Abstract

Rodent and clinical studies have documented that myeloid cell infiltration of tumors is associated with neutrophilia, lymphocytopenia and poor patient outcomes. This contrasts with lymphocyte infiltration of tumors, which is associated with improved outcomes. Lifestyle parameters such as high fat diets and omega (ω)-6 polyunsaturated fatty acids (PUFA) intake may influence these inflammatory parameters including extramedullary myelopoiesis that can contribute to a metastatic “niche”. While, tumor secretion of growth factors (GFs) and chemokines regulate tumor-immune-cell crosstalk, in this chapter, we also emphasize how lifestyle choices, including, obesity, high-fat and high ω-6 PUFA dietary content, contribute to inflammation and myeloid cell infiltration of tumors. A relationship between obesity and high-fat diets (notably the saturated fats in Western diets) and tumor incidence, metastasis, and poor outcomes is generally accepted. However, the mechanisms of dietary promotion of inflammatory microenvironments and targeted drugs to inhibit the clinical sequel remain an unmet challenge. One approach, modification of dietary intake may have a preventative or therapeutic approach to regulate tumor-associated inflammation and remains an attractive, but little studied intervention.

Original languageEnglish (US)
Title of host publicationAdvances in Experimental Medicine and Biology
PublisherSpringer New York LLC
Pages145-156
Number of pages12
Volume1036
DOIs
StatePublished - Jan 1 2017

Publication series

NameAdvances in Experimental Medicine and Biology
Volume1036
ISSN (Print)0065-2598
ISSN (Electronic)2214-8019

Fingerprint

Tumors
Lipids
Nutrition
Fats
Infiltration
Neoplasms
High Fat Diet
Myeloid Cells
Unsaturated Fatty Acids
Therapeutics
Life Style
Obesity
Omega-6 Fatty Acids
Myelopoiesis
Inflammation
Diet Therapy
Lymphopenia
Lymphocytes
Crosstalk
Chemokines

Keywords

  • High fat diet
  • Immune escape
  • Infiltration
  • Invasion
  • MDSC
  • Metastasis
  • PUFA
  • Seed and soil
  • TAM
  • Vasculogenesis

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Khadge, S., Sharp, J. G., McGuire, T. R., Thiele, G. M., & Talmadge, J. E. (2017). Lipid inflammatory mediators in cancer progression and therapy. In Advances in Experimental Medicine and Biology (Vol. 1036, pp. 145-156). (Advances in Experimental Medicine and Biology; Vol. 1036). Springer New York LLC. https://doi.org/10.1007/978-3-319-67577-0_10

Lipid inflammatory mediators in cancer progression and therapy. / Khadge, Saraswoti; Sharp, John G; McGuire, Timothy R; Thiele, Geoffrey Milton; Talmadge, James E.

Advances in Experimental Medicine and Biology. Vol. 1036 Springer New York LLC, 2017. p. 145-156 (Advances in Experimental Medicine and Biology; Vol. 1036).

Research output: Chapter in Book/Report/Conference proceedingChapter

Khadge, S, Sharp, JG, McGuire, TR, Thiele, GM & Talmadge, JE 2017, Lipid inflammatory mediators in cancer progression and therapy. in Advances in Experimental Medicine and Biology. vol. 1036, Advances in Experimental Medicine and Biology, vol. 1036, Springer New York LLC, pp. 145-156. https://doi.org/10.1007/978-3-319-67577-0_10
Khadge S, Sharp JG, McGuire TR, Thiele GM, Talmadge JE. Lipid inflammatory mediators in cancer progression and therapy. In Advances in Experimental Medicine and Biology. Vol. 1036. Springer New York LLC. 2017. p. 145-156. (Advances in Experimental Medicine and Biology). https://doi.org/10.1007/978-3-319-67577-0_10
Khadge, Saraswoti ; Sharp, John G ; McGuire, Timothy R ; Thiele, Geoffrey Milton ; Talmadge, James E. / Lipid inflammatory mediators in cancer progression and therapy. Advances in Experimental Medicine and Biology. Vol. 1036 Springer New York LLC, 2017. pp. 145-156 (Advances in Experimental Medicine and Biology).
@inbook{7b390ef795084587a3bef433de428551,
title = "Lipid inflammatory mediators in cancer progression and therapy",
abstract = "Rodent and clinical studies have documented that myeloid cell infiltration of tumors is associated with neutrophilia, lymphocytopenia and poor patient outcomes. This contrasts with lymphocyte infiltration of tumors, which is associated with improved outcomes. Lifestyle parameters such as high fat diets and omega (ω)-6 polyunsaturated fatty acids (PUFA) intake may influence these inflammatory parameters including extramedullary myelopoiesis that can contribute to a metastatic “niche”. While, tumor secretion of growth factors (GFs) and chemokines regulate tumor-immune-cell crosstalk, in this chapter, we also emphasize how lifestyle choices, including, obesity, high-fat and high ω-6 PUFA dietary content, contribute to inflammation and myeloid cell infiltration of tumors. A relationship between obesity and high-fat diets (notably the saturated fats in Western diets) and tumor incidence, metastasis, and poor outcomes is generally accepted. However, the mechanisms of dietary promotion of inflammatory microenvironments and targeted drugs to inhibit the clinical sequel remain an unmet challenge. One approach, modification of dietary intake may have a preventative or therapeutic approach to regulate tumor-associated inflammation and remains an attractive, but little studied intervention.",
keywords = "High fat diet, Immune escape, Infiltration, Invasion, MDSC, Metastasis, PUFA, Seed and soil, TAM, Vasculogenesis",
author = "Saraswoti Khadge and Sharp, {John G} and McGuire, {Timothy R} and Thiele, {Geoffrey Milton} and Talmadge, {James E}",
year = "2017",
month = "1",
day = "1",
doi = "10.1007/978-3-319-67577-0_10",
language = "English (US)",
volume = "1036",
series = "Advances in Experimental Medicine and Biology",
publisher = "Springer New York LLC",
pages = "145--156",
booktitle = "Advances in Experimental Medicine and Biology",

