Carcinogenesis Flashcards

1
Q

What are the three common characteristics of all cancers

A

It is a genetic disorder caused by DNA mutations

Genetic alterations in cancer cells are transmitted to daughter cells

Mutations and epigenetic alterations give cancer cells hallmarks

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2
Q

Name some of the hallmak=rks of cancer

A

Self sufficent in growth signals, insensitive to inhibitory ones

Evasion of apoptosis and limitless reproductive potential

Systained angiogenesis and altered cell metabolism,

Evasion of immune surveillance, and evasion and metastasis

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3
Q

What ccancers can ionising radiation lead to

A

Acute and chronic myeloid leukaemia, papillary carcinoma of thyroid

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4
Q

What cancers can non-ionising radiation cause (UVB, sunlight)

A

Squamous cell carcinoma, basal cell carcinoma, malignant carcinoma of skin

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5
Q

What are oncogenes

A

Cells which control growth and differentiation

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6
Q

What different types of oncogenes are there

A

Proto-oncogenes: FOr cell growth and differentiation

Growth factor/growth factor receptors (these induce cell growth)

Signal transducers: relay receptor activation to nucleus

Cell cycle regulators mediate progression though the cell cycle

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7
Q

What do tumour supressor genes do

A

Regulate cell growth, decrease risk of tumour formation

notable examples are p53 and retinoblastoma

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8
Q

What does p53 do

A

Tumour supressor gene,

regulates cell cycle and DNA repair, papoptosis. Can be damaged by mutation or loss of alleles.

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9
Q

What is the knudson two-hit hypothesis

A

Both copies of the gene must be knocked out for tumour formation (such as with p53)

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10
Q

At what point is p53 active in the cell cycle

A

During G1 checkpoint, if DNA is found to be damaged, p53 gene is activated, preventing access to S phase, arresting the cell cycle

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11
Q

Describe the cell cycle in order

A

G1 -> S -> G2 - > M -> G1

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12
Q

What other Tumour supressor gene acts like p53

A

Rb

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13
Q

What do apoptosis regulators do

A

prevent apoptosis in normal cells but promote ti in mutated cells with un-repairable DNA

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14
Q

How does BCL2 and cytochrome C regulate apoptosis

A

BCL2 stablises mitochondrial membrane, blocking cytochrome C release. Disruption og BCL2 allows cytocchrome C to leavemitochondria and activate apoptosis.

Follicular lymphoma gets around this

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15
Q

What is telomerase and what happens woth cancers

A

They shorten with serial cell divisions, eventually causing senescence.

Cancer cells show upregulation of telomerase

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16
Q

What is angiogenesis and how is it linked to cancers

A

The new blood vessel formation is needed for tumour survival and growth. Cancers usually produce fibroblast growth factor and vascular endothelial growth factor, both angiogenic, responsible for blood vessel creation

17
Q

What is dysplasia?

A

disordered cell growth, often precancerous cells.

Theoretically reversible with removal of stressor. Otherwise can progress to irreversible carcinoma

18
Q

What is neoplasia

A

Unregulated, clonal, irreversible growth. Neoplastic tumours can be benign or malignant

19
Q

What are the characteristics of a benign tumour

A

Remains localised, slow growing, closely resembles tissue from which they grow, often circumscribed or encapsulated

20
Q

What are the characteristics of malignant tumours

A

Invades surrounding tissues, many can metastasize. Often rapidly growing, varies in resemblance to tissue of origin, irregular margin

21
Q

What is the difference between in situ and invasive carcinoma

A

In situ means an epithelial neoplasm exhibiting all cellular features of malignancy, but hasnt invaded through the epithelial basement membrane, separating form potential routes of metastasis

22
Q

What are some characteristic signs of malignanct cells

A

Increased nuclear/cytoplasmic ratio

Nuclear pleomorphism and hyperchromasia
Irregular chromatin distribution, prominent nucleoli
Irregular nuclear membranes

23
Q

Name characteristics of benign cells

A

Low nuclear to cytoplasmic ratio

All nuclei of similar size, not hyperchromatic, vesiclular, evenly distributed chromatin, smooth nuclear membranes