排序方式: 共有178条查询结果,搜索用时 15 毫秒
71.
Kivanc Görgülü Kalliope N. Diakopoulos Jiaoyu Ai Benjamin Schoeps Derya Kabacaoglu Angeliki-Faidra Karpathaki Katrin J. Ciecielski Ezgi Kaya-Aksoy Dietrich A. Ruess Alexandra Berninger Marlena Kowalska Marija Stevanovic Sonja M. Wörmann Thomas Wartmann Yue Zhao Walter Halangk Svetlana Voronina Alexey Tepikin Hana Algül 《Gastroenterology》2019,156(1):203-217.e20
72.
Corbin Pontious Sabrina Kaul Marcus Hong Phil A. Hart Somashekar G. Krishna Luis F. Lara Darwin L. Conwell Zobeida Cruz-Monserrate 《Pancreatology》2019,19(7):951-956
Cathepsin E (CTSE) is an intracellular, hydrolytic aspartic protease found to be expressed in cells of the immune and gastrointestinal systems, lymphoid tissues, erythrocytes, and cancer cells. The precise functions are not fully understood; however, various studies have investigated its numerous cell-type specific roles. CTSE expression has been shown to be a potential early biomarker for pancreatic ductal adenocarcinoma (PDAC). PDAC patients have low survival rates mostly due to the lack of early detection methods. CTSE-specific activity probes have been developed and tested to assist in tumor imaging and functional studies investigating the role of CTSE expression in PDAC tumors. Furthermore, a CTSE protease-specific, photodynamic therapy pro-drug was developed to explore its potential use to treat tumors that express CTSE. Since CTSE is expressed in pancreatic diseases that are risk factors for PDAC, such as pancreatic cysts and chronic pancreatitis, learning about its function in these disease types could assist in early PDAC detection and in understanding the biology of PDAC progression. Overall, CTSE expression and activity shows potential to detect PDAC and other pancreatic diseases. Further research is needed to fully understand its functions and potential translational applicability. 相似文献
73.
Pancreatic ductaladeno carcinoma (PDAC) is a deadly cancer characterized by multiple molecular alterations, the presence of an intense stroma, poor perfusion, and resistance to therapy. In addition to standard imaging techniques, experimental imaging strategies, such as those utilizing molecular probes, nanoparticle-based agents, and tagged antibodies are actively being explored experimentally. It is hoped that advances in these technologies will allow for detecting PDAC at an early stage, and could serve to validate experimental therapies, rapidly identify non-responders, and assist in the design of novel therapeutic strategies tailored to the patient’s molecular profile. 相似文献
74.
GLI1 is regulated through Smoothened-independent mechanisms in neoplastic pancreatic ducts and mediates PDAC cell survival and transformation 总被引:3,自引:0,他引:3
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75.
76.
Nai-Ming Chen Albrecht Neesse Moritz Lino Dyck Benjamin Steuber Alexander O. Koenig Clara Lubeseder-Martellato Thore Winter Teresa Forster Hanibal Bohnenberger Julia Kitz Kirsten Reuter-Jessen Heidi Griesmann Jochen Gaedcke Marian Grade Jin-San Zhang Wan-Chi Tsai Jens Siveke Hans-Ulrich Schildhaus Elisabeth Hessmann 《Gastroenterology》2017,152(6):1507-1520.e15
77.
Masashi Okada Keita Shibuya Atsushi Sato Shizuka Seino Shuhei Suzuki Manabu Seino Chifumi Kitanaka 《Oncotarget》2014,5(13):5100-5112
Cancer cells with self-renewal and tumor-initiating capacity, either quiescent (cancer stem cells, CSCs) or proliferating (cancer stem-like cells, CSLCs), are now deemed responsible for the pervasive therapy resistance of pancreatic cancer, one of the deadliest human cancers characterized by high prevalence of K-Ras mutation. However, to date, much remains unknown how pancreatic CSCs/CSLCs are regulated. Here we show that the K-Ras – JNK axis plays a pivotal role in the maintenance of pancreatic CSCs/CSLCs. In vitro inhibition of JNK, either pharmacological or genetic, caused loss of the self-renewal and tumor-initiating capacity of pancreatic CSLCs. Importantly, JNK inhibition in vivo via systemic JNK inhibitor administration, which had no discernible effect on the general health status of mice, efficiently depleted the CSC/CSLC population within pre-established pancreatic tumor xenografts. Furthermore, knockdown of K-Ras in pancreatic CSLCs with K-Ras mutation led to downregulation of the JNK pathway as well as in loss of self-renewal and tumor-initiating capacity. Together, our findings suggest that pancreatic CSCs/CSLCs are dependent on K-Ras activation of JNK and also suggest that the K-Ras – JNK axis could be a potential target in CSC/CSLC-directed therapies against pancreatic cancer. 相似文献
78.
The efficacy of adjuvant therapy for pancreatic invasive intraductal papillary mucinous neoplasm (IPMN)
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79.
80.
Tomoyuki Abe Hironobu Amano Tsuyoshi Kobayashi Keiji Hanada Masahiro Nakahara Hideki Ohdan Toshio Noriyuki 《European journal of surgical oncology》2018,44(10):1573-1579