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BIOL21742 > Different molecules and their functions > Flashcards

Different molecules and their functions Flashcards

1
Q

TNF-α

A

Tumour necrosis factor-alpha

Immune activation in the cancer-destruction pathway

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2
Q

TGF-β

A

Transforming growth factor-beta

  • Pre-malignant cells - tumour suppressor, apoptosis, etc
  • Malignant cells - tumour promoting, immune evasion, metastasis, etc
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3
Q

IL-1β

A

Interleukin 1-beta

  • Immune activation in the cancer-destruction pathway
  • Angiogenesis stimulating
  • Inhibit cancer cell proliferation

Supports and inhibits cancer development

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4
Q

IL-2

A

Interleukin 2

Activation of CD8+ cells and NK cells

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5
Q

CXCL8

A

C-X-C motif chemokine 8, or IL-8 (interleukin-8)

Angiogenesis of tissues

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6
Q

IL-10

A

Interleukin-10

Immune suppression

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7
Q

IL-12

A

Interleukin-12

Maturation of APCs

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8
Q

IL-23

A

Interleukin-23

Immune activation in the cancer-destruction pathway

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9
Q

CXCL10

A

C-X-C motif chemokine 10, or IP-10 (Interferon-gamma-induced protein 10)

Immune activation in the cancer-destruction pathway

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10
Q

IFN-γ

A

Interferon-gamma

Immune activation in the cancer-destruction pathway

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11
Q

NO

A

Nitrous oxide

Immune activation in the cancer-destruction pathway

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12
Q

PD1/PDL1

A
  • Programmed cell death protein
  • Programmed death-ligand 1

Immune suppression

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13
Q

EGF

A

Epidermal growth factor

Proliferation and survival of cancer cells

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14
Q

FGF

A

Fibroblast growth factor

  • Proliferation and survival of cancer cells
  • Angiogenesis of tissues
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15
Q

PDGF

A

Platelet-derived growth factor

Angiogenesis of tissues

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16
Q

VEGF

A

Vascular endothelial growth factor

Angiogenesis of tissues

17
Q

MMPs

A

Matrix metalloproteases

Tissue remodelling and fibrosis

18
Q

Chatepsins

A

Tissue remodelling and fibrosis

19
Q

CD8

A

Cluster of differentiation 8

  • Cytotoxic T-cells
20
Q

CD4

A

Cluster of differentiation 4

  • Helper T cells
  • T-regulatory cells
21
Q

CD25

A

Cluster of differentiation 25

  • T-regulatory cells
22
Q

p16

A

p-16 kilo-dalton

  • Tumour suppressor - inhibit cyclin E (cyclin 2), arresting the cell cycle

Activated by Ets (E26 transformation-specific/E-twenty-six/eryhtroblast transformation specific)

23
Q

p21

A

p-21 kilo-dalton

  • Tumour suppressor - inhibit cyclin E (cyclin 2) and cyclin D (CDK4/6), arresting the cell cycle

Activated by p53

24
Q

p53

A

p-53 kilo-dalton

  • Tumour suppressor - arrests proliferative cycle and induces apoptosis
25
Q

BCR-Abl

A

Normal Abl is a proto-oncogene

BCR-Abl has its SH3 domain attached to the BCR subunit and doesn’t properly associate with the core, resulting in its constitutive activation

26
Q

v-Abl

A

Normal Abl is a proto-oncogene

v-Abl has its SH3 domain completely removed, resulting in Abl’s constitutive activation

27
Q

RB

A

Tumour suppressor - transcriptional repressor, regulates cell cycle - G0 to G1, dephosphorylation causes RB to bind to E2F and repress genes that promote entry into G1/S

Involved in retinoblastoma

28
Q

HER2

A

Human epidermal growth factor receptor 2

RTK oncogene - cell growth, differentiation, and survival

Breast cancer

Pertuzumab and trastuzumab - treatment

29
Q

Myc

A

Oncogenic transcription factor

Involved in cell proliferation, differentiation, metabolism, and apoptosis (various parts in tumour growth)

Normally dimerises with Max and binds to E-boxes(? whatever that)

Half-life of ~20 mins, rapid degradation by the proteasome

> 70% of cancers involve its constitutive activation, this is due to it losing its death timer and being amplified due to its survival and production (?), resulting in it activating not only its high-affinity targeting genes but also its low-affinity targeting genes which often results in tumorigenesis

Though none have clinical use currently, potentially targetting its dimerisation with Max, targeting myc itself, targeting myc mRNA translation, or targeting myc mRNA generation

30
Q

pTEN

A

Dephosphorylates PIP3 into PIP2

Tumour suppressor

31
Q

PI3K

A

Phosphorylates PIP2 into PIP3

Proto-oncogene as PIP3 can activate Akt which can potentially have oncogenic properties (cell survival/cycle) if dysregulated (Akt inhibits CDKIs - cell cycle promoted)

32
Q

Ras

A

Protein that is activated by RTKs and activates pathways that promote cell survival and proliferation

Proto-oncogene - its over activation results in pathways like the Akt and MAPK pathways to promote tumorigenic growth

BIOL21742 (21 decks)

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