scholarly journals c‐Jun N‐terminal kinase in pancreatic tumor stroma augments tumor development in mice

2017 ◽  
Vol 108 (11) ◽  
pp. 2156-2165 ◽  
Author(s):  
Takeshi Sato ◽  
Wataru Shibata ◽  
Yohko Hikiba ◽  
Yoshihiro Kaneta ◽  
Nobumi Suzuki ◽  
...  
Keyword(s):  
Pancreatic Tumor ◽  
Tumor Development ◽  
Tumor Stroma

scholarly journals Dynamic Stromal Alterations Influence Tumor-Stroma Crosstalk to Promote Pancreatic Cancer and Treatment Resistance

Cancers ◽  
2021 ◽  
Vol 13 (14) ◽  
pp. 3481
Author(s):  
Kendelle J. Murphy ◽  
Cecilia R. Chambers ◽  
David Herrmann ◽  
Paul Timpson ◽  
Brooke A. Pereira
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Development ◽  
Treatment Resistance ◽  
Tumor Stroma ◽  
Response To Treatment ◽  
Ductal Adenocarcinoma ◽  
Cell Phenotype ◽  
Stromal Compartment ◽  
Clinical Prognosis ◽  
Functional Value

Many cancer studies now recognize that disease initiation, progression, and response to treatment are strongly influenced by the microenvironmental niche. Widespread desmoplasia, or fibrosis, is fundamental to pancreatic cancer development, growth, metastasis, and treatment resistance. This fibrotic landscape is largely regulated by cancer-associated fibroblasts (CAFs), which deposit and remodel extracellular matrix (ECM) in the tumor microenvironment (TME). This review will explore the prognostic and functional value of the stromal compartment in predicting outcomes and clinical prognosis in pancreatic ductal adenocarcinoma (PDAC). We will also discuss the major dynamic stromal alterations that occur in the pancreatic TME during tumor development and progression, and how the stromal ECM can influence cancer cell phenotype, metabolism, and immune response from a biochemical and biomechanical viewpoint. Lastly, we will provide an outlook on the latest clinical advances in the field of anti-fibrotic co-targeting in combination with chemotherapy or immunotherapy in PDAC, providing insight into the current challenges in treating this highly aggressive, fibrotic malignancy.

scholarly journals Solid-pseudopapillary neoplasm of the pancreas in a patient with familial adenomatous polyposis: a case report

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Daishi Naoi ◽  
Koji Koinuma ◽  
Hideki Sasanuma ◽  
Yasunaru Sakuma ◽  
Hisanaga Horie ◽  
...  
Keyword(s):  
Familial Adenomatous Polyposis ◽  
Pancreatic Tumor ◽  
Laparoscopic Resection ◽  
Tumor Development ◽  
Colonic Polyps ◽  
Pancreatic Tumors ◽  
Beta Catenin ◽  
Adenomatous Polyposis ◽  
Solid Pseudopapillary Neoplasm ◽  
Extracolonic Manifestations

Abstract Background Familial adenomatous polyposis (FAP) is characterized by the presence of hundreds to thousands of colonic polyps, and extracolonic manifestations are likely to occur. Pancreatic tumors are rare extracolonic manifestations in patients with FAP, among which solid-pseudopapillary neoplasm (SPN) are extremely rare. We report here a patient with an SPN of the pancreas found during the follow-up of FAP. Case presentation A 20-year-old woman was diagnosed with FAP 3 years previously by colonoscopy which revealed less than 100 colonic polyps within the entire colon. She complained of left upper abdominal pain and a 10-cm solid and cystic pancreatic tumor was found by computed tomography scan. Solid and cystic components within the tumor were seen on abdominal magnetic resonance imaging. Simultaneous laparoscopic resection of the distal pancreas and subtotal colectomy was performed. Histopathological findings confirmed the pancreatic tumor as an SPN without malignancy. Abnormal staining of beta-catenin was observed by immunohistochemical study. Multiple polyps in the colorectum were not malignant. Molecular biological analysis from peripheral blood samples revealed a decrease in the copy number of the promoter 1A and 1B region of the APC gene, which resulted in decreased expression of the APC gene. Conclusions A rare association of SPN with FAP is reported. The genetic background with relation to beta-catenin abnormalities is interesting to consider tumor development. So far, there are few reports of SPN in a patient with FAP. Both lesions were treated simultaneously by laparoscopic resection.

The contribution of Lymphotoxin from PanINs to pancreatic tumor development

Pancreatology ◽  
2017 ◽  
Vol 17 (3) ◽  
pp. S21
Author(s):  
Gitta Maria Wanner-Seleznik ◽  
Theresia Reding ◽  
Conny Waschkies ◽  
Anurag Gupta ◽  
Daniela Lenggenhager ◽  
...  
Keyword(s):  
Pancreatic Tumor ◽  
Tumor Development

scholarly journals Evaluation of pancreatic tumor development in KPC mice using multi-parametric MRI

2018 ◽  
Vol 18 (1) ◽  
Author(s):  
Ravneet Vohra ◽  
Joshua Park ◽  
Yak-Nam Wang ◽  
Kayla Gravelle ◽  
Stella Whang ◽  
...  
Keyword(s):  
Pancreatic Tumor ◽  
Tumor Development ◽  
Kpc Mice

scholarly journals Role of MSC in the Tumor Microenvironment

Cancers ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2107 ◽  
Author(s):  
Ralf Hass
Keyword(s):  
Tumor Microenvironment ◽  
Cancer Cells ◽  
Tumor Development ◽  
Tumor Stroma ◽  
Cell Types ◽  
Cellular Interactions ◽  
Cell Functions ◽  
Metastatic Behavior ◽  
Stem Cell Niches

The tumor microenvironment represents a dynamically composed matrix in which tissue-associated cancer cells are embedded together with a variety of further cell types to form a more or less separate organ-like structure. Constantly mutual interactions between cells of the tumor microenvironment promote continuous restructuring and growth in the tumor. A distinct organization of the tumor stroma also facilitates the formation of transient cancer stem cell niches, thereby contributing to progressive and dynamic tumor development. An important but heterogeneous mixture of cells that communicates among the cancer cells and the different tumor-associated cell types is represented by mesenchymal stroma-/stem-like cells (MSC). Following recruitment to tumor sites, MSC can change their functionalities, adapt to the tumor’s metabolism, undergo differentiation and synergize with cancer cells. Vice versa, cancer cells can alter therapeutic sensitivities and change metastatic behavior depending on the type and intensity of this MSC crosstalk. Thus, close cellular interactions between MSC and cancer cells can eventually promote cell fusion by forming new cancer hybrid cells. Consequently, newly acquired cancer cell functions or new hybrid cancer populations enlarge the plasticity of the tumor and counteract successful interventional strategies. The present review article highlights some important features of MSC within the tumor stroma.

scholarly journals MicroRNAs of the mir-17~92 cluster regulate multiple aspects of pancreatic tumor development and progression

Oncotarget ◽  
2017 ◽  
Vol 8 (22) ◽  
pp. 35902-35918 ◽  
Author(s):  
Brian Quattrochi ◽  
Anushree Gulvady ◽  
David R. Driscoll ◽  
Makoto Sano ◽  
David S. Klimstra ◽  
...  
Keyword(s):  
Pancreatic Tumor ◽  
Tumor Development
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