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pancreatic cancer microenvironment

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https://www.readbyqxmd.com/read/28507714/targeting-the-tumour-microenvironment-with-an-enzyme-responsive-drug-delivery-system-for-the-efficient-therapy-of-breast-and-pancreatic-cancers
#1
Brigitte Renoux, Florian Raes, Thibaut Legigan, Elodie Péraudeau, Balkis Eddhif, Pauline Poinot, Isabelle Tranoy-Opalinski, Jérôme Alsarraf, Oleksandr Koniev, Sergii Kolodych, Stéphanie Lerondel, Alain Le Pape, Jonathan Clarhaut, Sébastien Papot
The development of novel therapeutic strategies allowing the destruction of tumour cells while sparing healthy tissues is one of the main challenges of cancer chemotherapy. Here, we report on the design and antitumour activity of a low-molecular-weight drug delivery system programmed for the selective release of the potent monomethylauristatin E in the tumour microenvironment of solid tumours. After intravenous administration, this compound binds covalently to plasmatic albumin through Michael addition, thereby enabling its passive accumulation in tumours where extracellular β-glucuronidase initiates the selective release of the drug...
May 1, 2017: Chemical Science
https://www.readbyqxmd.com/read/28499439/the-role-of-tgf-%C3%AE-and-its-crosstalk-with-rac1-rac1b-signaling-in-breast-and-pancreas-carcinoma
#2
REVIEW
Catharina Melzer, Ralf Hass, Juliane von der Ohe, Hendrik Lehnert, Hendrik Ungefroren
This article focusses on the role of TGF-β and its signaling crosstalk with the RHO family GTPases RAC1 and RAC1b in the progression of breast and pancreatic carcinoma. The aggressive nature of these tumor types is mainly due to metastatic dissemination. Metastasis is facilitated by desmoplasia, a peculiar tumor microenvironment and the ability of the tumor cells to undergo epithelial-mesenchymal transition (EMT) and to adopt a motile and invasive phenotype. These processes are controlled entirely or in part by TGF-β and the small RHO GTPase RAC1 with both proteins acting as tumor promoters in late-stage cancers...
May 12, 2017: Cell Communication and Signaling: CCS
https://www.readbyqxmd.com/read/28494747/new-diagnostic-and-therapeutic-aspects-of-pancreatic-ductal-adenocarcinoma
#3
Harald Mangge, Tobias Niedrist, Wilfried Renner, Stefan Lyer, Christoph Alexiou, Johannes Haybaeck
Pancreatic ductal adenocarcinoma (PDAC) is devastating. Because of its silent nature, the disease is often only diagnosed once it has reached an advanced, frequently inoperable stage. To date, we have no biomarkers that facilitate earlier diagnosis, leaving sufficient time for curative therapy that effectively lowers the very high mortality rate of this cancer entity. Because of this, the life expectancy of patients with PDAC is low (i.e. < 6% five-year survival rates). New data, including particular genetic signatures and features of the stromal architecture of PDAC tumors, may better explain their aggressiveness, their relatively long-lasting painless expansion, and why chemotherapy so frequently fails...
May 10, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28493710/nuclear-localizing-peptide-conjugated-redox-sensitive-polymersomes-for-delivering-curcumin-and-doxorubicin-to-pancreatic-cancer-micro-tumors
#4
Tayebeh Anajafi, Junru Yu, Abbas Sedigh, Manas K Haldar, Wallace W Muhonen, Seth Oberlander, Heather Wasness, Jamie Froberg, Md Shahjahan Molla, Kalpana S Katti, Yongki Choi, John B Shabb, D K Srivastava, Sanku Mallik
Improving the therapeutic index of anticancer agents is an enormous challenge. Targeting decreases the side effects of the therapeutic agents by delivering the drugs to the intended destination. Nanocarriers containing the nuclear localizing peptide sequences (NLS) translocate to the cell nuclei. However, the nuclear localization peptides are non-selective and cannot distinguish the malignant cells from the healthy counterparts. In this study, we designed a "masked" NLS peptide which is activated only in the presence of overexpressed matrix metalloproteinase-7 (MMP-7) enzyme in the pancreatic cancer microenvironment...
May 11, 2017: Molecular Pharmaceutics
https://www.readbyqxmd.com/read/28486750/stromal-spock1-supports-invasive-pancreatic-cancer-growth
#5
Veronique L Veenstra, Helene Damhofer, Cynthia Waasdorp, Anne Steins, Hemant M Kocher, Jan Paul Medema, Hanneke W van Laarhoven, Maarten F Bijlsma
Pancreatic ductal adenocarcinoma (PDAC) is marked by an abundant stromal deposition. This stroma is suspected to harbor both tumor-promoting as well as -suppressing properties. This is underscored by the disappointing results of stroma targeting in clinical studies. Given the complexity of tumor-stroma interaction in PDAC, there is a need to identify the stromal proteins that are predominantly tumor-promoting. One possible candidate is SPOCK1 that we previously identified in a screening effort in PDAC. We extensively mined PDAC gene expression datasets, and used species-specific transcript analysis in mixed-species models for PDAC to study the patterns and driver mechanisms of SPOCK1 expression in PDAC...
