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TY - JOUR. T1 - Characterization of a newly established human pancreatic carcinoma cell line, UK Pan-1. AU - Fralix, Kimberly D.. AU - Ahmed, Mansoor M.. AU - Mattingly, Cynthia. AU - Swiderski, Carol. AU - McGrath, Patrick C.. AU - Venkatasubbarao, Kolaparthi. AU - Kamada, Nanao. AU - Mohiuddin, Mohammed. AU - Strodel, William E.. AU - Freeman, James W.. PY - 2000/5/1. Y1 - 2000/5/1. N2 - BACKGROUND. A highly tumorigenic cell line designated as UK Pan-1 was established in a surgically removed human pancreatic adenocarcinoma and characterized as having many of the genotypic and phenotypic alterations commonly found in pancreatic tumors. METHODS. The cell line was characterized by its morphology, growth rate in monolayer culture and soft agar, tumorigenicity in nude mice, and chromosomal analysis. Furthermore, the status of p53, Ki-ras mutation and transforming growth factor (TGF)-β receptor expression were determined. The characteristics of UK Pan-1 were compared with those of other commonly ...

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Abstract Background Pancreatic carcinoma usually is a fatal disease with no cure, mainly due to its invasion and metastasis prior to diagnosis. We analyzed the gene expression profiles of paired primary pancreatic tumors and metastatic lesions from Ela-c-myc transgenic mice in order to identify genes that may be involved in the pancreatic cancer progression. Differentially expressed selected genes were verified by semi-quantitative and quantitative RT-PCR. To further evaluate the relevance of some of the selected differentially expressed genes, we investigated their expression pattern in human pancreatic cancer cell lines with high and low metastatic potentials. Results Data indicate that genes involved in posttranscriptional regulation were a major functional category of upregulated genes in both primary pancreatic tumors (PT) and liver metastatic lesions (LM) compared to normal pancreas (NP). In particular, differential expression for splicing factors, RNA binding/pre-mRNA processing factors and

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https://www.nature.com/articles/s41598-020-65804-5. San Diego, California., June 8, 2020 - Researchers at the Human BioMolecular Research Institute and ChemRegen, Inc., have reported on a small molecule p53 Activator Wnt Inhibitor-2 (PAWI-2) that potently inhibits human pancreatic cancer stem cells. Writing June 8, 2020 in the journal Scientific Reports, the team describes how they tested PAWI-2, a synthetic, drug-like compound that can be used to decrease human pancreatic cancer. Pancreatic cancer remains a major health problem in the United States and soon will be the second most common cause of mortality due to cancer. A majority of pancreatic cancer patients are often resistant to clinical therapies. Thus, it remains a challenge to develop an efficacious clinically useful pancreatic cancer therapy said Jiongjia Cheng, Ph.D., lead author of the study. Using a non-toxic small molecule to decrease pancreatic cancer is very attractive.. Medicinal chemistry leads to safe anti-cancer ...

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TY - JOUR. T1 - KAI1 expression is up-regulated in early pancreatic cancer and decreased in the presence of metastases. AU - Guo, Xiaozhong. AU - Friess, Helmut. AU - Graber, Hans U.. AU - Kashiwagi, Mikiya. AU - Zimmermann, Arthur. AU - Korc, Murray. AU - Büchler, Markus W.. PY - 1996/11/1. Y1 - 1996/11/1. N2 - KAI1 is a metastasis suppressor gene for prostate cancer that is located on chromosome 11p11.2-13. Using Northern blot analysis and in situ hybridization, we studied expression of KAI1 mRNA in specimens from 14 normal pancreases and 27 primary pancreatic cancers, and then correlated the findings with the clinical and histopathological parameters of the patients. Northern blot analysis showed increased steady-state levels of KAI1 mRNA expression in 24 of 27 (89%) pancreatic cancer samples. In situ hybridization showed enhanced KAI1 mRNA levels in the pancreatic cancer cells in 82% cancer tissues. The stroma surrounding the cancer mass and normal pancreatic tissue adjacent to the cancer ...

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Pancreatic cancer is known to be the deadliest of all common cancers. Despite all efforts in pancreatic cancer treatment, the five-year survival rates at diagnosis over the past 20 years have only increased from 5% to 8%. Assuming that pancreatic cancer is going to become the second most frequent cause of cancer related death in the next 20 years, we are all encouraged to treat patients in clinical trials to gain improvements in this devastating disease. Areas covered: This review will provide a summary of pancreatic cancer treatment over the last 20 years, starting with the pivotal study in 1997 which showed the superiority of gemcitabine over 5-FU in advanced pancreatic cancer and is marked as the beginning of a new era in pancreatic cancer treatment ...

