Tumor-Associated Macrophages in Pancreatic Ductal Adenocarcinoma: Origin, Polarization, Function, and Reprogramming
Макрофаги, ассоциированные с опухолью, при протоковой аденокарциноме поджелудочной железы: происхождение, поляризация, функции и репрограммирование
2021-01-11
SCID: 54.1/aasxxmvs
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immune escapemacrophage polarizationpancreatic ductal adenocarcinomatumor microenvironmenttumor-associated macrophages
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Abstract (AI)
Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy. PDAC is only cured by surgical resection in its early stage, but there remains a relatively high possibility of recurrence. The development of PDAC is closely associated with the tumor microenvironment. Tumor-associated macrophages (TAMs) are one of the most abundant immune cell populations in the pancreatic tumor stroma. TAMs are inclined to M2 deviation in the tumor microenvironment, which promotes and supports tumor behaviors, including tumorigenesis, immune escape, metastasis, and chemotherapeutic resistance. Herein, we comprehensively reviewed the latest researches on the origin, polarization, functions, and reprogramming of TAMs in PDAC.
Key Findings
1
M2-skewed tumor-associated macrophages promote tumorigenesis, immune escape, metastasis, and resistance to chemotherapy.
2
Pancreatic ductal adenocarcinoma is highly lethal and is curable by surgical resection only when detected at an early stage.
3
The PDAC tumor microenvironment drives tumor-associated macrophages toward an M2-like state.
4
The review examines tumor-associated macrophage origin, polarization, functions, and potential reprogramming strategies in PDAC.
5
Tumor-associated macrophages are among the most abundant immune-cell populations in the PDAC tumor stroma.
Research Object
Tumor-associated macrophages in pancreatic ductal adenocarcinoma and the pancreatic tumor microenvironment
Research Subject
The origin, M2 polarization, tumor-promoting functions, and reprogramming of tumor-associated macrophages, including their roles in tumorigenesis, immune escape, metastasis, and chemotherapeutic resistance
Publication Details
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2021-01-11
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