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BIOL266 > Cancer > Flashcards

Cancer Flashcards

1
Q

What is cancer?

A

Uncontrolled growth and division of cells

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2
Q

Cancer in late 1800s

A

Scientists assumed that cancer spread in a radical fashion from the initial growth - treated by Halsted radical mastectomy

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3
Q

Cancer in 1960s

A

Bernard Fisher suggested that cancer did not spread in an orderly fashion

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4
Q

Three theories of cause of cancer

A

Virus, Environment, Genetics

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5
Q

Peyton Rous (1908)

A

Studied chickens with tumours, transplanted tutor cells formed chickens that developed a tumour. Cancer presumed to be spread by a small unit, maybe virus -> Rous Sarcoma Virus

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6
Q

Sarcoma

A

connective tissue cancer

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7
Q

Dennis Burkitt (1950s)

A

Identified children in Uganda that developed a cancer -> Burkitt’s lymphoma

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8
Q

Anthony Epstein & Yvonne Barr

A

Analyzed tissue samples identified a virus in Burkitt’s lymphoma -> Epstein-Barr Virus

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9
Q

Why was it a breakthrough that some cancers were caused by viruses?

A

Because viruses can be treated by vaccines

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10
Q

Which cancers were treated by vaccines?

A

HPV (cervical), HepB and C (liver)

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11
Q

What is the strongest proof that cancer was caused by the environment?

A

% of people with lung cancer increased as cigarettes became popular

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12
Q

Ernest Wynder & Evarts Graham (1950s)

A

Demonstrated link between cigarette smoke and cancer

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13
Q

Why did scientists presume that genetics caused cancer?

A

Cancer cell gives rise to more cancer cells & some cancers are inherited

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14
Q

Michael Bishop & Harold Varmus (1967) ***

A

Studied RSV and found that the virus had 4 genes, in contrast to related viruses that don’t cause cancer have only 3 genes

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15
Q

What is the extra gene in RSV that Michael Bishop & Harold Varmus found?

A

Src - oncogene, cancer-causing gene. It is found in normal chickens, therefore, the virus picked up the gene from the chicken genome

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16
Q

Are there human genes that cause cancer?

A

Robert Weinberg (1970) isolated cancer genes from a normal cell and added them normal cells -> First gene found that turned normal cells into cancerous cells was Ras

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17
Q

What are oncogenes?

A

Genes which when mutated or over activated drive a cell towards uncontrolled growth

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18
Q

What are proto-ongenes?

A

Normal cells that promote normal cell growth (when mutated, become oncogenes)

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19
Q

How are oncogenes converted to proto-oncogenes?

A

1) Mutation of the DNA to an activated form
2) Duplication of the gene to lead to a higher amount of the protein
3) Chromosome rearrangement to alter the expression of the gene and result in a higher amount of protein

20
Q

What are tumour suppressors?

A

Normally, these genes restrain cell growth. When mutated to a non-active form drive the cell towards uncontrolled growth.

21
Q

Most tumour suppressors are ________ regulators of cell growth

A

Negative

22
Q

Examples of tumour suppressors

A

Rb (first tumour suppressors discovered), BRCA1, p53

23
Q

Oncogene vs Tumour supressors

A

Oncogenes act dominant -> only a single mutated copy is necessary for cell become cancerous
Tumour suppressors act recessive -> both copies must be mutated for cancer to develop

24
Q

Properties of cancer cells: Proliferation

A

Proliferation of cancer cells in culture is not subject to density-dependent inhibition (when they cover the entire surface of a plate, they start growing on top of each other, in contrast to normal cells that have their growth inhibited)

if deprived of nutrients and growth factors, cancer cells still pass the restriction point

25
Q

Properties of cancer cells: Autocrine growth stimulation

A

Some cancer cells produce their own growth factors that stimulate their proliferation

26
Q

Properties of cancer cells: Accumulation of mutations

A

Cancer cells accumulate mutations in proto-oncogenes and tumour suppressor genes and in pathways where these genes function

27
Q

3 main pathways implicated in cancer

A

1) Rb (initiation of cell division) - tumour suppressor
2) Ras (RTK-Ras-PI3K pathway) - proto-oncogene
3) p53 pathway (cell cycle arrest due to DNA damage) - tumour suppressor

28
Q

What will the Ras-Raf-Mek-ERK pathway lead to if implicated in cancer?

