Newly discovered anti-cancer activity of Furazolidone and some research suggestions

Main Points:

Researchers have found that furazolidone – an antibacterial drug – can effectively be used for the treatment of acute myeloid leukemia (AML), i.e. a form of cancer.

Published in:

PLoS ONE

Study Further:

Acute myeloid leukemia (AML):

AML is the cancer of myeloid line of blood cells i.e. blood cells related to or derived from bone marrow or the spinal cord. This cancer especially affects white blood cells called as myeloid cells and progresses rapidly.

Bone marrow aspirate showing acute myeloid leukemia. Several blasts have Auer rods. (Credit: Wikipedia)
Bone marrow aspirate showing acute myeloid leukemia. Several blasts have Auer rods. (Credit: Wikipedia)
Structure of Furazolidone
Structure of Furazolidone

Furazolidone:

Furazolidone is an antibacterial drug commonly used for diarrhea or enteritis – inflammation of intestines – caused by bacteria or protozoan infections in human and animals. It is a very popular antibiotic in China.

It is also used for giardiasis, i.e. infection of the gut by a water-borne microscopic protozoan giardia.

This drug is in use for more than 6 decades.

Therapeutic strategies for AML:

Currently, Arabinosylcytosine (Ara-C) and anthracycline- based chemotherapy are the frontline induction therapy for AML but the results are different in different subjects and conditions. These therapies result in only “less than 2 years of median survival and no more than 40% of 5-year overall survival (OS)”. Some other compounds such as gemcitabine, paclitaxel, and simvastatin have also been studied for the treatment of AML.

Research:

In the new study, researchers worked on 1200 off-patent marketed drugs and natural compounds approved by the Food and Drug Administration (FDA) and found that furazolidone has potent anti-leukemic activity in a series of AML cells. Not only it has anti-leukemic activity, it is also able to increase the stability of tumor suppressor p53 protein in AML cells.

p53:

p53 is a tumor suppressor gene, i.e. it works to stop the tumor formation. If you are interested in reading more about p53 than this paragraph is important. This gene produces p53 protein that has the ability to bind to the DNA resulting in the stimulation of another gene to generate p21 protein. P21 protein interacts with cdk2, i.e. a cell division-stimulating protein, forming a complex that prevents the cell to pass into the next stage of cell division (Summary: p53 makes p21 that complexes with cdk2 that prevents cell division progress). In the recent years, researchers are working hard to use its potential against cancer in different ways.

Research suggestions:

After studying this, I think we can research on the following points,

1. Mechanisms of FZD in the treatment of AML

2. Effects of FZD in the median survival and overall survival

3. Whether other drugs of the same class such as Nitrofuran derivatives or drugs for giardiasis have similar effects or not?

4. What would be the effect of the combination therapy of FZD and anthracycline- based chemotherapy?

5. Whether FZD is also potent against other forms of cancer or not?

References:

Genes and Diseases – NCBI Bookshelf

Acute myelogenous leukemia (AML) – MayoClinic

Xueqing Jiang, Lin Sun, Jihui Julia Qiu, Xiujing Sun, Sen Li, Xiyin Wang, Chi Wai Eric So, Shuo Dong mail (2013). A Novel Application of Furazolidone: Anti-Leukemic Activity in Acute Myeloid Leukemia PLoS ONE DOI: 10.1371/journal.pone.0072335

Usman Zafar Paracha

Usman Zafar Paracha is Assistant Professor, Pharmaceutics, in Hajvery University, Lahore, Pakistan.