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Despite intense efforts over the past 30 years, human pancreatic β cell lines have not been available. Here, we describe a robust technology for producing a functional human β cell line using targeted oncogenesis in human fetal tissue. Human fetal pancreatic buds were transduced with a lentiviral ve …

1240 The epidermal growth factor receptor (EGFR) is overexpressed in up to 60% of pancreatic cancer specimens. Recently, erlotinib (a small-molecule tyrosine kinase inhibitor, TKI) was approved for pancreatic cancer treatment. There is an association between TKI response in non-small cell lung cancer (NSCLC) and specific activating mutations in the EGFR tyrosine kinase (TK) domain. The applicability of this paradigm in pancreatic cancer was analyzed by evaluating the presence of activating EGFR TK mutations and EGFR pathway activation in a large cohort of pancreatic adenocarcinoma patients. Pancreatic adenocarcinoma is characterized by an exuberant desmoplastic reaction, masking precise analysis of tumor cells. State-of-the-art laser capture microdissection (LCM) allowed us to selectively isolate pancreatic ductal adenocarcinoma cells from their surrounding stromal elements. DNA, protein, and mRNA were extracted from 30 human frozen pancreatic cancer specimens following LCM of tissue sections ...

Occupational exposure to hydrocarbon solvents has been found to be associated with an increased risk of exocrine pancreatic cancer (EPC), the human tumor with the highest prevalence of K-ras mutations. Ras genes are critical DNA targets for chemical carcinogens. We analysed the relationship between past occupational exposure to hydrocarbon solvents and mutations in codon 12 of the K-ras gene in 107 incident cases of EPC. Information on occupational factors and life-style was obtained from personal interviews conducted during hospital stay. Occupational exposure to hydrocarbon solvents (aliphatic, aromatic, chlorinated, benzene, other organic solvents) was examined using two methods: expert assessment and the Finnish job-exposure matrix (Finjem). Exposure among K-ras mutated EPC cases (n = 83) was compared with that of K-ras wild-type EPC cases (n = 24). An association between K-ras mutations and solvent exposure was observed with Finjem but barely so with the expert assessment. Over 7-fold ...

TY - JOUR. T1 - Stable transduction of human pancreatic adenocarcinoma cells, rat fibroblasts, and bone marrow-derived stem cells with recombinant adeno- associated virus containing the rat preproisulin II gene. AU - Bochan, M. R.. AU - Sidner, R. A.. AU - Shah, R.. AU - Cummings, O. W.. AU - Goheen, M.. AU - Jindal, R. M.. PY - 1998/1/1. Y1 - 1998/1/1. UR - http://www.scopus.com/inward/record.url?scp=0031978015&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0031978015&partnerID=8YFLogxK. U2 - 10.1016/S0041-1345(97)01353-5. DO - 10.1016/S0041-1345(97)01353-5. M3 - Article. C2 - 9532125. AN - SCOPUS:0031978015. VL - 30. SP - 453. EP - 454. JO - Transplantation Proceedings. JF - Transplantation Proceedings. SN - 0041-1345. IS - 2. ER - ...

INTRODUCTION: Until now, studies examining the relationship between socioeconomic status and pancreatic cancer incidence have been inconclusive.. AIM: To prospectively investigate to what extent pancreatic cancer incidence varies according to educational level within the European Prospective Investigation into Cancer and Nutrition (EPIC) study.. METHODS: In the EPIC study, socioeconomic status at baseline was measured using the highest level of education attained. Hazard ratios by educational level and a summary index, the relative indices of inequality (RII), were estimated using Cox regression models stratified by age, gender, and center and adjusted for known risk factors. In addition, we conducted separate analyses by age, gender and geographical region.. RESULTS: Within the source population of 407, 944 individuals at baseline, 490 first incident primary pancreatic adenocarcinoma cases were identified in 9 European countries. The crude difference in risk of pancreatic cancer according to ...

ROCKVILLE, Md., Jan. 20, 2017 (GLOBE NEWSWIRE) - Rexahn Pharmaceuticals, Inc. (NYSE MKT:RNN), a clinical stage biopharmaceutical company developing next generation targeted therapeutics for the treatment of cancer, today announced an update on the safety and efficacy of RX-3117 in an ongoing Phase IIa clinical trial in metastatic pancreatic cancer at the American Society for Clinical Oncology (ASCO) 2017 Gastrointestinal Cancer Symposium in San Francisco California.. The data on progression free survival in metastatic pancreatic cancer patients treated with RX-3117 is very encouraging with 20% of patients exhibiting progression free survival of greater than 5.6 months (with one patient having progression free survival of 7.2 months). A majority of the patients enrolled in the trial have already failed 3 or more prior cancer therapies. Current options for these patients are usually limited to palliative or best supportive care; there are no drugs approved for metastatic pancreatic cancer ...

MANHATTAN BEACH, Calif., Nov. 9, 2012 /PRNewswire/ -- The Pancreatic Cancer Action Network is pleased to announce Abraxane® extends survival for patients with advanced pancreatic cancer. According to Celgene Corporation, Abraxane in combination with gemcitabine when given to advanced pancreatic cancer patients who had not received previous treatment demonstrated a statistically significant improvement in overall survival compared to patients receiving gemcitabine alone. (Logo: http://photos.prnewswire.com/prnh/20111004/LA79914LOGO). The phase III study included 861 metastatic pancreatic cancer patients from around the world. Full results from the clinical trial will be presented at the American Society of Clinical Oncologys 2013 Gastrointestinal Cancers Symposium being held in January. Historically, few effective treatment options for pancreatic cancer have existed. We are thrilled to have a new treatment option for patients with advanced pancreatic cancer. We look forward to learning more ...

