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Samenvatting Moderne oncologie

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Samenvatting over moderne oncologische middelen: BCR-ABL-remmers, EGFR-remmers, ALK-remmers, CKIT-remmers, BRAF-remmers, HER2-remmers en bevacizumab. Werkingsmechanisme, bijwerkingenprofiel en subtypen binnen elke geneesmiddelgroep worden beschreven. Daarnaast worden de volgende indicaties besproke...

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  • September 18, 2019
  • 12
  • 2019/2020
  • Summary
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HC moderne oncologie 1
mAb’s Monoclonal antibody. Antilichamen binden extracellulair op de,
groeifactorreceptor of binden aan de endogene liganden die normaal
aangrijpen op de groeifactorreceptor, en neutraliseren deze.
Nib’s Kinaseremmers. Remmen intracellulair het intracellulaire deel van de
groeifactorreceptor of remmen intracellulaire eiwitten die betrokken
zijn bij signaaltransductie.
Belangrijke groeifactor receptoren:

- EGFR
- HER2
- KIT

Elke groeifactor receptor is ingedeeld in verschillende subtypen (vb. A-KIT, B-KIT, C-KIT).

Belangrijke intracellulaire pathways:

- RAS-RAF-MEK-ERK-pathway
- PI3K-AKT-MTOR-pathway
- JAK-STAT-pathway




Tumoren ontstaan door overmatige expressie van een bepaalde groeifactorreceptor, intracellulair
eiwit, of door het ontstaan van eiwitten die bij gezonde mensen niet tot expressie komen. Deze
eiwitten/receptoren kunnen getarget worden met monoklonale antilichamen (Mab’s) of
tyrosinekinaseremmers (Nib’s).

Remmer laag in de cascade heeft minder de voorkeur, omdat de therapie dan minder selectief is
waardoor veel systemisch toxiciteit geïnduceerd wordt.

Werkingsmechanisme Geneesmiddel Type kanker Bijwerking
HER2-remmer (subdomein Trastuzumab HER2+ borstkanker Vermindering
IV) van LVEF
(hartfalen)
HER2-remmer (subdomein Pertuzumab Her2+ borstkanker Vermindering
II) van LVEF
(hartfalen)
ALK-remmer (bindt EML- Crizotinib EML-ALK+ Visusstoornis
ALK) longcarcinoom
ALK-remmer Ceritinib EML-ALK+
longcarcinoom

, ALK-remmer Alectinib EML-ALK+
longcarcinoom
BRAF-remmer Dabrafenib BRAF+ melanoom Erytheem en
fototoxiciteit
(mijd het
zonlicht)
MEK-remmer Tramatenib BRAF+-melanoom Erytheem en
fototoxiciteit
(mijd het
zonlicht)
EGFR-remmer Erlotinib EGFR+ longcarcinoom Erytheem en
diarree
EGFR-remmer Lapatinib EGFR+ longcarcinoom Erytheem en
diarree
EGFR-remmer Afatinib EGFR+ longcarcinoom Erytheem en
diarree
EGFR-remmer Gefitinib EGFR+ longcarcinoom Erytheem en
diarree
Cetuximab
BCR-ABL-remmer Ponatinib CML
BCR-ABL-remmer Nilotinib CML
BCR-ABL-remmer Dasatinib CML
BCR-ABL-remmer Bosutinib CML
BCR-ABL (C-KIT en JAK)- Imatinib CML Reversibele
remmer depygmentatie
(grijs haar)
Figure 1: voornaamste bijwerkingen op basis van de receptorexpressie op bepaalde weefsels.
HER2: hartcellen
BCR-ABL:
EML-ALK:
C-KIT: pigmentcellen
RAF en MEK: huidcellen
EGFR: epitheelcellen
MTOR: hyperglycemie/-lipidemie

- Erlotinib
- Lapatinib
- Afatinib
- Gefitinib

Neratinib

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