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FunMed Week 4 - cancer > Cancer > Flashcards

Cancer Flashcards

1
Q

what is cancer?

A

- group of diseases characterised by unregulated growth of malignant tumours

- around 200 different types

- normally need a number of mutations to occur for cancer to occur (multi hit)

- can be solid or haemotological

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2
Q

how are cancers different to normal cells regarding cell signals?

A

cancer cells can survive without cell signals - autonomous. (unlike normal cells)

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3
Q

name different cells found in cancer tissues

A

complex tissue:

  • functional tissue (perenchyma)
  • stroma (support tissue)
  • cancer cells
  • stem cells
  • inflammatory cells
  • endothelial cells
  • parasite cells
  • fibroblasts
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4
Q

describe the overview of carniogenesis

A
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5
Q

what are the 8 hallmarks of cancer?

A

all contribute to sustaining proliferative signalling -> then to tumour developement and malignant progression

  1. self sufficiency in growth signals
  2. insensitivity to anti-growth signals
  3. evading apoptosis
  4. limitless reproductive potential
  5. sustained angiogenesis
  6. tissue invasion and metastasis
  7. deregulating cellular energetics
  8. avoiding immune detection
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6
Q

explain self-suffienciency in growth signals

(what is it like in normal cells - how different in oncogenes?)

A
  • normal cells need mitogenic growth signals before they can move into proliferative state
  • many oncogenes can mimick normal growth signals and generate own growth signals (autocrine signalling)
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7
Q

explain how cancer cells are insensitive to anti-growth signals

A
  • normal cells have multiple anti-proliferative signals

- anti-growth singals block proliferation by:

a) force cells out of G0
b) cells may be induced to relinquish their proliferative potential by being induced to enter into post mitotic state associated with differentation

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8
Q
  1. are tumour cell populations determined just by rate of cell proliferation?
  2. how is limitless replicative potential achieved by cancer cells?
A
  1. NO - also by rate of apoptosis
  2. maintain telomeres - so prevent apoptosis
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9
Q

what are three main groups of genes that implicate cancer?

A

1. oncogenes

2. tumour supressor genes:

a) gatekeepers (regulate cell cycle)
b) care takers (DNA repair)

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10
Q

what are oncogenes?

what are proto-oncogenes?

A

oncogene: gene that encodes protein capable of inducing cancer

proto-oncogene: normal gene from which oncogene derives from. many encode growth factors, growth factor receptors or signalling molecules. activated by mutations. enhanced cell signalling in uncontrolled way

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11
Q

why do cancer cells want to not be differentiated?

A

once differentiated, no longer divide.

onco-genes reduce differentation

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12
Q

what are the five categories of proto-oncogenes?

A

1. growth factors

2. growth factor receptors

3. signal-transduction proteins

4. transcription factors

5. anti-apoptotic proteins

mutations change structure in these proto-oncogenes -> oncogenes

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13
Q

give over view of cell signalling in normal cell

A
  • growth factor binds to receptor. two receptors interact (dimerization)
  • intracelllar side: phosphorylation of tyrosine
  • siganlling proteins bind to P-tyrosine
  • causes cascade of phosphorylation events
  • activates two pathways: MAPK pathway and PI3 Kinase Pathway

- once pathways are activated, activate gene expression and transcription factors occur.

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14
Q

what happens if overexpress growth factors?

A

get hyperplasia (Hyperplasia, or hypergenesis, is an enlargement of an organ or tissue caused by an increase in the amount of organic tissue that results from cell proliferation)

  • can be precancerious or not lead to cancer
  • genes are often amplified
  • autocrine loops and unregulated growth
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15
Q

what are examples of hyperplasia and cancer?

A

hyperplasia leads to increased growth: can be:

benign - VEGF (vascular endothelial growth factor) - (up regulate the synthesis of blood vessels.): leads t benign prostatic hyperplasia (enlarged prostate). benign growth

malignant - platelet derived growth factor (PGDR) - leads to glioblastoma

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16
Q

whats an example of overpression of growth factors?

