29 Flashcards

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1
Q

cancer

A

uncontrolled proliferation of cells

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2
Q

what are 4 features of cancer?

A

Ignore inhibitory growth signals:
Normal cells stop dividing when they contact one another to indicate that there’s no room left & they form a monolayer
Cancer cells continue to divide, pile up & force the tissue out of place

Growth occurs independent of stimulatory growth signals
Normal cells require checkpoints, external signals to proceed through the cycle

Capable of continuous division
Normal cells senesce after ~50 divisions due to shorter telomere
Cancer Telomerase continues to restore telomere length, telomeres remain the same length & the cells don’t die off

Aneuploidy
Normal cells die off if c’some number deviates from the norm
Cancer cells are more tolerant of aneuploidy up to a certain point

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3
Q

carcinogen

A

chemical that causes cancer, a type of mutagen

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4
Q

A _____ is something that causes the DNA to be mutated, it is a ______ when it causes cancer

A

mutagen

carcinogen

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5
Q

how does increasing the rate of mitosis lead to cancer?

A

increases the opportunities for mutations

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6
Q

what are external factors that cause cancer?

A

Mutagens: mutate DNA
Radiation
Chemicals –> Carcinogens

Stimulates the rate of mitosis

Hormones (ex: breast tissue & prostate gland)

Chronic tissue injury  increases rate in stem cells needed to repair damage (ex: heregulin in lungs) 

Agents causing inflammation which generates oxidizing agents  white blood cells are recruited to kill off foreign agents, but if their activities are excessive then their oxidative products (from the mitochondrion) will lead to too much harm 

Viruses stimulate mitosis of their host, ex: HPV & cervical cancer, hepatitis & liver cancer
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7
Q

how many mutations are required for cancer to develop?

A

6-8

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8
Q

what are 6 diff categories of genes mutated in cancer?

A

Oncogenes – mutated or over-expressed products stimulate mitosis even though normal growth signals are absent

Tumor suppressor genes – genes normally inhibit mitosis when a mutation is detected (ex: p53 – halts cell cycle until mutation is resolved or directs cell to death if it’s unable to be resolved, if there is a mutation then the cell will divide)

Genes that regulate apoptosis – genes indicate to the cell to undergo apoptosis when damage is unresolvable, mutation enables cells to ignore this signal

Genes that maintain telomeres, telomerase - normal cells die when their telomeres are too short after so many divisions, cancer cells regain the ability to express their telomerase & are immortal

Metastasis genes: enables cells of the tumor to separate from the primary tumor & migrate, includes 2 kinds:
Mutations in genes that enable the cells to adhere to one another, ex: cadherin genes holding epithelial cells together
Mutations in genes that enable cells to adhere to their substrate, ex: integrin genes required for attachment to the basal lamina

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9
Q

hyperplasia

A

faster growth than neighboring cells

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10
Q

dysplasia

A

irregular growth

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11
Q

describe the progression of cancer

A

comes from a single lineage of cells that undergo progressive mutations

Comes from a single cell 

During mitosis one cell receives a mutation, if this mutation is cancer-causing then this will lead to a lineage of cells with the same mutation & a tumor will develop

Growth advantage 

Descendants will the suffer further mutations & further deregulates the cell cycle 

Eventually, more mutations occurred (6-8) & the cells are completely unregulated leading to cancer
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12
Q

explain the relation of cancer with age

A

increasing probability of cancer with an increase in age

cancer has less to with chemical exposure & more to do with increased longevity

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13
Q

how do you prevent viruses from causing cancer?

A

vaccines

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14
Q

what viruses cause cancer?

A

o 2 papilloma viruses
o Hepatitis B & C
o Epstein-Barr virus a type of herpes virus
o T-cell leukemia (HTLV-1 & HTLV-2)

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15
Q

how does radiation lead to cancer treatment?

A

damages cancer cells to the point where they cannot be repaired.

Normal cells seize to divide until the damage can be fixed, but cancer cells continue to divide & die off

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16
Q

what are the probs with radiation & chemotherapy?

A

don’t always kill all the cancer cells

can induce mutations in normal cells which can later result in cancer

can escape

can become resistant to chemotherapy

17
Q

how are antibodies being used in cancer treatment?

A

breast cancer - excess growth receptors called Her2, antibody is used to block the receptor disabling it to interact with growth factors

toxins or radioactive compounds are attached to antibodies & delivered to cells (only to cancer cells, not normal cells)

18
Q

what challenge arises when antibodies are being used in cancer therapies?

A

when normal cells & cancer cells have the same receptor b/c you don’t want to kill the normal cells

easy when the cancer cells contain a mutated receptor

19
Q

how is cancer development prevented with gene therapy?

A

Adding back p53 gene (many cancer cells are missing this)

Gene silencing using dsRNA – destroys a mutated cancer gene without affecting normal genes
Heterozygous genotype required

20
Q

how is nanotechnology used in cancer treatment?

A

nanoparticles: balls of metal are coated with sugar

delivered at the site of the tumor & taken in by cancer cells

patient is then placed in a magnetic field & the metal cooks the cells

21
Q

how is immunotherapy used to combat cancer?

A

inducing a patient’s own immune sys to target cancer cells

  1. Harvest tumour cells – biopsy
  2. Separate into smaller subsets
  3. Treat with cytokine (IL2) to stimulate growth
    White blood cells are stimulated & proliferate
  4. Select cultures that kill tumour cells
  5. Re-introduce cells back to patient
22
Q

when is immunotherapy ineffective in cancer cells?

A

when there is metastasis b/c migrated cells will appear diff than original cells