ILT2 and ILT4 Drive Myeloid Suppression via Both Overlapping and Distinct Mechanisms.

Solid tumors are dense three-dimensional (3D) multicellular structures that enable efficient receptor-ligand trans interactions via close cell-cell contact. Immunoglobulin-like transcript (ILT)2 and ILT4 are related immune-suppressive receptors that play a role in the inhibition of myeloid cells within the tumor microenvironment. The relative contribution of ILT2 and ILT4 to immune inhibition in the context of solid tumor tissue has not been fully explored.

Tumor histoculture captures the dynamic interactions between tumor and immune components in response to anti-PD1 in head and neck cancer.

Dynamic interactions within the tumor micro-environment drive patient response to immune checkpoint inhibitors. Existing preclinical models lack true representation of this complexity. Using a Head and Neck cancer patient derived TruTumor histoculture platform, the response spectrum of 70 patients to anti-PD1 treatment is investigated in this study.

Mitochondrial dependency in progression of acute myeloid leukemia.

Acute myeloid leukemia (AML) is a clonal hematopoietic malignant disorder which arises due to dysregulated differentiation, uncontrolled growth and inhibition of apoptosis leading to the accumulation of immature myeloid progenitor in the bone marrow. The heterogeneity of the disease at the molecular and cytogenetic level has led to the identification of several alteration of biological and clinical significance. One of the alterations which have gained attention in recent times is the altered energy and metabolic dependency of cancer originally proposed by Warburg.

Epstein-Barr virus latent membrane protein-2A alters mitochondrial dynamics promoting cellular migration mediated by Notch signaling pathway.

Recently, migration and invasion of breast cancer cells have been linked with dysregulated mitochondrial dynamics. Mitochondria are essential cellular organelles that undergo continuous dynamic cycles of fission and fusion. It has been proposed that a delicate balance between these two processes is important for many pathophysiological outcomes including cancer.

Alteration of mitochondrial proteome due to activation of Notch1 signaling pathway.

The Notch signaling pathway, a known regulator of cell fate decisions, proliferation, and apoptosis, has recently been implicated in the regulation of glycolysis, which affects tumor progression. However, the impact of Notch on other metabolic pathways remains to be elucidated. To gain more insights into the Notch signaling and its role in regulation of metabolism, we studied the mitochondrial proteome in Notch1-activated K562 cells using a comparative proteomics approach.

Molecular cross talk between Notch1, Shh and Akt pathways during erythroid differentiation of K562 and HEL cell lines.

Erythropoiesis is a tightly regulated process dependent on extrinsic signals conveyed by the bone marrow niche. The signalling pathways thus activated or repressed do not act in isolation; rather an intricate cross talk among these pathways ensues homoeostasis within the erythroid compartment. In this study, we describe the effects of two such signalling pathways namely the Notch1 and the Shh pathway on erythropoiesis in immortalised K562 and HEL cell lines as well as the cross talk that ensues between them.