Pancreatic cancer is considered the third most deadly form of the disease and leads to a great deal of mortality annually. Pancreatic cancer is not easy to detect owing to where the organ is located. Another reason that makes pancreatic cancer deadly is that it can become resistant to chemotherapy. One of the ways the treatment of pancreatic cancer can be more efficient is the development of a drug that can prevent it from becoming treatment resistant.. In August 2018, Aretha Franklin lost the fight to pancreatic cancer. Other prominent figures that have died from pancreatic cancer include Steve Jobs, Patrick Swayze, Joan Crawford, and Luciano Pavarotti.. This form of cancer is mostly diagnosed at a late stage and chemotherapy will cease to have an effect on the tumors. A combination of early diagnosis and preventing the tumors from becoming resistant to treatment can be a key to extending the life of suffers. According to researchers, cracking this code can extend the life of diagnosed patients ...

Introduction. Solid pseudopapillary neoplasm (SPN) of the pancreas is rare, accounting for 2-3 % of primary pancreatic tumours (1). It was first described by Frantz in 1959 and has since then been referred to as: solid and cystic tumour, solid and papillary neoplasm, Frantzs tumour, papillary-cystic neoplasm and papillary epithelial neoplasm. It was finally defined by the World Health Organization (WHO) in 2000 as a solid pseudopapillary neoplasm of the pancreas (2). SPN is considered a low malignant potential neoplasm, due to its benign morphology and the fact that it rarely metastasizes (3). Even though pancreatic tumours generally have bad prognosis, SPN shows good prognosis, which makes the disease entity unique in this disease group. To predict malignant behavior of SPN, several morphological criteria are needed (angioinvasion, invasion to surrounding tissue or unequivocal perineural invasion) and if present, the tumour should be designated as solid pseudopapillary carcinoma (SPC) (4). We ...

There has been a long standing interest in the identification of medicinal plants and derived natural products for developing cancer therapeutics. Our study focuses upon pancreatic cancer, due to its high mortality rate, that is attributed in part to the lack of an effective chemotherapeutic agent. Previous reports on the use of medicinal plant extracts either alone or alongside conventional anticancer agents in the treatment of this cancer have shown promising results. This work aims to investigate the therapeutic properties of a library of medicinal plants from Bangladesh. 56 extracts of 44 unique medicinal plants were studied. The extracts were screened for cytotoxicity against the pancreatic adenocarcinoma cell line Panc-1, using a label-free biosensor assay. The top cytotoxic extracts identified in this screen were tested on two additional pancreatic cancer cell lines (Mia-Paca2 and Capan-1) and a fibroblast cell line (Hs68) using an MTT proliferation assay. Finally, one of the most promising

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Pancreatic cancer has long carried poor prognosis. The development of new therapeutic approaches is particularly urgent. Inactivation of the tumor-suppressor gene p16(INK4a/CDKN2), a specific inhibitor of the cyclin-dependent kinases CDK4 and CDK6, is the most common genetic alteration in human pancreatic cancer, making it an ideal target for gene replacement. Here we transfected tumor cells using a recombinant adenovirus containing the wt-p16 cDNA (Ad5RSV-p16). The overexpression of p16 decreased cell proliferation in all four human pancreatic tumor cell lines (NP-9, NP-18, NP-29, and NP-31). However, G1 arrest and senescence were observed in only three. In contrast, the fourth (NP-18) showed a significant increase in apoptosis. This differential behavior may be related to the differences found in the expression level of E2F-1. Experiments on subcutaneous pancreatic xenografts demonstrated the effectiveness of p16 in the inhibition of pancreatic tumor growth in vivo. Taken together, our results ...

Evidence of a protective effect of several antioxidants and other nutrients on pancreatic cancer risk is inconsistent. The aim of this study was to investigate the association for prediagnostic plasma levels of carotenoids, vitamin C, retinol and tocopherols with risk of pancreatic cancer in a case-control study nested within the ... read more European Prospective Investigation into Cancer and Nutrition (EPIC). 446 incident exocrine pancreatic cancer cases were matched to 446 controls by age at blood collection, study center, sex, date and time of blood collection, fasting status and hormone use. Plasma carotenoids (- and -carotene, lycopene, -cryptoxanthin, canthaxanthin, zeaxanthin and lutein), - and -tocopherol and retinol were measured by reverse phase high-performance liquid chromatography and plasma vitamin C by a colorimetric assay. Incidence rate ratios (IRRs) with 95% confidence intervals (95%CIs) for pancreatic cancer risk were estimated using a conditional logistic regression ...

Like weeds sprouting from cracks in the pavement, cancer often forms in sites of tissue damage. That damage could be an infection, a physical wound, or some type of inflammation. Common examples include stomach cancer caused by H. pylori infection, Barretts esophagus caused by acid reflux, and even smoking-induced lung cancer.. Exactly how tissue damage colludes with genetic changes to promote cancer isnt fully understood. Most of what scientists know about cancer concerns advanced stages of the disease. Thats especially true for cancers such as pancreatic cancer that are usually diagnosed very late.. Researchers in Scott Lowes lab at the Sloan Kettering Institute are now trying to zero in on the earliest stages of pancreatic cancer development.. If we understood how these tumors form, maybe we could catch them before the cancer has progressed to an incurable stage, says Direna Alonso Curbelo, a postdoctoral fellow in the Lowe lab who is the first author of a new paper published February 3 ...

