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Review
. 2017 Jul 5:17:68.
doi: 10.1186/s12935-017-0437-3. eCollection 2017.

Chemotherapy and tumor microenvironment of pancreatic cancer

Qiaofei Liu  1 , Quan Liao  1 , Yupei Zhao  1
Affiliations
Review

Chemotherapy and tumor microenvironment of pancreatic cancer

Qiaofei Liu et al. Cancer Cell Int. .

Abstract

Pancreatic cancer is an extremely dismal malignance. Chemotherapy has been widely applied to treat this intractable tumor. It has exclusive tumor microenvironment (TME), characterized by dense desmoplasia and profound infiltrations of immunosuppressive cells. Interactions between stromal cells and cancer cells play vital roles to affect the biological behaviors of pancreatic cancer. Targeting the stromal components of pancreatic cancer has shown promising results. In addition to the direct toxic effects of chemotherapeutic drugs on cancer cells, they can also remodel the TME, eventually affecting their efficacy. Herein, we reviewed the following four aspects; (1) clinical landmark advances of chemotherapy in pancreatic cancer, since 2000; (2) interactions and mechanisms between stromal cells and pancreatic cancer cells; (3) remodeling effects and mechanisms of chemotherapy on TME; (4) targeting stromal components in pancreatic cancer.

Keywords: Cancer associated fibroblasts; Chemotherapy; Myeloid derived suppressor cells; Pancreatic cancer; Pancreatic stellate cells; Tumor associated macrophages; Tumor microenvironment.

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Figures

Fig. 1
Fig. 1
The landscape of tumor microenvironment (TME) of pancreatic cancer: (1) the PSCs, CAFs, MDSCs and TAMs promote the malignant biological behaviors of pancreatic cancer through eight aspects; (2) the phenotypes and functions of PSCs, CAFs, MDSCs and TMAs in TME of pancreatic cancer are dynamically changed and they can regulate each other; (3) bone marrow is the most importance origination for TAMs and MDSCs, and as well the bone marrow contributes to the PSCs and CAFs; (4) the cancer cells, including bulk cells and cancer stem cells (CSCs) in tumor tissue, are the main triggers to induce the architecture of TME, after chemotherapy, the damaged cancer cells, apoptotic cancer cells or immunogenic death of cancer cells can secrete varieties of signals to act on the stroma cells in TEM or to expand, recruit and activate bone marrow derived cells to remodel the TME, eventually affecting the efficacy of treatments or even leading to drug resistance
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