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G-CSF-Mediated Metastatic Niche Development in the Omentum
- The omentum is a common site of metastasis for various cancers like ovarian, gastric, colorectal, and pancreatic cancers due to complex mechanisms including anatomic features, cellular interactions, and immune system responses.
- Metastatic niche development involves detachment from the primary tumor, survival in the peritoneal cavity, migration to the omentum, adhesion, invasion, and proliferation.
- The omental structure, circulation of peritoneal fluid, immune cell-rich 'milky patches', and adhesion molecules like CD44 and integrins contribute to the metastatic process.
- Adipocytes in the omentum provide energy sources and signaling molecules to support tumor growth, while stromal cells stimulate angiogenesis and cancer cell proliferation.
- Tumor-associated macrophages (TAMs) and M2 macrophages in the omentum promote metastatic growth by facilitating angiogenesis, ECM remodeling, and immune evasion.
- Neutrophils, influenced by factors like G-CSF, prepare the metastatic niche through NETosis, creating structures that aid in cancer cell capture and spread to other parts of the body.
- G-CSF triggers neutrophil migration into the omentum, leading to the formation of 'pre-metastatic niche'; G-CSF, IL-8, and GRO induce NETosis in neutrophils, aiding in metastasis.
- NETs act as traps for circulating cancer cells, promoting their adhesion to the omentum; the NET structures play a crucial role in the omental metastatic cascade.
- The physical trapping and anchoring function of NETs, along with proteolytic enzymes on NETs, facilitate cancer cell invasion and remodeling of the extracellular matrix, promoting metastatic growth.
- The diverse mechanisms involved in omental metastasis underscore the complexity of the process, necessitating consideration of anatomical, cellular, and immune components for developing targeted therapies.
- The dual role of G-CSF in neutropenia treatment and omental metastasis highlights the importance of carefully evaluating its use in patients at risk of metastasis; targeting NET formation could be a potential approach for future cancer treatments.
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