TY - JOUR. T1 - A phase i study of IMP321 and gemcitabine as the front-line therapy in patients with advanced pancreatic adenocarcinoma. AU - Wang-Gillam, Andrea. AU - Plambeck-Suess, Stacey. AU - Goedegebuure, Peter. AU - Simon, Peter O.. AU - Mitchem, Jonathan B.. AU - Hornick, John R.. AU - Sorscher, Steven. AU - Picus, Joel. AU - Suresh, Rama. AU - Lockhart, Albert. AU - Tan, Benjamin. AU - Hawkins, Williams G.. PY - 2013/6/1. Y1 - 2013/6/1. N2 - Purpose This phase I study was conducted to determine the safety profile and maximum tolerated dose (MTD) of IMP321, a soluble lymphocyte activation gene-3 (LAG-3) Ig fusion protein and MHC Class II agonist, combined with gemcitabine in patients with advanced pancreatic adenocarcinoma. Patients and methods Patients with advanced pancreatic adenocarcinoma were treated with gemcitabine (1,000 mg/m2)(level 1), gemcitabine (1,000 mg/m 2) plus IMP 321 at 0.5 mg (level 2) and 2.0 mg (level 3), respectively. Safety, toxicity, and immunological markers at ...

To address the role of β(1) integrins in pancreatic cancer progression, we stably knocked down β(1) integrin subunit expression in human FG-RFP pancreatic cancer cells using lentiviral-based RNA interference. We then examined the effects of β(1) integrin subunit knockdown on pancreatic cancer cell adhesion, migration and proliferation on tumor microenvironment-specific extracellular matrix proteins in vitro and on tumor progression in vivo using a clinically relevant fluorescent orthotopic mouse model of pancreatic cancer. Knockdown of the β(1) integrin subunit inhibited cell adhesion, migration and proliferation on types I and IV collagen, fibronectin and laminin in vitro. In vivo, knockdown of the β(1) integrin subunit reduced primary tumor growth by 50% and completely inhibited spontaneously occurring metastasis. These observations indicate a critical role for the β(1) integrin subunit in pancreatic cancer progression and metastasis in particular. Our results suggest the β(1) integrin

CCL Dec - Onivyde Combination Boosts OS in Post-Gemcitabine Pancreatic Cancer Patients - Onivyde Combination Boosts OS in Post-Gemcitabine Pancreatic Cancer Patients   A phase III study of Onivyde (irinotecan liposome injection), in combination with fluorouracil and leucovorin, demonstrated improvements in median overall survival in post-gemcitabine metastatic pancreatic cancer patients. The study, NAPOLI-1, was the basis of approval by the FDA in this indication, and the results were recently published in The Lancet.

TY - JOUR. T1 - Phase II trial of salvage therapy with trabectedin in metastatic pancreatic adenocarcinoma. AU - Belli, Carmen. AU - Piemonti, Lorenzo. AU - DIncalci, Maurizio. AU - Zucchetti, Massimo. AU - Porcu, Luca. AU - Cappio, S.. AU - Doglioni, Claudio. AU - Allavena, Paola. AU - Ceraulo, D.. AU - Maggiora, Paola. AU - Dugnani, Erica. AU - Cangi, Mariagiulia. AU - Garassini, Greta. AU - Reni, Michele. PY - 2016/3/1. Y1 - 2016/3/1. N2 - Purpose: No standard salvage chemotherapy has been identified for metastatic pancreatic adenocarcinoma (mPA), and there is an urgent need for active agents against this disease. This phase II trial explored the activity of trabectedin in mPA progressing after gemcitabine-based first-line chemotherapy. Methods: Patients with gemcitabine-resistant disease received trabectedin 1.3 mg/m2 as a 3-h intravenous continuous infusion every 3 weeks until disease progression or unacceptable toxicity or for a maximum of 6 months. The primary endpoint was ...

Acquired 5-Fluorouracil Resistance in Human Pancreatic Carcinoma Cells. A Paradigm for Chemoresistance Mechanisms in Pancreatic Cancer

The role of tuberous sclerosis complex (TSC) in the pathogenesis of pancreatic cancers remains largely unknown. The present study shows that neurogenin 3 directed Cre deletion of Tsc1 gene induces the development of pancreatic acinar carcinoma. By cross-breeding the Neurog3-cre mice with Tsc1(loxp/loxp) mice, we generated the Neurog3-Tsc1-/- transgenic mice in which Tsc1 gene is deleted and mTOR signaling activated in the pancreatic progenitor cells. All Neurog3-Tsc1-/- mice developed notable adenocarcinoma-like lesions in pancreas starting from the age of 100 days old. The tumor lesions are composed of cells with morphological and molecular resemblance to acinar cells. Metastasis of neoplasm to liver and lung was detected in 5% of animals. Inhibition of mTOR signaling by rapamycin significantly attenuated the growth of the neoplasm. Relapse of the neoplasm occurred within 14 days upon cessation of rapamycin treatment. Our studies indicate that activation of mTOR signaling in the pancreatic ...

