Inhibiting tumor necrosis factor-alpha diminishes desmoplasia and inflammation to overcome chemoresistance in pancreatic ductal adenocarcinoma

Zhao, Xianda; Fan, Wei; Xu, Zhigao; Chen, Honglei; He, Yulong; Yang, Guowei; Ye, Gang; Hu, Hongping; Tang, Shihui; Wang, Ping; Zhang, Zheng; Xu, Peipei; Mu, Yu

doi:10.18632/oncotarget.13212

Cited by 73 publications

(67 citation statements)

References 32 publications

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“…Interestingly, overexpression of tubulins has been linked to poor response to microtubule‐targeting anticancer drugs . Moreover, elevated levels of tumor necrosis factor have been previously reported in pDAC but not in controls, and were associated with poor survival . In addition, increased levels of tumor necrosis factor were found in pDAC compared to other pancreatic malignancies including pNET, which is in line with our results.…”

Section: Discussionsupporting

confidence: 91%

“…In our study, we detected ion species that exhibited a similar mass to the molecules reported as basic fibroblast growth factor receptor 1, type I and type II collagen, tubulin beta‐2C chain, and tumor necrosis factor receptor, among others . Interestingly, basic fibroblast growth factor, collagens, tubulins, and tumor necrosis factor have all been reported in association with pDAC. We detected these molecules in higher intensities in pDAC compared to pNET.…”

Section: Discussionsupporting

confidence: 76%

See 1 more Smart Citation

Development of a Class Prediction Model to Discriminate Pancreatic Ductal Adenocarcinoma from Pancreatic Neuroendocrine Tumor by MALDI Mass Spectrometry Imaging

Casadonte¹,

Kriegsmann

Perren

et al. 2018

Proteomics Clinical Apps

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Purpose To define proteomic differences between pancreatic ductal adenocarcinoma (pDAC) and pancreatic neuroendocrine tumor (pNET) by matrix‐assisted laser desorption/ionization mass spectrometry imaging (MALDI MSI). Experimental design Ninety‐three pDAC and 126 pNET individual tissues are assembled in tissue microarrays and analyzed by MALDI MSI. The cohort is separated in a training (52 pDAC and 83 pNET) and validation set (41 pDAC and 43 pNET). Subsequently, a linear discriminant analysis (LDA) model based on 46 peptide ions is performed on the training set and evaluated on the validation cohort. Additionally, two liver metastases and a whole slide of pDAC are analyzed by the same LDA algorithm. Results Classification of pDAC and pNET by the LDA model is correct in 95% (39/41) and 100% (43/43) of patients in the validation cohort, respectively. The two liver metastases and the whole slide of pDAC are also correctly classified in agreement with the histopathological diagnosis. Conclusion and clinical relevance In the present study, a large dataset of pDAC and pNET by MALDI MSI is investigated, a class prediction model that allowed separation of both entities with high accuracy is developed, and differential peptide peaks with potential diagnostic, prognostic, and predictive values are highlighted.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 76%

Development of a Class Prediction Model to Discriminate Pancreatic Ductal Adenocarcinoma from Pancreatic Neuroendocrine Tumor by MALDI Mass Spectrometry Imaging

Casadonte¹,

Kriegsmann

Perren

et al. 2018

Proteomics Clinical Apps

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“…Our previous studies have shown that TNF-α and TGF-β cytokines can upregulate ZIP14 levels in muscle cells [21]. These cytokines can be detected in the conditioned media of PDAC cell lines and sera of PDAC patients [9,[28][29][30][31][32]. It remains to be tested in future studies whether blocking TNF-α or TGF-β signaling in muscles can reduce Zip14 expression.…”

Section: Discussionmentioning

confidence: 96%

Upregulation of ZIP14 and Altered Zinc Homeostasis in Muscles in Pancreatic Cancer Cachexia

Shakri

Zhong

et al. 2019

Cancers

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Pancreatic ductal adenocarcinoma (PDAC) is a lethal cancer type in which the mortality rate approaches the incidence rate. More than 85% of PDAC patients experience a profound loss of muscle mass and function, known as cachexia. PDAC patients with this condition suffer from decreased tolerance to anti-cancer therapies and often succumb to premature death due to respiratory and cardiac muscle wasting. Yet, there are no approved therapies available to alleviate cachexia. We previously found that upregulation of the metal ion transporter, Zip14, and altered zinc homeostasis are critical mediators of cachexia in metastatic colon, lung, and breast cancer models. Here, we show that a similar mechanism is likely driving the development of cachexia in PDAC. In two independent experimental metastasis models generated from the murine PDAC cell lines, Pan02 and FC1242, we observed aberrant Zip14 expression and increased zinc ion levels in cachectic muscles. Moreover, in advanced PDAC patients, high levels of ZIP14 in muscles correlated with the presence of cachexia. These studies underscore the importance of altered ZIP14 function in PDAC-associated cachexia development and highlight a potential therapeutic opportunity for improving the quality of life and prolonging survival in PDAC patients.

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“…Exactly, in some cases, infiltration of tumors by activated T cells reduces the spread of metastasis. The connection of circulating malignant cells with platelets or macrophages may prevent them from NK cell-mediated killing, thereby overcoming immunosurveillance [31]. Systemic inflammation promotesconnection of circulating malignant cells to hepatic sinusoids, and this process is ruled by neutrophil-dependent upregulation of adhesion molecules.…”

Section: Inflammation and Metastasismentioning

confidence: 99%

Inflammation and cancer interconnection; simply as we think

Hussein¹,

Darwish²,

Soliman³

2020

Appl Sci Rep

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Microbiota variety is site specific depending on its location in the body and this diversity can get together with human health. At the last decades, inflammation is a primary protective response that sometimes goes away and becomes a main cofactor in the pathogenesis of numerous chronic human diseases, including malignant tumor. As well, microbes have the potency power to influence tumor growth and progression through a wide forms of routes; including alteration of tumor microenvironment, prolonged activation of inflammation, induction of genotoxic restraints and metabolism. In this review, we will set a general overview of inflammation has suspected to provide a major role in the pathogenesis and development of cancer as an important object for advanced cancer biology. Semin Cancer Biol. 2015; 35 Suppl:S151-S184. | Article | PubMed Abstract | PubMed FullText 50. Nickoloff BJ, Ben-Neriah Y and Pikarsky E. Inflammation and cancer: is the link as simple as we think? J Invest Dermatol. 2005; 124:x-xiv. | Article | PubMed Citation: Hussein AM, Darwish ZE and Soliman OH. Inflammation and cancer interconnection; simply as we think. Appl Sci Rep. 2020; 7:1. http://dx.

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Inhibiting tumor necrosis factor-alpha diminishes desmoplasia and inflammation to overcome chemoresistance in pancreatic ductal adenocarcinoma

Abstract: Background: Pancreatic ductal adenocarcinoma (PDAC) is one of the most

Cited by 73 publications

References 32 publications

Development of a Class Prediction Model to Discriminate Pancreatic Ductal Adenocarcinoma from Pancreatic Neuroendocrine Tumor by MALDI Mass Spectrometry Imaging

Development of a Class Prediction Model to Discriminate Pancreatic Ductal Adenocarcinoma from Pancreatic Neuroendocrine Tumor by MALDI Mass Spectrometry Imaging

Upregulation of ZIP14 and Altered Zinc Homeostasis in Muscles in Pancreatic Cancer Cachexia

Inflammation and cancer interconnection; simply as we think

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