May 9, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28477403/micro-rna-21-regulates-cancer-associated-fibroblast-mediated-frug-resistance-in-pancreatic-cancer
#6
Lulin Zhang, Jun Yao, Wenyao Li, Ce Zhang
Pancreatic adenocarcinoma (PDAC) is one of the leading cause of cancer death due to its highly aggressive biological nature and resistance to chemotherapies. Former study also indicated that miR-21 in cancer-associated fibroblasts (CAFs) is an important regulator of their activation. However, whether miR-21 in CAFs would regulate PDAC's tumor microenvironment and leading to drug resistance remain unknown. In this study, we evaluated the relationship among CAFs activation, miR-21 expression level and drug resistance using PDAC patient tumor samples...
May 5, 2017: Oncology Research
https://www.readbyqxmd.com/read/28476028/hif-2%C3%AE-dictates-the-susceptibility-of-pancreatic-cancer-cells-to-trail-by-regulating-survivin-expression
#7
Nanae Harashima, Keizo Takenaga, Miho Akimoto, Mamoru Harada
Cancer cells develop resistance to therapy by adapting to hypoxic microenvironments, and hypoxia-inducible factors (HIFs) play crucial roles in this process. We investigated the roles of HIF-1α and HIF-2α in cancer cell death induced by tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) using human pancreatic cancer cell lines. siRNA-mediated knockdown of HIF-2α, but not HIF-1α, increased susceptibility of two pancreatic cancer cell lines, Panc-1 and AsPC-1, to TRAIL in vitro under normoxic and hypoxic conditions...
April 17, 2017: Oncotarget
https://www.readbyqxmd.com/read/28475017/hypoxia-induces-oncogene-yes-associated-protein-1-nuclear-translocation-to-promote-pancreatic-ductal-adenocarcinoma-invasion-via-epithelial-mesenchymal-transition
#8
Honglong Wei, Zongzhen Xu, Feng Liu, Fuhai Wang, Xin Wang, Xueying Sun, Jie Li
Pancreatic ductal adenocarcinoma is one of the most lethal cancers. The Hippo pathway is involved in tumorigenesis and remodeling of tumor microenvironments. Hypoxia exists in the microenvironment of solid tumors, including pancreatic ductal adenocarcinoma and plays a vital role in tumor progression and metastasis. However, it remains unclear how hypoxia interacts with the Hippo pathway to regulate these events. In this study, expressions of yes-associated protein 1 and hypoxia-inducible factor-1α were found to be elevated in pancreatic ductal adenocarcinoma samples compared with those in matched adjacent non-tumor samples...
May 2017: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
https://www.readbyqxmd.com/read/28471108/dna-methylation-in-the-tumor-microenvironment
#9
Meng-Wen Zhang, Kenji Fujiwara, Xu Che, Shu Zheng, Lei Zheng
The tumor microenvironment (TME) plays an important role in supporting cancer progression. The TME is composed of tumor cells, the surrounding tumor-associated stromal cells, and the extracellular matrix (ECM). Crosstalk between the TME components contributes to tumorigenesis. Recently, one of our studies showed that pancreatic ductal adenocarcinoma (PDAC) cells can induce DNA methylation in cancer-associated fibroblasts (CAFs), thereby modifying tumor-stromal interactions in the TME, and subsequently creating a TME that supports tumor growth...
May 2017: Journal of Zhejiang University. Science. B
https://www.readbyqxmd.com/read/28461158/pancreatic-stellate-cells-increase-pancreatic-cancer-cells-invasion-through-the-hepatocyte-growth-factor-c-met-survivin-regulated-by-p53-p21
#10
Xiao-Peng Yang, Shang-Long Liu, Jian-Fei Xu, Shou-Gen Cao, Yu Li, Yan-Bing Zhou
Pancreatic stellate cells (PSCs) are a key cellular component of the pancreatic tumor microenvironment and are considered to contribute to tumor invasion and metastasis. Multiple cytokines and growth factors derived from PSCs are involved in malignant cancer progression, including hepatocyte growth factor (HGF). However, the molecular mechanisms by which HGF regulates cancer invasion and metastasis have not been completely elucidated. Here, we report that two pancreatic cancer (PC) cell lines, Panc-1 and SW1990, displayed different invasive and migratory abilities after treatment with HGF secreted by PSCs...