Pancreatic cancer tissues and cell lines. Sixteen human pancreatic cancer cell lines were used in this study: A818.4, AsPc-1, CFPAC-1, FA6, Hs766T, MDAPanc-3, MiaPaCa-2, PANC-1, PaTu-I, RWP-1, Suit-2, and T3M4 were obtained from Cancer Research UK cell production services. PK1, PK9, and PK59 were established and maintained at Tohoku University (20). All cell lines were kept in a humidified incubator at 37°C with 5% CO2 and cultured in E4 complete medium, supplemented with 10% fetal bovine serum, penicillin (0.1 μg/mL), and streptomycin (100 units/mL). The human pancreatic ductal epithelial cell line HPDE was a kind gift from Dr. Ming-Sound Tsao (University of Toronto, Canada) and was grown in keratinocyte medium as described before (21).. Pancreatic cancer tissues were obtained from the Human Biomaterials Resource Centre (Hammersmith Hospital, London, United Kingdom) and Tohoku University Hospital (Sendai, Japan) with full ethical approval from the host institutions. All tissues used were ...

By blocking production of GM-CSF in pancreatic cancer cells, the researchers found that they were able to disrupt accumulation of myeloid-derived suppressor cells, liberating the tumor-killing immune response. Our study suggests a therapeutic strategy for harnessing the anti-tumor potential of the immune system, Dr. Bar-Sagi explained. Our findings should be applicable to a significant proportion of human pancreatic cancer cases, as the vast majority of human pancreatic cancer samples that we tested express the GM-CSF protein prominently, Dr. Bar-Sagi added. The researchers are hopeful that their findings will open new doors in therapeutic research, eventually leading to new drug therapies that block the production or function of the GM-CSF protein to allow anti-tumor immune cells to attack the cancer cells and halt tumor development. Although the study focuses on pancreatic cancer, KRAS mutations are prevalent in a number of other cancers, including colon and lung cancer. From a research ...

The identification of circulating tumor antigens or their related autoantibodies provides a means for early cancer diagnosis as well as leads for therapy. We have used a proteomic approach to identify proteins that commonly induce a humoral response in pancreatic cancer. Aliquots of solubilized proteins from a pancreatic cancer cell line (Panc-1) were subjected to two-dimensional PAGE, followed by Western blot analysis in which sera of individual patients were tested for primary antibodies. Sera from 36 newly diagnosed patients with pancreatic cancer, 18 patients with chronic pancreatitis, 33 patients with other cancers, and 15 healthy subjects were analyzed. Autoantibodies were detected against either one or two calreticulin isoforms identified by mass spectrometry in sera from 21 of 36 patients with pancreatic cancer. One of 18 chronic pancreatitis patients and 1 of 15 healthy controls demonstrated autoantibodies to calreticulin isoform 1; none demonstrated autoantibodies to isoform 2. None of ...

TY - JOUR. T1 - Inhibition of constitutive NF-κB activity by IκBαM suppresses tumorigenesis. AU - Fujioka, Shuichi. AU - Sclabas, Guido M.. AU - Schmidt, Christian. AU - Niu, Jiangong. AU - Frederick, Wayne A.. AU - Dong, Qiang G.. AU - Abbruzzese, James L.. AU - Evans, Douglas B.. AU - Baker, Cheryl. AU - Chiao, Paul J.. PY - 2003/3/6. Y1 - 2003/3/6. N2 - We have demonstrated that nuclear factor-κB (NF-κB) is constitutively activated in human pancreatic adenocarcinoma and human pancreatic cancer cell lines but not in normal pancreatic tissues or in immortalized, nontumorigenic pancreatic epithelial cells, suggesting that NF-κB plays a critical role in the development of pancreatic adenocarcinoma. To elucidate the role of constitutive NF-κB activity in human pancreatic cancer cells, we generated pancreatic tumor cell lines that express a phosphorylation defective IκBα (S32, 36A) (IκBαM) that blocks NF-κB activity. In this study, we showed that inhibiting constitutive NF-κB activity ...

TY - JOUR. T1 - Immune infiltrates as predictive markers of survival in pancreatic cancer patients. AU - Protti, Maria Pia. AU - De Monte, Lucia. PY - 2013. Y1 - 2013. N2 - Pancreatic cancer is a devastating disease with dismal prognosis. The tumor microenvironment is composed by multiple cell types, molecular factors, and extracellular matrix forming a strong desmoplastic reaction, which is a hallmark of the disease. A complex cross-talk between tumor cells and the stroma exists with reciprocal influence that dictates tumor progression and ultimately the clinical outcome. In this context, tumor infiltrating immune cells through secretion of chemokine and cytokines exert an important regulatory role. Here we review the correlation between the immune infiltrates, evaluated on tumor samples of pancreatic cancer patients underwent surgical resection, and disease free and/or overall survival after surgery. Specifically, we focus on tumor infiltrating lymphocytes (TILs), mast cells (MCs) and ...

Physical exams mainly focus on the abdomen to check for any masses or fluid buildup, which could indicate pancreatic cancer. Pancreatic cancer can also spread to lymph nodes; the lymph nodes will be looked at carefully for swelling during a physical examination.. Imaging tests use x-rays, magnets, sound waves, or radioactive chemicals to produce pictures of the inside of the body. For pancreatic cancer, these will include computed tomography (CT) scans, magnetic resonance imaging (MRI) scans, somatostatin receptor scintigraphy, positron emission tomography (PET) scans, endoscopic ultrasounds, and angiography.. Blood tests for pancreatic cancer are used to make diagnoses and determine a patients treatment options. These tests may include a CA 19-9 test and CEA test.. Biopsies entail taking a sample of a suspected tumor so it can be examined under the microscope. Biopsies for pancreatic cancer are performed as a last resort and entail surgically removing a pancreatic tissue sample and ...

