Lecture 1 - introduction to cancer Flashcards

1
Q

what is cancer?

A

Abnormal growth of cells. cells grow when they should not (cell proliferation)

abnormally over growing cells spread to other parts of the body (metasis).

Cancer cells take over- affect normal cells, take nutrients, produce the wrong types of cells in organs affecting normal function

behave differently depending on cell type from which they originate: different- symptoms, age of onset, aggressiveness, invasiveness, response to treatment

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2
Q

what are leading cancers in the world?

A

tracheal, bronchus and lung cancer are the leading cause of cancer deaths worldwide.

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3
Q

what are examples of benign and malignant cancers?

A

some lumps or tumours are non-cancerous - benign. for example; lipoma, cysts, benign tumour of the small intestine, skin mole, benign brain tumour.

examples of malignant cancers are skin cancers, colorectal cancer, lung cancer

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4
Q

who gets cancer?

A

cancer increases with age. more males than females get cancer. cancer can affect any race, gender or person

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5
Q

what is cancer a disease of?

A

cancer is a disease of nerve cells, gut cells, red blood cells, skin cells - cells in general.

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6
Q

what is cell division?

A

new cells are made by cell division. cell division is needed for growth, healing and replacing old cells

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7
Q

describe what happens to the cells in cancer.

A

Normal cell division occurs. There is cell damage and no repair, leading to cell suicide or apoptosis. there is a balance between new cell growth and cell death.

In cancer cell division, there is loss of normal growth control which is the key to cancer. first mutation of cell, mutates to second, to third to fourth mutation and there is uncontrolled growth. cell death is greater than new cell growth.

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8
Q

What causes cancer?

A

Cancer is often a disease that strikes for no apparent reason.

Besides intrinsic factor such as heredity, diet and hormones, key extrinsic factors such as chemicals (eg smoking), radiation, alcohol use, chronic infections, unbalanced diet and viruses of bacteria.

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9
Q

What is the molecular basis of cancer?

A

genetic damage or mutations acquired by the action of environmental agents such as chemicals, viruses or radiation, but mutations actually cause cancer. development of cancer is usually a multi-stage process meaning multiple mutations occur over time.

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10
Q

what are examples of chemical carcinogens and types of cancers they are associated with?

A

Asbestos - lung cancer.
Benzene - leukemia
Leather dust - nasal, bladder
Napthylamine - bladder
Vinyl chloride - liver
Wood dust - nasal

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11
Q

what chemicals in cigarette smoke are carcinogenic ?

A

arsenic, benzene, cadmium, nickel, 2 napthylamine

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12
Q

what viruses are associated with what type of cancers?

A

Epstein-barr virus - burrkits lymphoma

HPV - cervical cancer

Hepatitis B virus - liver cancer

Human T-cell lymphotrophic virus - adult T cell leukaemia

cancer viruses-some of the viral genetic information carried in these nucleic acids is inserted into the chromosomes of the infected cell, and this causes the cell to become malignant.

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13
Q

what is ionising radiation?

A

ionising radiation causes DNA damage which can lead to cancer. Types of ionising radiation are: fallout, cosmic rays, gamma, beta, alpha particles, X rays and radon gas

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14
Q

What are hereditary conditions lead to cancer?

A

Hereditary cindtions can icnrease the risk for cancer

Xeroderma pigmentosum - skin cancer

Wilm’s tumour - kidney cancer

familial adenomatous polyposis - colon, rectum cancer

BRCA1/2 - breast and ovarian cancer

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15
Q

what are the targets of DNA damage?

A

the growth promoting port-oncogenes

the growth inhibitory tumour-suppressor genes (TSGs)

the genes that regulate programmed cell death, apoptosis- may be Oncogenes or TS genes

the genes that produce proteins which are involved in DNA damage response and repair - maybe Onc/TS

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16
Q

Describe oncogenes.

A

Genes that code for mutant forms of normal signalling molecules that regulate and control cell growth: proliferation, differentiation and survival (proto-oncogenes)

Genes coding for the following can mutate to cause cancer get mutated
Growth factors, Growth factor receptors, Cytosolic transducers, Nuclear transducers

oncogenes make or let cancer grow more

17
Q

descried the process of how normal cells grow.

A

for a normal cell to grow it requires a ‘signal’ which is usually a growth factor or hormone.

ligand which is the primary messenger, binds to the receptor causing signal transduction via second messengers. this leads to cellular responses and changes in gene expression/ induction or initiation of cell cycle.

no growth factor has no cell division

18
Q

what is the feature of oncogenic variations of Growth factors?

A

oncogenic variation of growth factors don’t require growth factors. even in the absence of a growth signal it is turned on without the need of an on switch.

there is intracellular signalling pathways leading to transcription factors and entering into the nuscleas, causing even induction and initiation of cell cycle.

19
Q

what is an example of oncogene?

A

oncogene - Ras in cancaner is alors on - drive cells to grow grow grow leading to cancer

20
Q

what are tumour suppressor genes?

A

Tumor suppressor genes are a family of normal genes that instruct cells to produce proteins that restrain cell growth and division.
Since tumor suppressor genes code for proteins that slow down cell growth and division, the loss of such proteins allows a cell to grow and divide in an uncontrolled fashion.

TSGs act like an ambulance- they
Hear a cell is “ hurt” and go an
Help repair it

TSGs prevent cancer cells growing

21
Q

how are tumour suppressor evens genetically acquired?

A

Tumour suppressor genes are recessive this means that both copies of the gene need to be missing Or “ broken”

22
Q

explain normal vs mutated p53.

A

p53 is a TSG.

in normal p53, then cellular damage occurs, p53 arrests the cell cycle until the damage is repaired. if the damage cannot be repaired then apoptosis occurs.

Mutated p53 does not arrest the cell cycle. the damaged cell continues to divide, which may result in cancer.

23
Q

what are defects in DNA?

A

defects in 3 types of DNA damage repair (DDR) systems contribute to different types of cancer: mismatch repair, nucleotide excision repair and recombination repair.

24
Q

what does a malignant neoplasms typically display?

A

A malignant neoplasm typically displays excessive growth, local invasiveness and the ability to form metastases. These Characteristics are acquired in a step-wise manner, a phenomenon termed tumour progression.

25
Q

how can DDr be used to fight cancer?

A

formation of many cancers it an error in a DDR and cancer cells lose the ability to check for DNA damage leading to cancer cells continuing to divide with damage. if we an develop a compound that blocks the remaining DDR pathways in a cancer cell with DDR errors that the adage it carries will be unsustainable and the cancer cells will be triggered to die.