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Cancer and genetics > Cancer cell biology > Flashcards

Cancer cell biology Flashcards

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1
Q

What is carcinogenesis?

A

Formation of cancer
By chemical, physical, viral carcinogens (mutagens)
mutagens can cause by cancer by damaging DNA= mutation

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2
Q

How do carcinogens cause DNA damage?

A
  1. Add chemically modified bases- point mutation

2. Strand breaks by deletion/translocation of chromosome

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3
Q

Risk factors of lung cancer

A
  1. Smoking tobacco
  2. Second hand smoke -those exposed to tobacco
  3. Asbestos
  4. Arsenic- in groundwater, human carcinogen
  5. radon
  6. Carcinogens- vehicle emissions and pollutants
  7. lung disease e.g TB and pneumonia leave scarring on lung tissue
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4
Q

How does asbestos contribute to lung cancer?

A

Naturally occurring minerals used in industries
Fibres easily shatter and suspend into the air and adhere to clothes
Particles can be inhaled and enter lungs
Damaging cells in lung

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5
Q

How does radon contribute to lung cancer?

A

Natural, radioactive gas found in soils and rocks

People who work in mines=exposed to radon

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6
Q

Example of a carcinogenic substance

A

Benzo-[A]-pyrene

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7
Q

How do carcinogens damage DNA? (3 steps)

A

1.Reacts with DNA
2. Forms an adduct with DNA
Adduct= formed when segment of chemical binds to DNA= distorts DNA double helix
3) Mutation

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8
Q

Why is it easy to study different stages of cancer in colorectal cancer?

A

Easy to get a biopsy

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9
Q

Where does colorectal cancer arise from?

A

Epithelium lining of colon and rectum

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10
Q

Where in the large intestine are stem cells that renew lining?

A

Intestinal crypts

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11
Q

Colorectal cancer

A

Small benign tumour (Adenoma) of gut epithelium
Form polyps (mass of abnormal tissue)
Polyps develop into carcinomas by mutations
Later stage- tumour cells break through epithelial basal lamina and spread through muscle of gut
Metastasize to lymph nodes via lymphatic vessels
And to liver, lungs and other organs

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12
Q

What is the most frequently mutated gene in colorectal cancer?

A

Ras (K-ras)

p53 (tumour suppressor gene)

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13
Q

K-Ras mutation in colorectal cancer

A

Point mutation

Activates it to become an oncogene

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14
Q

Cells found in colonic epithelium

A

Stem cells
Goblet cells
Enterocytes (absorb water and electrolytes)
Enteroendocrine cells (secrete hormones)

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15
Q

Cell renewal in colon epithelium?

A

Every 4-5 days

Continuous renewal= more susceptible to cancer forming

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16
Q

Role of Wnt signalling pathway

A

Highly conserved
Essential role in embryogenesis and cell growth (proliferation)
Wnt= glycoprotein
Produced by stromal cells at bottom of colonic crypts
Wnt acts locally- predominantly on intestinal cells
Drives proliferation

17
Q

Wnt signalling pathway (presence of Wnt)

A

Destruction complex= GSK3, B-catenin, APC, AXIN
2 receptors- frizzled and LRP
1. Wnt binds to receptors
2. Dishevelled protein binds to frizzled receptor
3. Destruction complex moves towards receptor
4. Axin binds to dsh-receptor complex
5. Releases B-catenin which translocates to the nucleus= transcription factor
6. -catenin transcribes genes required for cell proliferation (MYC and Cyclin-D)

18
Q

What happens when axin leaves the destruction complex?

A

Inactivates destruction complex
Blocks B-catenin phosphorylation and ubiquitylation
Allows unphopshorylated B-catenin to translocate to nucleus

19
Q

Wnt signalling pathway- when Wnt is absent

A

Destruction complex stays together and (turns on itself)
GSK3 phosphorylates B-catenin
B-catenin undergoes ubiquitylation (degradation in proteasomes)= inhibits proliferation genes
So no proliferation= cells stop dividing and differentiating
groucho keep Wnt genes inactivated

20
Q

Deregulated gene in colorectal cancers?

A

APC
APC= mutated/short protein formed by frameshift mutation (stop codon)
This deregulates destruction complex
So APC can’t bind to B-catenin
Meaning B-catenin is NOT degraded and functions as transcription factor= uncontrollable cell proliferation
In normal cells APC binds to B-catenin and deregulates it

21
Q

What is the earliest mutation in colorectal cancer?

A

APC

Mutation of APC= creates polyps

22
Q

What is familial adenomatous polyposis?

A

Autosomal dominant inherited condition
numerous adenomatous polyps form in the large intestine.
untreated= colorectal cancer

23
Q

MAPK/ERK pathway

A
  1. Growth factor binds to receptor
  2. Ras activated (GDP to GTP)
  3. RAF-MEK-ERK
  4. Cell proliferation
24
Q

What is the signalling pathway that activates oncogenic Ras?

A

MAPK/ERK pathway

25
Q

What are E-Cadherins?

A

Proteins that allow epithelial cells of colon to attach to one another

26
Q

What causes metastasis of colorectal cancer?

A

Breakdown of cell adhesion- loss of E cadherins

Increase levels of Matrix Metalloproteinases (MMPs) which help breakdown extracellular matrix (collagen and proteins)

27
Q

What is a neoplasm?

A

Mass of abnormal cells (tumour)

28
Q

Characteristics of malignant tumours

A
  1. Less differentiated cells (anaplastic)
  2. Pleomorphic=vary in shape and size
  3. High nuclear:cytoplasmic ratio
  4. Hyperchromatic (dark purple) nucleus (chrome= colour)
  5. Fast growing
  6. Many mitotic cells
29
Q

What does cancer in-situ mean?

A

All mentioned for malignant tumours and entire epithelium replaced by dysplastic cells

30
Q

Cancer?

A

Malignant tumour+cancer in-situ+ invasive and metastasizes to other places

31
Q

Nomenclature for cancers

A

-sarcoma
chondrosarcoma (malignant tumours in cartilage)
Adenocarcinoma (epithelial cells of glands tumour)
cytic= cells
normocytic= normal cells
chrome= colour

32
Q

Characteristics of benign tumours

A
  1. Differentiated cells
  2. Monomorphic cells- look the same
  3. Low nuclear:cytoplasmic ratio
  4. Normochromatic nucleus
  5. Slowly growing
  6. Few mitotic cells
  7. Not invasive
  8. Doesn’t metastasize
33
Q

Nomenclature of benign tumours

A

-oma
chondroma
adenoma

Cancer and genetics (3 decks)

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