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We identified an aberrant accumulation of cholesteryl ester in human pancreatic cancer specimens and cell lines, Li said. Depletion of cholesterol esterification significantly reduced pancreatic tumor growth and metastasis in mice.. Findings show that drugs like avasimibe, previously developed for treatment of atherosclerosis, reduced the accumulation of cholesteryl ester. The disease usually kills within a few months of diagnosis. It is hoped the potential new treatment might extend life of pancreatic cancer patients for a year, Cheng said.. The accumulation of cholesteryl ester is controlled by an enzyme called ACAT-1, and findings correlated a higher expression of the enzyme with a poor survival rate for patients. The researchers analyzed tissue samples from pancreatic cancer patients and then tested the drug treatment in a type of laboratory mice referred to as an orthotopic mouse model, developed at the IU School of Medicine. Specimens of human pancreatic tissues were obtained from the ...

Pancreatic cancer is associated with low responsiveness to conventional chemotherapies and its incidence nearly equals its death rate. This warrants the development of novel mechanism-based approaches for the management of pancreatic cancer. This study was designed to determine the potential of sanguinarine, a plant alkaloid known to possess strong antimicrobial, anti-inflammatory, and antioxidant activities, against human pancreatic carcinoma cells. Employing human pancreatic carcinoma AsPC-1 and BxPC-3 cells, we specifically evaluated the pro-apoptotic and cell cycle deregulatory effects of sanguinarine and evaluated the involvement of Bcl-2 family proteins and p53 as the mechanism of the biological effects of sanguinarine. Our data demonstrated that sanguinarine (at low concentrations of 0.1-10 ?M; for 24 h) treatment to AsPC-1 and BxPC-3 cells resulted in a dose dependent (i) inhibition of viability and growth, (ii) colony formation ability, (iii) induction of apoptosis, and (iv) G0-G1 phase ...

According to the results of a Phase II clinical trial, the addition of the investigational drug EndoTAG™-1 to chemotherapy with Gemzar® (gemcitabine) may improve survival among patients with inoperable pancreatic cancer. These results were presented at the 33rd Congress of the European Society for Medical Oncology (ESMO).. Pancreatic cancer has one of the highest mortality rates of all cancers. It accounts for approximately 2% of all newly diagnosed cancers in the United States each year but 5% of all cancer deaths. Pancreatic cancer is often called a silent killer because its symptoms are usually not recognizable until it has advanced and spread outside the pancreas. As a result the majority of pancreatic cancers are not diagnosed until they have reached advanced stages and are considered incurable.. Chemotherapy is a common treatment for advanced pancreatic cancer. However, due to the poor long-term survival achieved with chemotherapy alone, researchers continue to evaluate novel ways to ...

Natural killer (NK) cells play a key role in non-specific immune response in different cancers, including pancreatic cancer. However the anti-tumor effect of NK cells decreases during pancreatic cancer progression. The regulatory pathways by which NK cells facilitate tumor immune escape are unclear, therefore our purpose was to investigate the roles of the contributory factors. NK cells isolated from fresh healthy peripheral blood were co-cultured with normal human pancreatic ductal cells hTERT-HPNE and human pancreatic cancer cell lines SW1990 and BxPc-3 in vitro. Then NK cell function was determined by Flow cytometric analysis of surface receptors and cytotoxic granules in NK cells, NK cell apoptosis and cytotoxicity, and Enzyme-linked immunosorbent assay of cytokines. Expression level of MMP-9, IDO and COX-2 in hTERT-HPNE and SW1990 cells were detected by quantitative RT-PCR. Statistical differences between data groups were determined by independent t-tests using SPSS 19.0 software. Our results

TY - JOUR. T1 - Chemosensitization and inhibition of pancreatic cancer stem cell proliferation by overexpression of microRNA-205. AU - Chaudhary, Amit Kumar. AU - Mondal, Goutam. AU - Kumar, Virender. AU - Kattel, Krishna. AU - Mahato, Ram I. PY - 2017/8/28. Y1 - 2017/8/28. N2 - Treatment of pancreatic cancer with gemcitabine (GEM) is limited due to its rapid plasma metabolism and development of chemoresistance. MicroRNA (miRNA) regulates cancer stem cell (CSC) maintenance and induces chemoresistance in cancer cells. In this study, we observed differential downregulation of miR-205 (miR-205-5p) in human pancreatic cancer tissues and cells. Compared to GEM-sensitive MIA PaCa-2 cells, miR-205 was highly downregulated in GEM-resistant MIA PaCa-2R cells. Lentivirus-mediated overexpression of miR-205 inhibits MIA PaCa-2R cell proliferation after GEM-treatment. Further investigation confirmed that miR-205 alone significantly reduces the proliferation of CSCs and tumor growth in mouse models. However, ...

