Different molecules and their functions Flashcards
TNF-α
Tumour necrosis factor-alpha
Immune activation in the cancer-destruction pathway
TGF-β
Transforming growth factor-beta
- Pre-malignant cells - tumour suppressor, apoptosis, etc
- Malignant cells - tumour promoting, immune evasion, metastasis, etc
IL-1β
Interleukin 1-beta
- Immune activation in the cancer-destruction pathway
- Angiogenesis stimulating
- Inhibit cancer cell proliferation
Supports and inhibits cancer development
IL-2
Interleukin 2
Activation of CD8+ cells and NK cells
CXCL8
C-X-C motif chemokine 8, or IL-8 (interleukin-8)
Angiogenesis of tissues
IL-10
Interleukin-10
Immune suppression
IL-12
Interleukin-12
Maturation of APCs
IL-23
Interleukin-23
Immune activation in the cancer-destruction pathway
CXCL10
C-X-C motif chemokine 10, or IP-10 (Interferon-gamma-induced protein 10)
Immune activation in the cancer-destruction pathway
IFN-γ
Interferon-gamma
Immune activation in the cancer-destruction pathway
NO
Nitrous oxide
Immune activation in the cancer-destruction pathway
PD1/PDL1
- Programmed cell death protein
- Programmed death-ligand 1
Immune suppression
EGF
Epidermal growth factor
Proliferation and survival of cancer cells
FGF
Fibroblast growth factor
- Proliferation and survival of cancer cells
- Angiogenesis of tissues
PDGF
Platelet-derived growth factor
Angiogenesis of tissues
VEGF
Vascular endothelial growth factor
Angiogenesis of tissues
MMPs
Matrix metalloproteases
Tissue remodelling and fibrosis
Chatepsins
Tissue remodelling and fibrosis
CD8
Cluster of differentiation 8
- Cytotoxic T-cells
CD4
Cluster of differentiation 4
- Helper T cells
- T-regulatory cells
CD25
Cluster of differentiation 25
- T-regulatory cells
p16
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)
p21
p-21 kilo-dalton
- Tumour suppressor - inhibit cyclin E (cyclin 2) and cyclin D (CDK4/6), arresting the cell cycle
Activated by p53
p53
p-53 kilo-dalton
- Tumour suppressor - arrests proliferative cycle and induces apoptosis
BCR-Abl
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
v-Abl
Normal Abl is a proto-oncogene
v-Abl has its SH3 domain completely removed, resulting in Abl’s constitutive activation
RB
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
HER2
Human epidermal growth factor receptor 2
RTK oncogene - cell growth, differentiation, and survival
Breast cancer
Pertuzumab and trastuzumab - treatment
Myc
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
pTEN
Dephosphorylates PIP3 into PIP2
Tumour suppressor
PI3K
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)
Ras
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
