratio
  • invade surrounding tissue
  • more difficult to treat as less defined
  • enter circulation and metastasis
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15
Q

Properties of malignant tumours: (6)

A
  • less well differentiated
  • grow and divide rapidly
  • high nucleus to cytoplasm ratio
  • invade surrounding tissue
  • more difficult to treat as less defined
  • Metastasis
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16
Q

Define metastasis

A

entering circulating and seeding at a different site

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17
Q

Genetic predisposition examples (2)

A
  1. Li-frumeni syndrome

2. Chronic myloid leukemia (CML)

18
Q

What happens in Li-frumeni syndrome?

A

inherited mutation of one p53 gene. Normally functions as a tumour suppressor. Wild type then mutates and cancers form in childhood

19
Q

What happens genetically in CML

A

chromosomal translocation

20
Q

Environemental stressors examples (4)

A

Animal fat in prostate cancer
UV
Radium and oral cancer
Tabacco

21
Q

Many tumour cells have constitutively active pathways thus producing their own….

A

growth factors

22
Q

What are proto-oncogenes?

A

sds

23
Q

What are proto-oncogenes?

What happens to them?

A

genes whose normal function is to control cell growth. Converted into oncogenes by a GAIN OF FUNCTION mutation.

24
Q

3 e.g. of gain of funciton mutations

A

point mutation - always active
gene amplification - more protein
chromosomal translocation

25
Q

What are oncogenes?

A

Gene which encodes a protein able to transform cells - derived from proto-oncogene

26
Q

What are tumour suppressor genes (3 functions)

A

Gene which restrain cell growth, promote cell death and promote DNA repair

27
Q

…………………. of tumour suppressor genes leads to unregulated cell growth of damaged cells

A

LOSS OF FUNCTION

28
Q

Tumour suppressor genes are dominant or recessive?

A

Recessive - so both copies must be lost

29
Q

How does hereditary predisposition with tumour suppressor genes work?

A

You inherit one mutant and later in life the other mutates

30
Q

What is epigenetics?

A

Gene regulation:

Modifications to genomic and chromatin components and structure - alter gene transcription and hence protein expression

31
Q

What things does epigentics wrok with (3)?

A

Histom modificate
methylation
miRNA

32
Q

How many changes have taken place to make cancer

A

3-7 ( cells must survive each one to acquire the next, on different survival pathways)

33
Q

How many changes have taken place to make cancer

A

3-7 ( cells must survive each one to acquire the next, on different survival pathways)

34
Q

Benign tissue surrounding tumour frequently contains …

A

all but one of these mutations

35
Q

Will we cure cancer in the future?

A

more likely to transform it into a long term chronic disease what pt can live with

36
Q

Each cell in the cancer is….

A

a clone of a single cell

37
Q

Cells taken from the outside of a tumour do/don’t grow into cancer when implanted?

A

Don’t - indicating stem cells?

38
Q

Once metastasis has occurred prognosis is

A

poor

39
Q

In order for cells to break off and metastasise what must happen?

A

breakdown and degradation of the basal lamina (release of MMP and invadopodia)

40
Q

What is a transformed cell?

A

Survives longer than it should but is not full on caner