Different molecules and their functions

Question 1

TNF-α

Answer 1

Tumour necrosis factor-alpha

Immune activation in the cancer-destruction pathway

Question 2

TGF-β

Answer 2

Transforming growth factor-beta

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

Question 3

IL-1β

Answer 3

Interleukin 1-beta

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

Supports and inhibits cancer development

Question 4

IL-2

Answer 4

Interleukin 2

Activation of CD8+ cells and NK cells

Question 5

CXCL8

Answer 5

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

Angiogenesis of tissues

Question 6

IL-10

Answer 6

Interleukin-10

Immune suppression

Question 7

IL-12

Answer 7

Interleukin-12

Maturation of APCs

Question 8

IL-23

Answer 8

Interleukin-23

Immune activation in the cancer-destruction pathway

Question 9

CXCL10

Answer 9

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

Immune activation in the cancer-destruction pathway

Question 10

IFN-γ

Answer 10

Interferon-gamma

Immune activation in the cancer-destruction pathway

Question 11

NO

Answer 11

Nitrous oxide

Immune activation in the cancer-destruction pathway

Question 12

PD1/PDL1

Answer 12

• Programmed cell death protein
• Programmed death-ligand 1

Immune suppression

Question 13

EGF

Answer 13

Epidermal growth factor

Proliferation and survival of cancer cells

Question 14

FGF

Answer 14

Fibroblast growth factor

• Proliferation and survival of cancer cells
• Angiogenesis of tissues

Question 15

PDGF

Answer 15

Platelet-derived growth factor

Angiogenesis of tissues

Question 16

VEGF

Answer 16

Vascular endothelial growth factor

Angiogenesis of tissues

Question 17

MMPs

Answer 17

Matrix metalloproteases

Tissue remodelling and fibrosis

Question 18

Chatepsins

Answer 18

Tissue remodelling and fibrosis

Question 19

CD8

Answer 19

Cluster of differentiation 8

• Cytotoxic T-cells

Question 20

CD4

Answer 20

Cluster of differentiation 4

• Helper T cells
• T-regulatory cells

Question 21

CD25

Answer 21

Cluster of differentiation 25

• T-regulatory cells

Question 22

p16

Answer 22

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)

Question 23

p21

Answer 23

p-21 kilo-dalton

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

Activated by p53

Question 24

p53

Answer 24

p-53 kilo-dalton

• Tumour suppressor - arrests proliferative cycle and induces apoptosis

Question 25

BCR-Abl

Answer 25

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

Question 26

v-Abl

Answer 26

Normal Abl is a proto-oncogene v-Abl has its SH3 domain completely removed, resulting in Abl's constitutive activation

Question 27

RB

Answer 27

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

Question 28

HER2

Answer 28

Human epidermal growth factor receptor 2 RTK oncogene - cell growth, differentiation, and survival Breast cancer Pertuzumab and trastuzumab - treatment

Question 29

Myc

Answer 29

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

Question 30

pTEN

Answer 30

Dephosphorylates PIP3 into PIP2 Tumour suppressor

Question 31

PI3K

Answer 31

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)

Question 32

Ras

Answer 32

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