title: Omentum and bone marrow: how adipocyte-rich organs create tumour microenvironments conducive for metastatic progression.
abstract: A number of clinical studies have linked adiposity with increased cancer incidence, progression and metastasis, and adipose tissue is now being credited with both systemic and local effects on tumour development and survival. Adipocytes, a major component of benign adipose tissue, represent a significant source of lipids, cytokines and adipokines, and their presence in the tumour microenvironment substantially affects cellular trafficking, signalling and metabolism. Cancers that have a high predisposition to metastasize to the adipocyte-rich host organs are likely to be particularly affected by the presence of adipocytes. Although our understanding of how adipocytes influence tumour progression has grown significantly over the last several years, the mechanisms by which adipocytes regulate the metastatic niche are not well-understood. In this review, we focus on the omentum, a visceral white adipose tissue depot, and the bone, a depot for marrow adipose tissue, as two distinct adipocyte-rich organs that share common characteristic: they are both sites of significant metastatic growth. We highlight major differences in origin and function of each of these adipose depots and reveal potential common characteristics that make them environments that are attractive and conducive to secondary tumour growth. Special attention is given to how omental and marrow adipocytes modulate the tumour microenvironment by promoting angiogenesis, affecting immune cells and altering metabolism to support growth and survival of metastatic cancer cells.
authors.affiliation: Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI, USA.
authors.forename: H
authors.initials: H
authors.lastname: Chkourko Gusky
authors.affiliation: Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI, USA.|Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI, USA.
authors.forename: J
authors.initials: J
authors.lastname: Diedrich
authors.affiliation: Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.|Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
authors.forename: O A
authors.initials: OA
authors.lastname: MacDougald
authors.affiliation: Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI, USA. ipodgors@med.wayne.edu.|Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI, USA. ipodgors@med.wayne.edu.
authors.forename: I
authors.initials: I
authors.lastname: Podgorski
mesh_terms: D017667:Adipocytes / Q000378:metabolism / Q000502:physiology; D052436:Adipose Tissue, White / Q000473:pathology*; D001853:Bone Marrow / Q000473:pathology*; D002471:Cell Transformation, Neoplastic / Q000276:immunology / Q000473:pathology*; D018450:Disease Progression; D006801:Humans; D009362:Neoplasm Metastasis; D009369:Neoplasms / Q000276:immunology / Q000473:pathology*; D009765:Obesity / Q000150:complications / Q000276:immunology / Q000473:pathology*; D009852:Omentum / Q000473:pathology*; D059016:Tumor Microenvironment / Q000276:immunology / Q000502:physiology*
keywords: Adipose tissue; MAT; WAT; bone metastasis; omental metastasis