Fitzpatrick - Targeted Therapy and Biologicals Flashcards Preview

Hematology and Oncology > Fitzpatrick - Targeted Therapy and Biologicals > Flashcards

Flashcards in Fitzpatrick - Targeted Therapy and Biologicals Deck (23)
Loading flashcards...
1
Q

Bcr-abl inhibitor name and MOA

A
  • Imatibib or Dasintinib (CML tx).

- MOA - Occupies ATP cofactor binding stie on Bcl-abl, inhibiting transfer of phosphate to TK.

2
Q

Tx for Imatinib resistant CML

A

Dasatinib

3
Q

Selectivity of imatinib v. Dasatinib.

A
  • Imatinib - Bcr-abl c-kit, PDGFR = CML, GIST

- Dasatinib - Bcr-abl, src = CML(imatinib resistant forms), (Ph+)ALL

4
Q

Tx for Imatinib resistant GIST

A

Sunitinib

5
Q

HER2+ is expressed in 1/4 of ___ cancer

overexpression v expression means what for survival?

A

breast cancer

Overexpression=3yr survival v. expression=6-7yr survival

6
Q

Drugs that inhibit TK ERB Family signaling/target: HER2 receptor
Drugs that inhibit TK ERB Family signaling/target: EGFR receptor

A
HER2 = Lapatanib
EGFR2 = Erolotinib, Gefitinib, Lapatinib
7
Q

Drugs that inhibit TK signaling/target: PDGFR receptor, VEGFR receptor

A

Sunitinib and Sorafenib

8
Q

antibodies to drugs that inhibit EGFR receptors
antibodies to drugs that inhibit HER2 receptors
antibodies to drugs that inhibit VEGF LIGAND

A

EGFR receptor - PaCe = Panitumumab/Cetiximab
HER2 receptor - LapaTra = Trastuzumab
VEGF-ligand = bevacizumab

9
Q

Vemurafinib inhibits mutant ___

A

Mutant BRAF V600E = Metastatic Malignant Melanoma

10
Q

Drugs that inhibit TK signaling/target: BCR-Abl

A

Dasatinib, Imatinib

11
Q

EGFR-receptor target/Cetuximab ab = ___ clinical use

A

colorectal; H/N (**no KRAS mutation)

12
Q

EGFR-receptor target/panitumumab ab = ___ clinical use

A

Colorectal cancer (**no KRAS mutation)

13
Q

HER2+ receptor target/trastuzumab ab = ___ clinical use

A

Breast cancer

14
Q

VEGF ligand target/bevacizumab ab = ___ clinical use

A

Renal cell carcinoma

15
Q

Why is KRAS a determinant of response to antibodies that inhibit EGFR activation?

A

Mutant KRAS is permanently activated; bypasses EGFR TK signaling.

16
Q

Name the angiogenesis inhibitors (1 ab and 2 RTK inhibitors)

A

Ab - bevacizumab (targets a GF LIGAND –> used esp for RCC)

RTK inhibitors - Sunitinib, sorafenib

17
Q

Why does RCC respond well to angiogenesis inhibitors?

A

Bc arises from mutation in VHL. VHL degrades HIF. Impaired VHL=more HIF=highly vascularized tumor.

18
Q

Rituxomab treats what?

A

CD20+ B Cell Lymphoma

19
Q

Breast cancer drugs: three

A
  1. Lapatinib/Trastuzumab
  2. Anastrazole (aromatase inhibitor = reversible)
  3. Exemestane (aromatase inactivator = irreversible)
20
Q

NSCLC drugs

A

(EGFR) Erlotinib, Gefitinib

21
Q

Breast Cancer

A

Lapatinib - EGFR and HER2

22
Q

GIST and RCC

A

Sunatinib (c-kit, PDGFR, VEGFR)

23
Q

RCC and HCC

A

SoRAFenib (PDGFR, VEGFR)