A

This pathway regulates delayed response genes including Cdks and cyclins leading to uncontrolled cell growth

29
Q

Properties of cancer cells: Invasion

A

Cancer cells invade and colonise regions where normal cells would grow. Cancer cells secrete proteases that can digest through basal laminae and invade underlying connective tissues and adjacent normal tissue

30
Q

Properties of cancer cells: Increased life spans

A

Cannot undergo apoptosis and exhibit increased life spans

31
Q

Properties of cancer cells: Produce energy via lactate

A

Cancer cells do not use oxidative phosphorylation to produce energy. They produce lactate even in presence of oxygen (Warburg effect). Similar to embryonic cells and have high need of glucose

32
Q

Cancer prevention

A

John Bailer:
Main changes are weight loss and avoiding tobacco smoke
Early detection

33
Q

What are the 4 therapies of cancer?

A

Radiation, chemotherapy, target-specific inhibition, immunotherapy

34
Q

Radiation (kills any cells!!)

A

Intense beams of radiation focussed on cancer cells lead to DNA damage introducing either single stranded or double stranded breaks -> interferes with cell cycle

35
Q

Radiation leads to 2 varieties of cell death

A

1) Apoptosis: occurs before cell enter mitosis
2) Mitotic catastrophe: mis-segregation of chromosomes after mitosis resulting in multiple nuclei or micronuclei, may result in apoptosis or necrosis, which can be viewed as a signalling pathway leading to cell death

36
Q

Is p10 a tumour suppressor or oncogene?

A

p10 converts PIP3 into PIP2
PIP3 needed for cells to grow
So p10 is a tumour suppressor

37
Q

Chemotherapy (kills any cells!!)

A

Kills rapidly dividing cells -> bone marrow, hair follicles

38
Q

Emil Frei and William Peters - STAMP

A

Solid Tumour Autologous marrow Program. High dose of chemotherapy and transplanted patients own bone marrow back -> bad results

39
Q

Alkylating agents

A

Modify DNA by corsslinking bases on same or diff strands -> DNA damage -> p53 -> apoptosis

40
Q

Antimetabolites

A

Nucleotide mimetics are very similar to nucleotide bases in structure but once incorporated into the nucleic acid lead to DNA damage -> p53 -> prevent further cell division and can induce apoptosis

41
Q

Antifolates

A

Enzyme DHFR catalyses conversion of dihydrofolate to tetrahydrofolate which is a building block for thymidine and purines which needed for nucleic acid. Methotrexate inhibits DHFR -> less nucleic acid available so cannot support rapidly dividing cells -> treats cancer growth

42
Q

Anti-microtubule agents

A

Interferes with MT dynamics, spindle formation is disturbed, interfering with mitosis

43
Q

Topoisomerase inhibitors

A

Topoisomerase enzymes relive tension in DNA. Inhibition of topoisomerase -> tension in DNA -> DNA damage -> p53 -> apoptosis

44
Q

What is target- specific inhibition

A

Find a target in or on a cancer and inhibit its action with small molecules or antibodies

45
Q

Bert Vogelstein (1980s)

A

Compare normal cells to cancer cells and suggested that cancer cells accumulate mutations over years -> microevolutionary.

Passenger mutations: mutations that don’t cause any problem

Driver mutations: cause problem

46
Q

Some cancers are caused by one gene. Give one example and explain how it is treated, relating to microevolutionary process of cancer.

A

A form of lung cancer is caused by mutation of Alk gene. Treated with drug LDK BUT cells continue to mutate and become resistant. Solution: block diff pathways and use personalised combination of drugs

BIOL266 (3 decks)

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