April 29, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28460571/muc4-mucin-a-therapeutic-target-for-pancreatic-ductal-adenocarcinoma
#11
Shailendra K Gautam, Sushil Kumar, Andrew Cannon, Bradley Hall, Rakesh Bhatia, Mohd Wasim Nasser, Sidharth Mahapatra, Surinder Batra, Maneesh Jain
Pancreatic cancer (PC) is characterized by mucin overexpression and MUC4 is the most differentially overexpressed membrane bound mucins that plays functional role in disease progression and therapy resistance. Area covered: We describe the clinicopathological significance of MUC4, summarize mechanisms contributing to its deregulated expression, review preclinical studies aimed at inhibiting MUC4, and discuss how MUC4 overexpression provides opportunities for developing targeted therapies. Finally, we discuss the challenges for developing MUC4-based therapeutics, and identify areas where efforts should be directed to effectively exploit MUC4 as a therapeutic target for PC...
May 2, 2017: Expert Opinion on Therapeutic Targets
https://www.readbyqxmd.com/read/28455244/got1-mediated-anaplerotic-glutamine-metabolism-regulates-chronic-acidosis-stress-in-pancreatic-cancer-cells
#12
Jaime Abrego, Venugopal Gunda, Enza Vernucci, Surendra K Shukla, Ryan J King, Aneesha Dasgupta, Gennifer Goode, Divya Murthy, Fang Yu, Pankaj K Singh
The increased rate of glycolysis and reduced oxidative metabolism are the principal biochemical phenotypes observed in pancreatic ductal adenocarcinoma (PDAC) that lead to the development of an acidic tumor microenvironment. The pH of most epithelial cell-derived tumors is reported to be lower than that of plasma. However, little is known regarding the physiology and metabolism of cancer cells enduring chronic acidosis. Here, we cultured PDAC cells in chronic acidosis (pH 6.9-7.0) and observed that cells cultured in low pH had reduced clonogenic capacity...
April 26, 2017: Cancer Letters
https://www.readbyqxmd.com/read/28454427/chemoresistance-in-pancreatic-cancer-emerging-concepts
#13
Manu Gnanamony, Christopher S Gondi
Pancreatic cancer is one of the most lethal types of cancer in the world. The incidence of pancreatic cancer increases each year with no significant decrease in mortality. Pancreatic cancer is a complex disease, and this complexity is partly attributed to late diagnosis, an aggressive phenotype, environmental factors and lack of effective treatment options. Surgical resection followed by adjuvant chemotherapy is the treatment of choice for early stage cancer, whereas gemcitabine is the standard first line therapy for patients with advanced stage disease...
April 2017: Oncology Letters
https://www.readbyqxmd.com/read/28450156/microrna-7-impairs-autophagy-derived-pools-of-glucose-to-suppress-pancreatic-cancer-progression
#14
Dian-Na Gu, Ming-Jie Jiang, Zhu Mei, Juan-Juan Dai, Chen-Yun Dai, Chi Fang, Qian Huang, Ling Tian
Pancreatic cancer commonly addicts to aerobic glycolysis, and abnormally activates autophagy to adapt the stringent metabolic microenvironment. microRNA-7 (miR-7) was supposed to modulate various gastrointestinal cancer progression. We wonder whether miR-7 could destroy the reprogrammed metabolic homeostasis in pancreatic cancer via modulating the level of autophagy, and further affect tumor proliferation and survival. Herein, we first reported that pancreatic cancer could take advantage of autophagy as a survival strategy to provide essential glucose required for glycolysis metabolism...
April 25, 2017: Cancer Letters
https://www.readbyqxmd.com/read/28440551/alternating-ph-landscapes-shape-epithelial-cancer-initiation-and-progression-focus-on-pancreatic-cancer
#15
REVIEW
Stine F Pedersen, Ivana Novak, Frauke Alves, Albrecht Schwab, Luis A Pardo
We present here the hypothesis that the unique microenvironmental pH landscape of acid-base transporting epithelia is an important factor in development of epithelial cancers, by rendering the epithelial and stromal cells pre-adapted to the heterogeneous extracellular pH (pHe ) in the tumor microenvironment. Cells residing in organs with net acid-base transporting epithelia such as the pancreatic ductal and gastric epithelia are exposed to very different, temporally highly variable pHe values apically and basolaterally...
