Topic 10: Cancer 1 Flashcards

1
Q

what are major features that define cancer

A

cells that have uncontrollable proliferation and are able to invade and colonize other tissue

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2
Q

how can uncontrollable proliferation occur?

A

it happens when the balance of cell division and apoptosis is off rather
- increased cell division with normal apoptosis
- decreased apoptosis with normal cell division
- increased in both cell division and apoptosis

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3
Q

definition of oncogenesis

A

the microevoultionary process that usually takes years r decades for cancer to form and is generally an accumulation of mutations

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4
Q

what is a begin tumour?

A

is when cell profileration occurs but the cells stay in its appropriate tissue
- the size of the mass may cause issue which leads to removals

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5
Q

what is a malignant tumour?

A

it is when the proliferated cells leave their appropriate tissue and evade other sections by traveling through the bloodstream

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6
Q

what are all the hallmarks of cancer? (8) (tumourgenosis)

A
  • self sufficient growth signals
  • insensitivity to antigrowth signals
  • apoptosis inability
  • unlimited replication potential
  • tissue invasion (metastasis)
  • sustained angiogenesis
  • alluding immune destruction
  • increased mutation rate
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7
Q

carcinoma

A

cancer in the epithelial cell

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8
Q

sarcoma

A

cancer in the connective or muscle tissue

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9
Q

leukemia/lymhoma

A

cancer on the hematopoietic stem cells

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10
Q

adenoma

A

type of carcinoma; benign epithelial tumour in a duct of a gland

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11
Q

chondroma

A

benign tumour of cartilage

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12
Q

how can tumorigenesis start?

A

by a single mutation in a chromosome that slowly builds up with multiple mutations
- philadelphia chromosome: a translation in chronic myelogenous leukemia
other mutation can be
- deletion
- translocaion
- addtion
- point muation

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13
Q

what is the most common cancer of old age?

A

colon cancer

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14
Q

describe the process of the multi-hit model

A

(what leads to metastasis) basically an acclimation of undetected mutations
- a single mutation occurs and is not fixed then its descendants get mutated as well causing more profiltation and those descendants divide uncontrollably as well then tumour is growing

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15
Q

how do benign grow?
(carinoma example)

A
  • a polyp forms on the wall of organ
  • a benign cancerous tumor starts to grow
  • class 2 (adenoma) benign
  • class 3 (adenoma) benign
  • malignant carcinoma
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16
Q

what SPECIFIC of mutations cause cancer to grow?

A
  • loss of APC tumor suppressor
  • loss of K-ras oncogene
  • loss of tumor supressor gene in region of chomosome 18q
  • loss of p53 (tumour supressor)
17
Q

describe the process of metastasis

A

after growing in its section of tissue for awhile
- it loses its adherens & desomomes (cell-cell adhesion)
- penetrates through the basel lamina ( hemidesmosomes and actin linked cell matrixes break)
- intravasation: enters the blood vessel
- extravasation: exits the bloodstream into another tissue
- proliferates in the new tissue

18
Q

what do tumours do to survive in their mircoenvironment

A
  • have altered sugar metabolism
  • induce angiogenesis
19
Q

explain the altered sugar metabolism of cancer cells

A

they have a very high glucose uptake and they need to produce building blocks from glycolysisis. The increased glycolysis causes an increase in lactate which they use for energy

20
Q

what is angiogenesis

A

the extension of a capillary to the cancer site to fuel it
it occurs do the secretion of these growth factors
- basic FGF
- transforming growth factor alpha (TGF alpha)
- vascular endothelial growth factor (VEGF)

21
Q

explain how tumour cells VEGF expression

A

since the O2 levels are down in the cancer cells, they release hypoxia inducible factor occurs (HIF). This stimulates the production of VEGF so the a capillary network can grow towards it.

22
Q

what is replicative senescence (not die)

A

the cell division mechanism that counts how many times the cell has replicated and alerts it to stop dividing when telomere is too short

23
Q

how do they avoid replicative senescence

A

all somatic cells stop dividing when their telomere gets too short however, cancer cells can escape the built in limit of cell proliferation
- they maintain telomere expression (just like stem cells)
- they make another way based on homologous recombination for elongating their chromosome ends

24
Q

what is the difference between normal and cancer cells in culture

A

normal cells
- grow flat
- have finite divisions
- require growth fators
- respond to inhibitory growth factors

maglinant cells do the opposite