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2016 ; 35
(41
): 5337-5349
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The tumor microenvironment in esophageal cancer
#MMPMID26923327
Lin EW
; Karakasheva TA
; Hicks PD
; Bass AJ
; Rustgi AK
Oncogene
2016[Oct]; 35
(41
): 5337-5349
PMID26923327
show ga
Esophageal cancer is a deadly disease, ranking sixth among all cancers in
mortality. Despite incremental advances in diagnostics and therapeutics,
esophageal cancer still carries a poor prognosis, and thus, there remains a need
to elucidate the molecular mechanisms underlying this disease. There is
accumulating evidence that a comprehensive understanding of the molecular
composition of esophageal cancer requires attention to not only tumor cells but
also the tumor microenvironment (TME), which contains diverse cell populations,
signaling factors and structural molecules that interact with tumor cells and
support all stages of tumorigenesis. In esophageal cancer, environmental
exposures can trigger chronic inflammation, which leads to constitutive
activation of pro-inflammatory signaling pathways that promote survival and
proliferation. Antitumor immunity is attenuated by cell populations such as
myeloid-derived suppressor cells and regulatory T cells, as well as immune
checkpoints like programmed death-1. Other immune cells such as tumor-associated
macrophages can have other pro-tumorigenic functions, including the induction of
angiogenesis and tumor cell invasion. Cancer-associated fibroblasts secrete
growth factors and alter the extracellular matrix to create a tumor niche and
enhance tumor cell migration and metastasis. Further study of how these TME
components relate to the different stages of tumor progression in each esophageal
cancer subtype will lead to development of novel and specific TME-targeting
therapeutic strategies, which offer considerable potential especially in the
setting of combination therapy.
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