April 25, 2017: BioEssays: News and Reviews in Molecular, Cellular and Developmental Biology
https://www.readbyqxmd.com/read/28440296/gold-nanoclusters-assisted-delivery-of-ngf-sirna-for-effective-treatment-of-pancreatic-cancer
#16
Yifeng Lei, Lixue Tang, Yangzhouyun Xie, Yunlei Xianyu, Lingmin Zhang, Peng Wang, Yoh Hamada, Kai Jiang, Wenfu Zheng, Xingyu Jiang
Pancreatic cancer is one of the deadliest human cancers, whose progression is highly dependent on the nervous microenvironment. The suppression of gene expression of nerve growth factor (NGF) may have great potential in pancreatic cancer treatment. Here we show that gold nanocluster-assisted delivery of siRNA of NGF (GNC-siRNA) allows efficient NGF gene silencing and pancreatic cancer treatment. The GNC-siRNA complex increases the stability of siRNA in serum, prolongs the circulation lifetime of siRNA in blood and enhances the cellular uptake and tumour accumulation of siRNA...
April 25, 2017: Nature Communications
https://www.readbyqxmd.com/read/28438662/never-let-it-go-stopping-key-mechanisms-underlying-metastasis-to-fight-pancreatic-cancer
#17
REVIEW
E Giovannetti, C L van der Borden, A E Frampton, A Ali, O Firuzi, G J Peters
Pancreatic ductal adenocarcinoma (PDAC) is an extremely aggressive neoplasm, predicted to become the second leading cause of cancer-related deaths before 2030. This dismal trend is mainly due to lack of effective treatments against its metastatic behavior. Therefore, a better understanding of the key mechanisms underlying metastasis should provide new opportunities for therapeutic purposes. Genomic analyses revealed that aberrations that fuel PDAC tumorigenesis and progression, such as SMAD4 loss, are also implicated in metastasis...
April 21, 2017: Seminars in Cancer Biology
https://www.readbyqxmd.com/read/28436934/biopolymers-codelivering-engineered-t-cells-and-sting-agonists-can-eliminate-heterogeneous-tumors
#18
Tyrel T Smith, Howell F Moffett, Sirkka B Stephan, Cary F Opel, Amy G Dumigan, Xiuyun Jiang, Venu G Pillarisetty, Smitha P S Pillai, K Dane Wittrup, Matthias T Stephan
Therapies using T cells that are programmed to express chimeric antigen receptors (CAR T cells) consistently produce positive results in patients with hematologic malignancies. However, CAR T cell treatments are less effective in solid tumors for several reasons. First, lymphocytes do not efficiently target CAR T cells; second, solid tumors create an immunosuppressive microenvironment that inactivates T cell responses; and third, solid cancers are typified by phenotypic diversity and thus include cells that do not express proteins targeted by the engineered receptors, enabling the formation of escape variants that elude CAR T cell targeting...
April 24, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28435988/the-key-genes-of-chronic-pancreatitis-which-bridge-chronic-pancreatitis-and-pancreatic-cancer-can-be-therapeutic-targets
#19
Shuang Li, Rui Li, Heping Wang, Lisha Li, Huiyu Li, Yulin Li
An important question in systems biology is what role the underlying molecular mechanisms play in disease progression. The relationship between chronic pancreatitis and pancreatic cancer needs further exploration in a system view. We constructed the disease network based on gene expression data and protein-protein interaction. We proposed an approach to discover the underlying core network and molecular factors in the progression of pancreatic diseases, which contain stages of chronic pancreatitis and pancreatic cancer...
April 24, 2017: Pathology Oncology Research: POR
https://www.readbyqxmd.com/read/28407685/extra-pancreatic-invasion-induces-lipolytic-and-fibrotic-changes-in-the-adipose-microenvironment-with-released-fatty-acids-enhancing-the-invasiveness-of-pancreatic-cancer-cells
#20
Takashi Okumura, Kenoki Ohuchida, Masafumi Sada, Toshiya Abe, Sho Endo, Kazuhiro Koikawa, Chika Iwamoto, Daisuke Miura, Yusuke Mizuuchi, Taiki Moriyama, Kohei Nakata, Yoshihiro Miyasaka, Tatsuya Manabe, Takao Ohtsuka, Eishi Nagai, Kazuhiro Mizumoto, Yoshinao Oda, Makoto Hashizume, Masafumi Nakamura
Pancreatic cancer progression involves components of the tumor microenvironment, including stellate cells, immune cells, endothelial cells, and the extracellular matrix. Although peripancreatic fat is the main stromal component involved in extra-pancreatic invasion, its roles in local invasion and metastasis of pancreatic cancer remain unclear. This study investigated the role of adipose tissue in pancreatic cancer progression using genetically engineered mice (Pdx1-Cre; LSL-KrasG12D; Trp53R172H/+) and an in vitro model of organotypic fat invasion...
March 14, 2017: Oncotarget
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