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36

NCCN Guidelines for Patients

®

:

Acute Lymphoblastic Leukemia, Version 1.2017

4

Cancer treatments

Targeted therapy

Targeted therapy

Targeted therapy is treatment with drugs that target

a specific or unique feature of cancer cells. Because

these drugs specifically target cancer cells, they may

be less likely to harm normal cells throughout your

body. The targeted therapy drugs that are used for

ALL are listed in

Guide 5

and are described next.

Guide 5. Targeted therapy drugs for

ALL

Generic name Brand name

(sold as)

Type of drug

Blinatumomab Blincyto™

Monoclonal

antibody

Bosutinib

Bosulif

®

TKI

Dasatinib

Sprycel

®

TKI

Imatinib

mesylate

Gleevec

®

TKI

Nilotinib

T

asigna

®

TKI

Ponatinib

Iclusig

®

TKI

Rituximab

Rituxan

®

Monoclonal

antibody

Tyrosine kinase inhibitors

TKI (

t

yrosine

k

inase

i

nhibitor) therapy is a type of

targeted therapy. TKIs are used for a subtype of ALL

in which the leukemia cells have the Philadelphia

chromosome. This subtype is called Ph-positive ALL.

The Philadelphia chromosome contains the abnormal

BCR-ABL

fusion gene.

TKIs target the abnormal BCR-ABL protein that

helps leukemia cells grow. This protein is made by

the

BCR-ABL

gene. It is a type of protein called a

tyrosine kinase. TKIs block (inhibit) the BCR-ABL

protein from sending the signals that cause too many

leukemia cells to form.

TKIs are made in the form of a pill that is

swallowed. TKIs are typically not used alone to

treat ALL. Instead, a TKI is added to a combination

chemotherapy regimen. The use of TKIs has greatly

improved treatment outcomes for this type of ALL.

TKI drug resistance

A treatment response is an improvement in disease

that is caused by treatment. Drug resistance is when

ALL doesn’t respond to a drug. There is more than

one type of drug resistance.

Primary resistance is when ALL doesn’t respond

at all to a drug taken for the first time. This type of

resistance is rare in ALL. Secondary resistance is

more common. It is when ALL responds to a drug at

first and then stops responding over time.

A number of factors may cause or lead to secondary

resistance. Most often, it is caused by mutations

in the part of the

BCR-ABL

gene that makes the

BCR-ABL protein. These mutations change the

shape of the BCR-ABL protein. This can affect how

well certain TKIs work. New mutations can happen

over time during TKI therapy. This can cause the TKI

to stop working.

But, each TKI drug works in a slightly different

way. One TKI drug may be able to work against a

mutation that another TKI can’t. Therefore, switching

to a different TKI may result in a treatment response

after a prior TKI stops working.