Pancreatic ductal adenocarcinoma has a poor prognosis due to late diagnosis and a lack of effective therapeutic options. Thus, it is important to better understand its molecular mechanisms and to develop more effective treatments for the disease. The ternary complex factor Net, which exerts its strong inhibitory function on transcription of proto-oncogene gene c-fos by forming ternary complexes with a second transcription factor, has been suspected of being involved in pancreatic cancer and other tumors biology. In this study, we found that the majority of pancreatic ductal adenocarcinoma tissues and cell lines had weak or no expression of Net, whereas significantly high level of Net expression occurred in paired adjacent normal tissues we studied. Furthermore, using in vitro and in vivo model systems, we found that overexpression of Net inhibited cell growth and survival and induced cell apoptosis in human pancreatic ductal adenocarcinoma cell PL45; the mechanisms by which Net inhibited the cell cycle

TY - JOUR. T1 - Ex vivo organotypic culture system of precision-cut slices of human pancreatic ductal adenocarcinoma. AU - Misra, Sougat. AU - Moro, Carlos F.. AU - Del Chiaro, Marco. AU - Pouso, Soledad. AU - Sebestyén, A.. AU - Löhr, Matthias. AU - Björnstedt, Mikael. AU - Verbeke, Caroline S.. PY - 2019/12/1. Y1 - 2019/12/1. N2 - Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis, which is mainly due to late diagnosis and profound resistance to treatment. The latter is to a large extent attributed to the tumor stroma that is exceedingly prominent in PDAC and engages in complex interactions with the cancer cells. Hence, relevant preclinical models of PDAC should also include the tumor stroma. We herein describe the establishment and functional validation of an ex vivo organotypic culture of human PDAC that is based on precision-cut tissue slices from surgical specimens and reproducibly recapitulates the complex cellular and acellular composition of PDAC, including its ...

PRIMARY OBJECTIVES:. I. To evaluate progression-free survival (PFS) associated with temozolomide alone or temozolomide and capecitabine in patients with advanced pancreatic neuroendocrine tumors.. SECONDARY OBJECTIVES:. I. To evaluate response rates (RR) associated with temozolomide alone or temozolomide and capecitabine treatment in patients with advanced pancreatic neuroendocrine tumors.. II. To evaluate overall survival (OS) associated with temozolomide alone or temozolomide and capecitabine in patients with advanced pancreatic neuroendocrine tumors.. III. To evaluate the toxicity associated with temozolomide alone or temozolomide and capecitabine treatment in patients with advanced pancreatic neuroendocrine tumors.. IV. To evaluate the usefulness of methyl guanine methyltransferase (MGMT) status (by immunohistochemistry [IHC] and promoter methylation) for predicting response in pancreatic neuroendocrine tumor patients treated with either temozolomide or temozolomide and capecitabine.. V. To ...

Pancreatic neuroendocrine tumors constitute about 2% of all gastrointestinal neoplasms. Approximately half of the pancreatic neuroendocrine tumors are nonfunctional. Due to lack of specific symptoms, most patients with nonfunctional pancreatic neuroendocrine tumors present with locally advanced or metastatic disease. Second primary malignancies are seen very rarely in these patients. Colon carcinoma ranks third in frequency among primary sites of cancer in both men and women in western countries. Presence of a metachronous colon adenocarcinoma in a patient with nonfunctional pancreatic neuroendocrine tumor has not been reported before. We present a patient who had an asymptomatic mass in the head of the pancreas, detected by ultrasonography in 1996. The patient did not consent to operation. In 2002, after the diagnosis of an unresectable, nonfunctional pancreatic neuroendocrine tumor, interferon alpha-2b and octreotide were started. A year after biological treatment, he refused further ...

2009) Pancreatic cancer stem cells: insights and perspectives. profiling analysis showed that CSLCs (CD44+/CD133+/EpCAM+) exhibit differential expression of more than 1,600 mRNAs, including (2,C4). A large number of studies have shown clear evidence in support of the presence of CSLCs and their clinical implications because the rare subpopulations of CSLCs have been recognized from most tumors, such as prostate, lung, breast, pancreas, brain, gastric, and colorectal tumors. These CSLCs are involved in cell growth, migration/invasion, and apoptosis resistance, attributing to treatment resistance and metastasis, leading to poor clinical end result (2,C4). However, the pathogenesis of CSLCs during tumorigenesis and tumor progression has not been well documented. Although significant improvements have been made in the fight against cancers, pancreatic malignancy (PC) remains one of the most aggressive and lethal malignant diseases in the world, and remains the 4th leading cause of cancer-related ...

In this report, we have identified a subpopulation of highly tumorigenic cancer cells within human pancreatic adenocarcinomas using a xenograft model in which primary human pancreatic adenocarcinoma cells were implanted in immunocompromised mice. These highly tumorigenic cancer cells were identified by expression of the cell surface markers CD44, CD24, and ESA. These cells displayed several features typically seen in stem cells, including the ability to both self-renew and generate differentiated progeny, the ability to differentiate to recapitulate the phenotype of the tumor from which they were derived, and activation of developmental signaling pathways.. We chose to examine expression of the markers CD44, CD24, and ESA based on studies in breast cancer, in which CD44+CD24−/low ESA+ cells were identified as putative cancer stem cells ( 5). We found that cells that expressed CD44, CD24, and ESA represented the most highly tumorigenic population of pancreatic cancer cells, with injection of as ...