A

HER2 or ErbB2

  • tyrosine kinase receptor known as HER2 or ErbB2
  • overexpression leads to: uncontrolled growth, survival of cells containing mutations, invasion of tumour cells, migration tumour cells
17
Q

explain the ras pathway and how mutation leads to kras cancer

A
  • when ras switched on: (normally ras is switched on by binding to GTP) can switch on ERK and AKT pathways. (ras regulates the pathways by turning on / off the ERK and AKT pathways)
  • mutated ras (kras): hydrolysis of bound GTP (first stage in pathway) occurs v slowly. GTP is bound to ras in unhydroloysed form - ras is permenantly switched on. continois proliferation and growth.
18
Q

ras oncogene - is it rare / common?

A
  • one of the most frequent mutations in human tumours

- need to know stats?? see slides

19
Q

explain c-MYC proto-oncogene

A
  • proto-oncogene: c-MYK (~50% of cancers)
  • promotion of transcription of cyclin genes (promotes cell cycle progression)
  • c-MYK is correlated with agressive tumour pattern and poor clinical outcome

( - causes increased growth, metabolism, cell adhesion, differentiation and metastasis)

  • seen in: Burkitt lymphoma, breast cancer
20
Q

can c-MYC induce cancer on its own?

A

NO

need secondary mutations to occur in:

  • proliferative arrest
  • apoptosis
  • sencescence

MYC OVEREXPRESSION ALONE DOES NOT INDUCE TUMOURIGENESIS

21
Q

how can cancer cells avoid apoptosis? (general)

A

- mutations in anti-apoptotic proteins - e.g. BCL-2

  • if not directed to apoptosis -> survive with mutation, up regulation of anti-apoptotic genes
22
Q

which genes normally regulate apoptosis?

A

Bax: pro-apoptotic protein

Bcl2: anti-apopotic protein

a balance is required for normal apoptosis

(overpression of bcl-2 -> cancer)

23
Q

what are the two types of tumour suppressor genes?

A

1. gate keeepers

  • directly suppress growth / restrict proliferation (e.g. check point control genes)

2. care takes

  • maintains genetic stability (like DNA repair)
24
Q

what do mutations in tumour supressor genes cause?

A

- act recessively ot release cells from growth control

  • increase probability of other mutations in other classes ( if DNA repair / apoptosis is not occuring - mutations)
  • may prevent apoptosis
25
Q

explain three gate keeper genes

A

Bax (pro-apoptotic protein)

- allows cancer cells to survive even when challenged with chemotheropeautic or DNA damaging compounts that normally triger cytotoxic response

p53

normal function

  • transcription factor (activates transcription)
  • causes cells with mutations to undergo cycle arrest, allows DNA repair or entry to apopotic pathway
  • p53 activated by DNA damage, hypoxia or cell injury
  • p53 activation activates p21 -> inhibits cyclin complexes (prevents cell leaving G1 / entering S-phase

mutated function

  • cell progresses with cell cycle with cell damage -> cells accumulate mutations -> cancer

mutated pRB (retinoblastoma):

  • pRb prevents cell cycle progression past G1 phase by inhibiting expression of S-phase genes
  • mutation in Rb gene = retinoblastoma
26
Q

what do cartaker genes do?

give e.gs and how often they occur?

A

DNA repair proteins

  • repair DNA damage during cell cycle arrest
  • maintain genomic stability

Examples:

  • BRAC1 and BRAC2 are most commonly mutated genes in familial breast (50%) and ovarian cancer (70-80%)
  • carriers mutant BRAC1 and BRAC2 - have a 50-70% risk of developing breast cancer before aged 70
  • BRAC2 leads to more aggressive prostate cancer
27
Q

what are BRAC1 and BRAC2 directly involved in during normal function?

A

- BRAC1 and BRAC2 repair damaged dsDNA crosslinks at the G2 / M checkpoint

  • loss of BRAC1 / 2 results in strand breaks and aneuploidy after cell division
28
Q

describe what happens in normal / mutatted BRAC1?

A

BRAC1:

  • normally: triggers the activation of the CDK inhibitor: p21WAF-1 and p53, so can control cell cycle
  • also involved in DNA repair
  • mutations lead to genomic instability
29
Q

describe what BRCA2 normally does / what a mutation does

A

BRAC2:

  • normally facilitates HR
  • BRAC2 deficient cells: cant recruit RAD51 (protein that binds to ssDNA and needed in dsDNA repair)
  • mutations: cant repair ss and dsb DNA breaks
30
Q

what are neoplastic cells?

A
  • cells that have lost control of normal processes such as growth. once neoplasm has started, not reversible

FunMed Week 4 - cancer (9 decks)

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