}

TY - CHAP

T1 - Lipid inflammatory mediators in cancer progression and therapy

AU - Khadge, Saraswoti

AU - Sharp, John G

AU - McGuire, Timothy R

AU - Thiele, Geoffrey Milton

AU - Talmadge, James E

PY - 2017/1/1

Y1 - 2017/1/1

N2 - Rodent and clinical studies have documented that myeloid cell infiltration of tumors is associated with neutrophilia, lymphocytopenia and poor patient outcomes. This contrasts with lymphocyte infiltration of tumors, which is associated with improved outcomes. Lifestyle parameters such as high fat diets and omega (ω)-6 polyunsaturated fatty acids (PUFA) intake may influence these inflammatory parameters including extramedullary myelopoiesis that can contribute to a metastatic “niche”. While, tumor secretion of growth factors (GFs) and chemokines regulate tumor-immune-cell crosstalk, in this chapter, we also emphasize how lifestyle choices, including, obesity, high-fat and high ω-6 PUFA dietary content, contribute to inflammation and myeloid cell infiltration of tumors. A relationship between obesity and high-fat diets (notably the saturated fats in Western diets) and tumor incidence, metastasis, and poor outcomes is generally accepted. However, the mechanisms of dietary promotion of inflammatory microenvironments and targeted drugs to inhibit the clinical sequel remain an unmet challenge. One approach, modification of dietary intake may have a preventative or therapeutic approach to regulate tumor-associated inflammation and remains an attractive, but little studied intervention.

AB - Rodent and clinical studies have documented that myeloid cell infiltration of tumors is associated with neutrophilia, lymphocytopenia and poor patient outcomes. This contrasts with lymphocyte infiltration of tumors, which is associated with improved outcomes. Lifestyle parameters such as high fat diets and omega (ω)-6 polyunsaturated fatty acids (PUFA) intake may influence these inflammatory parameters including extramedullary myelopoiesis that can contribute to a metastatic “niche”. While, tumor secretion of growth factors (GFs) and chemokines regulate tumor-immune-cell crosstalk, in this chapter, we also emphasize how lifestyle choices, including, obesity, high-fat and high ω-6 PUFA dietary content, contribute to inflammation and myeloid cell infiltration of tumors. A relationship between obesity and high-fat diets (notably the saturated fats in Western diets) and tumor incidence, metastasis, and poor outcomes is generally accepted. However, the mechanisms of dietary promotion of inflammatory microenvironments and targeted drugs to inhibit the clinical sequel remain an unmet challenge. One approach, modification of dietary intake may have a preventative or therapeutic approach to regulate tumor-associated inflammation and remains an attractive, but little studied intervention.

KW - High fat diet

KW - Immune escape

KW - Infiltration

KW - Invasion

KW - MDSC

KW - Metastasis

KW - PUFA

KW - Seed and soil

KW - TAM

KW - Vasculogenesis

UR - http://www.scopus.com/inward/record.url?scp=85039436289&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85039436289&partnerID=8YFLogxK

U2 - 10.1007/978-3-319-67577-0_10

DO - 10.1007/978-3-319-67577-0_10

M3 - Chapter

VL - 1036

T3 - Advances in Experimental Medicine and Biology

SP - 145

EP - 156

BT - Advances in Experimental Medicine and Biology

PB - Springer New York LLC

ER -