Cancer #3 Flashcards

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1
Q

Carcinomas

A

cancers that a rise from epithelial cells
~ 90% of cancers
~ solid

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2
Q

Sarcomas

A

cancers that originate in supporting tissues
e.g. bone (osteo), fibrous tissue (fibre) or muscle (myo)
~ solid

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3
Q

Leukemias

A

cancer of leukocytes, malignant blood cells that proliferate in the blood stream
~ liquid

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4
Q

Lymphomas

A

cancers of lymphocytes, typically form solid masses in lymph nodes
~ liquid

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5
Q

Driver gene mutation

A

mutation that directly or indirectly confers a selective growth advantage to the cell in which it occurs
(cancer requires a collection, 5-8, of driver mutations)

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6
Q

Passenger mutation

A

mutation that has no direct or indirect effect on the selective growth advantage of the cell in which it occurred

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7
Q

What are the four most important properties of cancer cells? (can be caused by oncogene activation)

A
~ self-sufficiency in growth signallung
~ insensitivity to signals suppressing growth
~ enabling replicative immortality
~ genome instability and mutation
~ ability to avoid apoptosis
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8
Q

What is the common characteristic found in cancer susceptibility genes?

A

genes have roles as +ve or -ve regulators of cell proliferation

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9
Q

Oncogenes

A

dominantly acting cancer-susceptibility genes
~ normally protons-oncogenes
~ arise from genetic change that increases in the protein’s activity
~ mutations are genetically dominant

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10
Q

Proto-oncogene

A

function in growth signalling pathways that promote cell proliferation or inhibit apoptosis

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11
Q

Name the six functional classes of cellular oncogenes.

A
~ growth factors/mitogens
~ growth factors/mitogen receptors
~ signal transduction component
~ transcription factors
~ cell cycle regulators/drivers
~ cell death inhibitors
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12
Q

Mitogens

A

stimulate cell division by binding to a receptor in the cell membrane and activating signal transduction pathways that acts through Ras to stimulate

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13
Q

growth factors/mitogen receptors oncogenic mutations e.g. EGFR

A

EGFR = epidermal growth factor receptor
Very common in lots of cancers, mutations include:
~ amplification = more receptors
~ deletion = truncated reporter that fires w/o mitogen

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14
Q

signal transduction component oncogenic mutations

A

mutated Ras looses its intrinsic GTPase activity = permanently active = constant downstream signally w/o activation

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15
Q

transcription factors oncogenic mutations

A

Mutation in Myc protein:
~ amplification (lots of gene)
~ point mutation (stabilises Myc)
~ translocation (increased gene expression)

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16
Q

cell cycle regulators/drivers oncogenic mutations

A

~ CCND1 gene encodes Cyclin D –> its amplification is involved in lots of cancers as it promotes UNSCHEDULED entry into S phase
~ Over amplification of CDK4 gene (Cdk4) also found in many cancers

17
Q

cell death inhibitors oncogenic mutations

A

~ increased Bax production (due to p53 activation) = Bax dimers and induction of apoptosis
~ amplification of Mdm2 = more MDM2 = no p53 accumulation = no activation of DNA damage checkpoint

18
Q

Myc protein

A

acts in nucleus to stimulate cell growth and division

19
Q

Myc protein

A

acts in nucleus to stimulate cell growth and division

20
Q

Apoptosis

A

programmed cell death
~ controlled by Bcl2 family of proteins
~ EXTRINSIC (extracellular signalling proteins) or INTRINSIC (intracellular mitochondrial proteins) pathway

21
Q

Apoptosis

A

programmed cell death
~ controlled by Bcl2 family of proteins
~ EXTRINSIC (extracellular signalling proteins) or INTRINSIC (intracellular mitochondrial proteins) pathway

22
Q

MDM2 mechanism

A

no DNA damage = MDM2 ubiquitinates P53 (targets it for degradation)
DNA damage = MDM2 + p53 are phosphorylated = p53 accumulation

23
Q

MDM2 mechanism

A

no DNA damage = MDM2 ubiquitinates P53 (targets it for degradation)
DNA damage = MDM2 + p53 are phosphorylated = p53 accumulation

24
Q

Hayflick limit

A

normal cells in culture cease to divide after 50-70 doublings

25
Q

Oncogenes + telomerase

A

oncogenic mutation reactivate telomerase expression, maintaining telomere structure = immortality
~ telomerase activity found in ALL major cancers