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Case 12: Female Reproductive System > Cancer Hallmarks > Flashcards

Cancer Hallmarks Flashcards

1
Q

What is cancer

A

Uncontrolled proliferation of any cell due to faulty or missing signals that result in benign or malignant tumors

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2
Q

What is the 2 categories of cancer causes

A
  1. Hereditary
  2. Environmental
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3
Q

What is hereditary factors influence on cancer development

A

<10% cancer cases
Wide range of genetic factors that can be influenced after exposure to potential carcinogens

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4
Q

What is the 3 environmental factors causing cancer

A
  1. Chemical
  2. Radiation
  3. Infectious agents
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5
Q

How does chemical exposure cause cancer

A

Most common
Damage DNA directly or indirectly & causes cancer if key genes are affected

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6
Q

How does radiation exposure cause cancer

A

Damage DNA if exposed to UV, x-ray or gamma radiation

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7
Q

How does infectious agents cause cancer

A

Virus integrate into host DNA & effect gene expression
Bacteria cause chronic inflammation

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8
Q

What occurs in the G1 & S phase

A

G1: cell growth
S: DNA replication

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9
Q

What is the functions of control points

A

Ensure DNA integrity & if DNA errors the cycle will stop/repair/apoptosis

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10
Q

What control G1/S transition

A

P53

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11
Q

What proteins control transition between phases

A

Mitosis promoting factors, MPF

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12
Q

What is MPF’s composition

A

Protein dimer made of cyclin & cyclin dependent kinase (Cdk)

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13
Q

How does MPF become activated

A

Cyclin binds to Cdk & activated Cdk to phosphorylated other proteins causing activation & degradation of other proteins & cell transition between phases

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14
Q

What is the protein dimer is present mid G1

A

Retinoblastoma protein & transcriptional factor E2F

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15
Q

How does activation of pRB happen

A

After activation of Cdk it targets pRB that is phosphorylated & cause confirmation changes & E2F is released, activated & can bind to upstream genes that initiate expression of other cycling & genes form DNA replication

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16
Q

What is cyclin E effect on increasing own transcription

A

Phosphorylate more pRB to further activate E2F & promote more cyclone E expression or increase own expressions

17
Q

What is cyclin E function

A

Progress cell cycle from G1 to S phase when interacting with Cdk2

18
Q

What is somatic mutation theory

A

Over time exposure accumulation of multiple mutations in different genes but same cell that forms cancer cells

19
Q

What is the 3 types of cancer therapy

A

Surgery
Radiation therapy
Chemotherapy

20
Q

What is HPV effect on the cell cycle

A

Express E6 & E7 that inactivate regulatory gene products p53 & pRB

21
Q

What is E7 effects on cell cycle

A

E7 binds to pRB & can’t bind E2F & released from pRB & bind promotor of target genes & transcribed gene products drive cell into S phase

22
Q

What is E6 effects on cell cycle

A

E6 produce a protein that binds & inactive p53 that promotes unregulated cell division, cell growth, cell survival all characteristics of cancer

23
Q

What is the normal function of p53

A

Prevent cell growth & promote cell death when there is DNA damage
Upregulate p21 protein which block formation of cyclin D & Cdk4 complex that prevent pRB phosphorylation that halts the cell cycle progression by preventing activation of E2F

24
Q

What is HPV net effect on cell

A

Increased proliferation & avoidance of apoptosis despite DNA damage that can result in cervical cancer

25
Q

What is the relationship between epigenetic and cancer

A

Cancer cells have a change in methylation pattern of DNA that changes expression profile of affected gene & methylation is at the promotor region that block gene transcription
Loss of methylation activates gene & allow transcription when transcription factor binds

26
Q

What is the model of tumourigenesis

A

Carcinogens is a multi-step & multi gene model
Multistep: accumulations happen over time & not all at once
Multi gene: multiple genes are altered by mutation in the same cell
Long term exposure = development of cancer

27
Q

What happens if alteration in genes happen in regulatory circuit

A

Dysregulation of critical homeostatic pathways

28
Q

Can different cancers arise form different alterations of gene

A

Yes

29
Q

What proteins does chemotherapy target & why

A

Chemotherapy targets Ras protein
Central role in cellular process look proliferation, cell cycle progression, apoptosis & cell motility

Case 12: Female Reproductive System (10 decks)

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