Targeted treatment for APL
The way TRISENOX
® (arsenic trioxide) injection works is not completely understood, but it
appears to target the
underlying genetic causes of acute promyelocytic leukemia
(APL). In APL, two genes involved in the prevention of the disease actually trade places.
1-4
Normally these genes help to restrict tumor growth and to control the aging of white blood
cells.
5,6 In patients with APL, these genes combine to form a mutant gene that makes it
difficult for normal genes to do their job.
1-4 Because of this, APL cells may not age as they're
supposed to, and can increase in number to an unhealthy degree.
1-5
These leukemic cells are uniquely sensitive to TRISENOX.
2 TRISENOX helps to break down the
mutant proteins, enabling white blood cells to age properly.
1,2 TRISENOX may also
help APL cells to actually eliminate themselves through a natural process called apoptosis, or
"programmed cell death."
4,7 TRISENOX may also help to reactivate the functions of
the affected genes so they can get back to work and help to suppress tumors and kill APL
cells.
6,8
As a targeted treatment for APL, TRISENOX works with minimal chemotherapy-related side
effects.
>> Click here to learn more about potential side effects with TRISENOX therapy.
In clinical trials, most patients taking TRISENOX experienced some drug-related toxicity,
most commonly leukocytosis, gastrointestinal (nausea, vomiting, diarrhea, and abdominal pain),
fatigue, edema, hyperglycemia, dyspnea, cough, rash or itching, headaches, and dizziness.
These adverse effects have not been observed to be permanent or irreversible, nor do they
usually require interruption of therapy.
1. Grignani F, Fagioli M, Alcalay M, et al. Acute promyelocytic leukemia: from genetics to treatment. Blood. 1994;83:10-25.
2. Douer D, Tallman MS. Arsenic trioxide: new clinical experience with an old medication in hematologic malignancies. J Clin Oncol. 2005;23:2396-2410.
3. Miller WH Jr, Schipper HM, Lee JS, et al. Mechanisms of action of arsenic trioxide. Cancer Res. 2002;62:3893-3903.
4. Davison K, Mann KK, Miller WH Jr. Arsenic trioxide: mechanisms of action. Semin Hematol. 2002;39(2 Suppl 1):3-7.
5. Melnick A, Licht JD. Deconstructing a disease: RAR alpha, its fusion partners, and their roles in the pathogenesis of acute promyelocytic leukemia. Blood. 1999;93:3167-3215.
6. Hayakawa F, Privalsky ML. Phosphorlyation of PML by mitogen-activated protein kinases plays a key role in arsenic trioxide-mediated apoptosis. Cancer Cell. 2004;5:389-401.
7. Miller WH Jr. Molecular targets of arsenic trioxide in malignant cells. Oncologist. 2002;7Suppl 1:14-19.
8. Mann KK, Miller WH Jr. Death by arsenic: implications of PML sumoylation. Cancer Cell. 2004;5:307-309.