Cancer Flashcards

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1
Q

What is Cancer?

A

uncontrolled cellular proliferation

cells divide when they shouldn’t

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2
Q

What causes cancer?

A

all known cancers are caused by damage to DNA

1-How DNA is regulated

  1. Sequence of DNA
    - genes turning off and on- epigenetics
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3
Q

Cancer

A

• Mutations in cell’s own DNA

cells getting ready to divide make an error-proof reading mechanisms aren’t full proof

Errors during replication and mitosis – Carcinogens

-tabacco, benzene, charred food, uv light

aspetis-used for insulation, x-rays

viruses – Play a role in ~15% of cancers – Examples?

HPV-cervical cancer

virus that causes mono

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4
Q

How Many Mutations Does It Take?

A

• Number varies depending on which genes are mutated

-average 7 major genes mutated in tumors

;no sunscreen, mutation, cell divides possibility of another mutation( random error in replication

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5
Q

Why does the incidence of cancer increase with age?

A

around for longer. able to accumulate more mutuations, exposed to more carcinogens, immune system is not as great

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6
Q

What are the two types of genes most often associated with cancer? what do they act as?

A
  • oncogenes -gas pedal OP
  • tumor supressors -breaks TBS
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7
Q

• ____________ = Gene that when mutated or overexpressed can contribute to turning a normal cell into a cancer cell

A

protooncogene

tell to divide without a signal

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8
Q

Oncogenes

A

• Genes involved in growth and differentiation – Examples: growth factors, RTKs, GTPases, transcription factors

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9
Q

Oncogenes:3 basic types of activation ?

A
  1. Mutation that changes protein structure
  2. Increase in protein concentration
  3. Chromosomal Translocation
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10
Q

Mutation which changes protein structure

A

• Increase activity or cause loss of regulation

-change DNA, change shape, more stable, could be turned on all the time

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11
Q

– Increase in protein concentration

A

• Increase in expression, stability or gene duplication

-gene duplicated, always on, always making protein

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12
Q
A
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13
Q

-chromosomal translocation

A
  • • Constitutively expressed fusion protein (Bcr‐Abl) or expression in wrong cell or at wrong time
  • each genes on/off switch not controlled by own switch

can inhibit it with drug-cells continue to mutate —>have more mutations that develop

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14
Q

What are Tumor Suppressors?

A

• Genes which have a repressive effect on the regulation of the cell cycle or promote apoptosis

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15
Q

Tumor suppressors follow what hypothesis?

A

• Usually follow the “two‐hit hypothesis” – both copies of the gene must be non functional

-with one good copy-still have breaks

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16
Q
A
17
Q

p53 is known as?

A

“The Guardian of the Genome”

18
Q

What is P53?

A

Tumor suppressor

19
Q

What does P53 do?

A

regulates the cell cycle-halts the cell cycle if there’s damage to the DNA/ stress on the cell

-mutated in 50% of human cancers

inherited mutations =Li Fraumens syndrome

diagnosed with first cancer very early in life-continue to develop malgnancies throughout life

-screened very often-inherit mutation-even if it’s not cancerous - predisposes you

20
Q

What are the ten hallmarks of cancer

A
  1. Uncontrolled proliferation
  2. Evasion of growth suppressors (inactivation of tumor suppressors)
  3. Resistance to apoptosis
  4. Develop replicative immortality (activate telomerase)
  5. Induce angiogenesis
  6. Invasion and metastasis
  7. Genomic Instability
  8. inflammation
  9. Changed energy metabolism
  10. immune system invasion
21
Q

What is uncontrolled proliferation?

A

uncontrolled cell division

22
Q

• Resistance to apoptosis

A

damaged cells should die-cancer cells resistant -even w/o chemo they won’t die

23
Q

Develop replicative immortality (activate telomerase)

A

continue to divide over and over again-normal cells divide-telomeres shorter reach critical length- apoptosis.

-loose more DNA-loose important information

enzyme telomyerase lengthens telemeres over and over again

24
Q

• Induce angiogenesis

A

induce formation of new blood vessels as tumor larger cells inside can’t access nutrients, oxygen.

send signals for new blood vessels to form-new blood vessels difficult to remove because of blood vessels around the area

25
Q

Invasion and metastasis

A

move throughout body -when they branch out-difficult to get all of them-loose anchorage-dependency-don’t need ECM–set a secondary site elsewhere

26
Q

Genomic instability

A
  • cells not identical-have different mutations-try to kill several different mutations
  • extra chromosomes/missing chromosomes-cell continue to divide =more mutations less controls-accumulate more
27
Q

Inflammation

A

signals growth factors to repair tissues -the cancer does this-divides-keeps dividing

28
Q

Changed energy metabolism

A

-lots of cancer-don’t do aerobic respiration-glycolysis-lactate-instead of citric

29
Q

immune system invasion

A

-notices when something is off-destroys cells-grow and divide even when something is wrong

30
Q

Treatments

A
  • target therapies – Target specific pathways/proteins involved in tumor development • Angiogenesis inhibitors • Herceptin (breast) • Gleevec (CML) • Tamoxifen
  • gene therapy• Cancer Vaccines – Hepatitis B, HPV and Prostate
31
Q

Skin Cancer •

A

Most common cancer in the US –

Most commonly caused by uv radiation

32
Q

What does a tan tell you? • What does sunscreen do? • Can dark‐skinned people get skin caner?

A

-Tan=DNA damaged-change in pigment-change in melanin-produce for melanin to protect against more damage

sunscreen? absorbs UV light and gives off loss of heat as heat in sunscreen

dark skin- can get cancer

33
Q

1 in 8 women will develop invasive breast cancer • ____________ diagnosed cancer in women • Almost 300,000 new cases of breast cancer were expected to be diagnosed in 2011 – 2,140 cases in men • ~40,000 deaths were expected in 2011 • Overall 5 year survival rate is 89%

A

2nd most diagnosed

34
Q

What caused breast cancer?

A

– ? – Known risk factors include: • Smoking, obesity, alcohol, exposure to carcinogens, increased estrogen exposure • Only 5‐10% linked to inherited gene mutations – BRCA1 and BRCA2 (tumor suppressors) – Mutation in one copy of BRCA1 = 60% chance of developing breast cancer before age 50 compared to 2% chance if both copies are normal

35
Q

Lung cancer

A

#1 cause: smoking

Asbestos • Radon gas • Pollution • Exposure to carcinogens – Coal dust, gasoline, mustard gas • Radiation therapy to the lungs

36
Q

Cervical Cancer risk factor?

A

HPV