Cancer Genetics Flashcards

1
Q

What is cancer

A

All cancers are genetic diseases and changes in the DNA sequence of key genes which are known as cancer genes cause this abnormal division of the cells .

DNA polymerase can also make mistakes , changes can also occur due to exposure to mutagens such as UV

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2
Q

What causes cancer

A

Chemicals ( e.g. from smoking) and radiation can damage genes ( environment)

Viruses can introduce their own genes into cells ( exogenous factors)

By heredity , alteration in genes that make a person more susceptible to cancer can be passed to the next generation ( genetics - rate and common)

Meat cooked at high temps can also lead to an increased risk of cholesterol, pancreatic and prostate cancer

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3
Q

What is a benign tumour

A

Massive well differentiated cells that grow slowly and is capsulated and lack the ability to invade neighbouring tissues or to metastasise

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4
Q

What is a malignant tumour

A

Not limited in its growth and the cells are poorly differentiated and capable of dividing into adjacent issues and maybe capable of spreading distant issues at a microscopic level if there are new bed vessels it may be categorised as malignant

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5
Q

What do cancer cells look like

A
Large number of dividing cells
Large, variably shaped nuclei
Large nucleus to cytoplasm ratio
Variation in size and shape 
Loss of normal cell features
Disorganised arrangement 
Poorly defined tumour boundary
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6
Q

Microscopic appearance of cancer cells

A

Pronounced irregular microscopic membrane and there are increased activity of nucleoporins which causes an increase in the input of transcriptional factor

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7
Q

Carcinoma

A

Rise from epithelial cells - most common are lung, breast and colon

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8
Q

Sarcoma

A

Elle found in the supportive cells of the body . Bone, cartilage, fat connective tissue and muscle

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9
Q

Lymphomas

A

Cancers that arise in the lymph nodes and tissues of the body’s immune system

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10
Q

Leukemia

A

Cancers of cells that grow in the bone marrow and accumulate in the bloodstream

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11
Q

Cancers affecting children

A

Leukaemia s ( ALL) and in tissues which are undergoing a high rate of proliferation such as brain and testicular cancer

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12
Q

6 hallmarks of cancer

A
Self sufficiency in growth signals
Evading apoptosis 
Insensitivity to anti growth signals
Sustained angiogenesis 
Tissue invasion and metastasis 
Limitless replication potential 

( also deregulated metabolism and avoid immune destruction has been added)

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13
Q

The life time risk of developing cancer is a particular tissue is correlated with how often stem cells in the tissue divide

A

So intestine has high cell proliferation rate and so increased risk of cancer

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14
Q

Germ.one mutations

A

Present in egg or sperm cell
Are heritable ( family syndrome)
Rare
Germ line cells are the only cells that can undergo mitosis and meiosis

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15
Q

Somatic mutations

A

Occur in non germ line tissues
Are non heritable
Very common ( 90% of all cancers)

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16
Q

Diff types of mutations in cancer cells

A
Deletions
Duplications 
Inversions 
Translocations
Single base substitutions ( point mutations- silent, nonsense and missense ) 
Chromosomal instability 
Aneuploidy
17
Q

Multi step carcinogens is with tumour cells as an example

A

1) initiation where thee is irreversible genetic mutations and allows excessive cell prolif . Colon cancer starts with defect in tumour suppressor gene ( APC)

Then more mutations occur in DNA repair genes or other tumour suppressor genes ( p53) and other growth related genes ( K-Ras)

2) tumour becomes cancerous
3) over time accumulated damage can yield a highly malignant , metastatic tumour

18
Q

Example of distinct somatic mutations

A

Some cancers have distinct somatic mutations ( C>T) . The DNA damage from UV radiation leads to the formation of covalent bonds between two adjacent pyrimidines ( C and T) in the DNA molecule

Or in smokers - G to T transition

19
Q

Passenger mutations

A

Many mutations can be tolerated by somatic cells and have no effect but may be in the same genome where a driver mutation is located ( known as hatch hiking)

20
Q

Driver mutation

A

Leads to clinal expansion - may be in p53 and tumour suppressor

21
Q

Passenger vs driver mutation

A

Driver mutation will have greater effect on protein function than passenger mutation
And will have more frequent mutations than background mutation rate in a gene
But hard to determine as there is so much variation

22
Q

Oncogenes

A

Gene that has the potential to cause cancer and it regulates cell proliferation, differentiation and and apoptosis , one mutations is sufficient for role in cancer development ( dominant / gain of function )

23
Q

What is a tumour suppressor gene

A

Regulates cell during cell division and mutation - might be more important in progression of cancers than the proto oncogenes ( recessive/ loss of function )