Fitz- CML Module Flashcards Preview

IHO Week 4 > Fitz- CML Module > Flashcards

Flashcards in Fitz- CML Module Deck (11):
1

What is the general MOA for STIs?

They bind to to the ATP binding site of TK

2

What are the general SE of STIs?

Generally have fewer SE than conventional therapies because they are target toward the specific defect of a particular cancer.

CAN cause CHF and MYOCARDIAL INFARCTION
TERATOGENIC

3

Why is Imatinib so successful?

Targets a genetic defect that is perfectly selective to cancer cells

4

What are the TUs for imatinib?

Complete hematological/cytological response in 85-95% of pts w/ chronic CML

Delay death in 25% of pts in blast crisis

Gastroinstestinal stormal tumors expressing c-kit

5

Where does imatinib act?

Competitive antagonist at the ATP binding site of:

BCR-ABL
c-KIT--altered in GIST
PDGF

6

What does DASTAINIB specifically target?

SRC

A TK whose expression is up-regulated in several types of cancer

7

What are common toxicities associated w/ imatinib?

edema
BMS

8

What are the therapeutic uses for gefitinib and erolotinib? What is weird about it in terms of efficacy?

Metastatic non-small cell lung cancer after failure of standard chemotherapies

different populations experience varying efficacies--> having the right mutation means the diff between a cure and a response

9

What is the MOA for efitinib and erolotinib? what does it commonly target?

competitive antagonists of ATP binding site of EGFR TK

EGFR TK is overexpressed in epithelial derived cancers

10

Interstitial pneumonia is associated w/ what drugs?

Erlotinib and gefitinib

11

How does imatinib compare to the conventional therapy for the treatment of CML?

STIs are MOST successful at promoting remission, but don't cure the underlying cause of cancer.

They generally have LOWER toxicity and GREATER differential selectivity.