CHAPTER II
LITERATURE REVIEW
"Acute myeloid leukemia (AML) goes by many names, including acute myelocytic leukemia, acute myelogenous leukemia, acute granulocytic leukemia, and acute non-lymphocytic leukemia"
(Detailed Guide: Leukemia).
The word "acute" in acute myeloid leukemia refers to the fact the leukemia may progress at a rapid rate, and if/when the disease is not treated, within a few months, it would likely prove to be fatal. AML begins to develop in cells that traditionally develop into various types of blood cells. Most AML cases develop from cells that would transform into white blood cells (other than lymphocytes), however, a number AML cases develop in other kinds of blood-forming cells. AML starts to develop in the bone marrow, albeit, in the majority of cases it rapidly moves into the blood. At times, it may spread to other body parts, "including the lymph nodes, liver, spleen, central nervous system (brain and spinal cord), and testes" (Detailed Guide: Leukemia). Some other cancer types that may start in these organs and/or elsewhere, and then spread to the bone marrow are not leukemia.
Information presented in this literature review chapter, the researcher notes, "names" or reports a number of relevant points regarding AML. The three clinical studies presented in this study's introduction relate particularly relevant data regarding treatments of/for AML. The following three studies the researcher examines during this thesis include:
1. Study I: "Preclinical Studies of Vorinostat (Suberoylanilide Hydroxamic Acid) Combined with Cytosine Arabinoside and Etoposide for Treatment of Acute Leukemias" (Shiozawa, et al.).
2. Study II: "Nuclear Factor- B Modulation in Patients Undergoing Induction Chemotherapy for Acute Myelogenous Leukemia" (Strair, et al.).
3. Study III: "Preclinical Studies of Vorinostat (Suberoylanilide Hydroxamic Acid) Combined with Cytosine Arabinoside and Etoposide for Treatment of Acute Leukemias" (Shiozaw, et al.).
Treatment of AML
As researchers continue to study the suspected causes, diagnosis, and treatment of AML at various medical centers, university hospitals, and other institutions, they have begun to make progress in understanding ways changes in an individual's DNA may contribute to normal bone marrow cells developing into leukemia. With an increased understanding of the genes involved in particular translocations or other chromosomal changes frequently occurring in AML, more insight into why these cells become abnormal is gained, along with the potential for the development of newer targeted therapies against AML.
The following list depicts a number of these newer target therapies, however, the newer therapies are not limited to these:
Gene Expression Profiling: This lab technique to help identify and classify different cancers utilizes microarrays to simultaneously examines the patterns of various genes in the cancer cells, rather than examining single genes.
Detection of Minimal Residual Disease: "The polymerase chain reaction (PCR) test can identify AML cells based on their gene translocations or rearrangements. This test can find one leukemia cell among a million normal cells. A PCR test can be useful in determining how completely the treatment has destroyed the AML cells" (Detailed Guide: Leukemia).
Improving Chemotherapy
Stem Cell Transplants
Targeted Therapies
New targeted drugs that specifically attack some of the genetic changes seen in AML are now being developed.
About 1 person out of 3 with AML has a mutation in the FLT3 gene. Several new drugs, called FLT3 inhibitors, target this gene. They have shown activity against AML in early studies, especially when combined with chemotherapy. So far, they are only available in clinical trials. Other gene mutations, such as changes in the c-KIT gene, also appear to be important in some cases of AML, and may become important targets for new therapies. Drugs that target this gene, such as imatinib (Gleevec) and dasatinib (Sprycel) are already used against other types of leukemia, and are now being studied against AML.
Gemtuzumab ozogamicin (Mylotarg) is a monoclonal antibody that is often used in older patients if AML doesn't respond to chemotherapy or comes back after treatment. Doctors are now studying whether this drug might be useful if given with chemotherapy earlier in the course of the disease (Detailed Guide: Leukemia).
Study I
During Study I, "Epigenetic Modification of CCAAT/Enhancer Binding Protein Expression in Acute Myeloid Leukemia," Hackanson, et al., as noted earlier, confirm C/EBP mRNA as a target for miRNA-124a. Bjorn, et al. signify that C/EBP epigenetic alterations denote a frequent event in AML and epigenetic treatment may result in down-regulation of a key hematopoietic transcription facto. Hackanson, et al. point out that the "functional loss of CCAAT/enhancer binding protein (C/EBP), a master regulatory transcription factor in the hematopoietic system, can result in a differentiation...
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