The immune suppressive mechanisms
displayed by malignant cells are considered a central process in the
pathogenesis of cancer. Research in this area has gained significant
momentu mover the past 20 years, with several immune checkpoints
identified, including; CTLA-4, CD200/CD200R, Tim-3/Galectin-9 and
PD-L1/PD-1 (Figure 1). Whilst characterising the molecular basis of
leukaemia for risk stratification remains at the forefront of AML
research; this must now extend to understating how the seimmune
checkpoint path ways fit into the equation. A good example of why this
is important is to consider CD200expression level in AML, which is a
negative prognostic indicator [1]. CD200 is an immunosuppressive lig
and, that when engaged with its receptor CD200R, has the capacity to
attenuate T-cell and NK-cell anti-tumour activity in AML.
Interestingly, most cases of CBF AML express high levels of CD200, yet
CBF AML performs relatively well clinically. This paradox suggests
there is a complex interplay between AML molecular heterogeneity and
immune surveillance. Given the recent development and FDA approval of
several immune checkpoint therapies, a full understanding of these
processes and integration with standard molecular risk stratification is
warranted.
For More information
For more Lupine Publishers Open Access Journals Please visit our website
For more Oncology research journals articles Please Click
Here: https://lupinepublishers.com/cancer-journal/ 
