Acute myeloid leukemia (AML) is a cancer of blood and bone marrow,
caused by abnormal production of white blood cells. According to the recent 2020
statistics, an estimated number of 19,940 people in the United States will be diagnosed
with AML. The hematologic tumor microenvironment plays a critical role in the
progression of AML. Emerging evidence indicates that chemotherapy resistance and
disease relapse are linked through the signaling pathways associated with the tumor
microenvironment in AML. The leukemia cells communicate with the other noncancerous
cells of the tumor microenvironment through small vesicles that are within
the size of 30-120nm called exosomes, a type of extracellular vesicles. Exosomes
contain genetic information in their cargo, in the form of either protein, DNA, or noncoding
RNAs and communicate to the distinct cells through various signaling
pathways. The c-Myc oncogenic transcription factor protein is a master regulator of
oncogenic signaling pathways in various cancers, including AML. C-Myc has been
associated with the development of therapy resistance in AML, representing a key
target. The interconnection between exosomes, tumor microenvironment, c-Myc and
the development of progression, therapy resistance are discussed in this chapter and
thus, represents a fundamental knowledge of the recent advances in cancer signal
transduction and therapy.
Keywords: Acute myeloid leukemia, C-Myc, Drug resistance, Exosomes,
Oncogene, Tumor microenvironment, Tumor suppressor gene.
