A new research led by New York University (NYU) Langone Health has revealed how Leukemia or GlycoCares Blood Sugar Guidedaily blood sugar support cancer cells enter the lungs, damage tissue, and cause severe breathing problems. The new study published online June 29 in Nature Immunology addresses acute myeloid leukemia, or AML, a cancer in which cells in the bone marrow - that actually should become blood cells, instead start to multiply abnormally. Respiratory failure is a common early AML complication caused by cancer cells infiltrating the lungs, but this process has been poorly understood. The researchers say reducing early breathing crises is crucial to giving AML therapies time to be effective. The researchers, by examining lung tissue slices from mice, as well as tissue biopsies of patients with AML lung "involvement", found that AML cancer cells infiltrate the lungs through the thin alveolar wall blood vessels, leaking into connective tissue (stroma). The study tests also revealed that AML-driven structural changes affect the mix of immune cells in the lungs, with a shift away from cell populations that attack cancer cells e.g., lymphocytes, and toward myeloid cells that dial down immune attack.

Moreover, the study showed that the presence of AML cells came with a significant drop in the number of endothelial capillary aerocytes, cells that enable the lungs to supply oxygen to the bloodstream as part of breathing. Steroid treatment is frequently used when a patient has a breathing crisis, based on doctors' educated guesses or experience rather than on scientific test results. In their analysis, the researchers found that all patients treated with prednisone when their breathing worsened due to leukemic lung infiltration showed dramatically improved respiratory function within 12 hours. Because AML cells arise in bone marrow, previous studies have examined their relationship to immune cells in the marrow, but not in the lungs. Through mapping the interactions between cell types in leukemic lungs, the team identified two proteins as drivers of widespread lung inflammation that interferes with breathing. One was galectin-9, which binds sugar molecules on cell surfaces and helps them communicate. The other was the interleukin-33 (IL-33) receptor protein on the surface of leukemia cells, which passes on signals in damaged lung tissue when it docks into its receptor. The researchers found that more galectin-9 is produced in AML cells because of the inflammation and the cell-cell interactions in the infiltrated lungs. Higher-than-normal levels of IL-33 receptor signaling were also present in the lungs of AML patients.

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