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1.
Mol Cancer ; 19(1): 32, 2020 02 15.
Artigo em Inglês | MEDLINE | ID: mdl-32061257

RESUMO

Pancreatic ductal adenocarcinoma (PDAC) is an incurable cancer resistant to traditional treatments, although a limited number of early-stage patients can undergo radical resection. Immunotherapies for the treatment of haematological malignancies as well as solid tumours have been substantially improved over the past decades, and impressive results have been obtained in recent preclinical and clinical trials. However, PDAC is likely the exception because of its unique tumour microenvironment (TME). In this review, we summarize the characteristics of the PDAC TME and focus on the network of various tumour-infiltrating immune cells, outlining the current advances in PDAC immunotherapy and addressing the effect of the PDAC TME on immunotherapy. This review further explores the combinations of different therapies used to enhance antitumour efficacy or reverse immunodeficiencies and describes optimizable immunotherapeutic strategies for PDAC. The concordant combination of various treatments, such as targeting cancer cells and the stroma, reversing suppressive immune reactions and enhancing antitumour reactivity, may be the most promising approach for the treatment of PDAC. Traditional treatments, especially chemotherapy, may also be optimized for individual patients to remodel the immunosuppressive microenvironment for enhanced therapy.


Assuntos
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Carcinoma Ductal Pancreático/tratamento farmacológico , Imunoterapia/métodos , Neoplasias Pancreáticas/tratamento farmacológico , Microambiente Tumoral/imunologia , Animais , Carcinoma Ductal Pancreático/imunologia , Carcinoma Ductal Pancreático/patologia , Humanos , Neoplasias Pancreáticas/imunologia , Neoplasias Pancreáticas/patologia , Microambiente Tumoral/efeitos dos fármacos , Neoplasias Pancreáticas
2.
Asian Pac J Trop Med ; 8(6): 474-8, 2015 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-26194833

RESUMO

OBJECTIVE: To explore the protective effect and mechanism of Tetramethy1Pyrazine (TMP) on the pancreas function of acute pancreatitis rats. METHODS: A total of 75 SD rats were randomly divided into three groups (A, B, C) with 25 rats in each group. Group A served as sham operation group. In the groups B and C, AP model was prepared as by injecting taurocholic acid sodium. Group B was model group. After modeling, rats were administrated by intraperitoneal injection of normal saline. Group C was TMP treatment group, which was administrated by intraperitoneal injection of 0.6% TMP after modeling. The rat blood specimens in each group were collected with 1 mL/100 g solution after modeling of 2, 6, 12 and 24 h. Levels of amylase (AMS), blood urea nitrogen (BUN), creatinine (CR), TNF-α and IL-6 were detected, and 5 rats were sacrificed. Histopathological examination was performed in he pancreatic tissue specimens of each group to observe pancreatic tissue damage. RESULTS: After modeling in each time point, AMS, BUN, CR, TNF-α and IL-6 in groups B and C were significantly higher than that of in group A (P < 0.05). After modeling of 2 h, AMS, BUN and CR in group B increased significantly and reached the peak value at 6 h. After modeling of 12 h, serum level of TNF-α and IL-6 were significantly lower than that of in control group, while after 24 h of modeling, serum level of AMS, BUN, CR, TNF-α and IL-6 were significantly lower than that of in control group (P < 0.05). The histological observation showed that pancreatic tissue in rats of group A was normal without damage lesions. Massive bleeding, necrosis and serious injury were visible in pancreatic tissue of group B. The rat pancreatic tissue was bleeding in group C with small pieces of necrotic lesions. The degree of inflammatory cell infiltration was lower than group B, and the degree of injury was significantly lower than group B. CONCLUSIONS: TMP can significantly decrease the serum level of TNF-α and IL-6 in AP rats, inhibits inflammatory response of AP, and has significant protective effect on pancreatic tissue and function in AP rats.

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