TY - JOUR. T1 - Appropriateness of systemic treatments in unresectable metastatic well-differentiated pancreatic neuroendocrine tumors. AU - Strosberg, Jonathan R.. AU - Fisher, George A.. AU - Benson, Al B.. AU - Anthony, Lowell B.. AU - Arslan, Bulent. AU - Gibbs, John F.. AU - Greeno, Edward. AU - Iyer, Renuka V.. AU - Kim, Michelle K.. AU - Maples, William J.. AU - Philip, Philip A.. AU - Wolin, Edward M.. AU - Cherepanov, Dasha. AU - Broder, Michael S.. PY - 2015/2/28. Y1 - 2015/2/28. N2 - AIM: To evaluate systemic treatment choices in unresectable metastatic well-differentiated pancreatic neuroendocrine tumors (PNETs) and provide consensus treatment recommendations. METHODS: Systemic treatment options for pancreatic neuroendocrine tumors have expanded in recent years to include somatostatin analogs, angiogenesis inhibitors, inhibitors of mammalian target of rapamycin and cytotoxic agents. At this time, there is little data to guide treatment selection and sequence. We therefore assembled a ...

PRIMARY OBJECTIVES:. I. To evaluate if the addition of adjuvant everolimus to the R0 or R1 surgical resection of pancreatic neuroendocrine tumor metastases to the liver will result in an improvement in disease free survival.. SECONDARY OBJECTIVES:. I. To evaluate if the addition of adjuvant everolimus to the R0 or R1 surgical resection of pancreatic neuroendocrine tumor metastases to the liver will result in an improvement in overall survival.. II. To evaluate the toxicity associated with adjuvant everolimus following resection in patients with metastatic pancreatic neuroendocrine tumors to the liver.. OUTLINE: Patients are randomized to 1 of 2 treatment arms.. ARM A: Patients receive everolimus orally (PO) once daily (QD) on days 1-28. Treatment repeats every 28 days for up to 12 courses in the absence of disease progression or unacceptable toxicity.. ARM B: Patients receive placebo PO QD on days on days 1-28. Treatment repeats every 28 days for up to 12 courses in the absence of disease ...

TY - JOUR. T1 - EFFECTS OF HUMAN PANCREATIC TUMOUR GROWTH HORMONE RELEASING FACTOR ON GROWTH HORMONE AND SOMATOMEDIN C LEVELS IN PATIENTS WITH IDIOPATHIC GROWTH HORMONE DEFICIENCY. AU - Borges, João L.C.. AU - Gelato, Marie C.. AU - Rogol, Alan D.. AU - Lee Vance, Mary. AU - Macleod, Robert M.. AU - Lynn Loriaux, D.. AU - Rivier, Jean. AU - Blizzard, Robert M.. AU - Furlanetto, Richard. AU - Evans, William S.. AU - Kaiser, Donald L.. AU - Merriam, George R.. AU - Spiess, Joachim. AU - Vale, Wylie. AU - Thorner, Michael O.. PY - 1983/7/16. Y1 - 1983/7/16. N2 - Human pancreatic tumour growth hormone releasing factor (hpGRF-40) 10 μg/kg was administered intravenously to 6 normal young men and 12 adult patients who had presented in childhood with growth hormone (GH) deficiency (7 patients had isolated GH deficiency, 4 had multiple anterior pituitary hormone deficiencies, and 1 had Hand-Schüller-Christian [HSC] disease). hpGRF-40 administration increased serum GH concentrations in all normal ...

TY - JOUR. T1 - Genome-wide genetic and epigenetic analyses of pancreatic acinar cell carcinomas reveal aberrations in genome stability. AU - Jäkel, Cornelia. AU - Bergmann, Frank. AU - Toth, Reka. AU - Assenov, Yassen. AU - Van Der Duin, Daniel. AU - Strobel, Oliver. AU - Hank, Thomas. AU - Klöppel, Günter. AU - Dorrell, Craig. AU - Grompe, Markus. AU - Moss, Joshua. AU - Dor, Yuval. AU - Schirmacher, Peter. AU - Plass, Christoph. AU - Popanda, Odilia. AU - Schmezer, Peter. PY - 2017/12/1. Y1 - 2017/12/1. N2 - Pancreatic acinar cell carcinoma (ACC) is an aggressive exocrine tumor with largely unknown biology. Here, to identify potential targets for personalized treatment, we perform integrative genome-wide and epigenome-wide analyses. The results show frequently aberrant DNA methylation, abundant chromosomal amplifications and deletions, and mutational signatures suggesting defective DNA repair. In contrast to pancreatic ductal adenocarcinoma, no recurrent point mutations are detected. The ...

Telomerase activity was measured in surgically resected tissues of 20 human pancreatic ductal carcinomas, 12 adenomas, 5 pancreatitis tissues, 14 normal pancreatic ducts, and 13 normal pancreatic tissues (primarily made up of acinar cells) using a PCR-based telomerase assay. Relative telomerase activity was expressed as the equivalent telomerase intensity of the number of cells of a human pancreatic cancer cell line, MIA PaCa-2, per microgram of protein in the tissue samples. The median value (25th percentile, 75th percentile) of relative telomerase activity in pancreatic carcinomas was 13.2 (3.58, 244), which was significantly higher relative to normal tissues, normal ducts, pancreatitis tissues, and adenomas (P , 0.0001). When the cutoff value of relative telomerase activity was set at 1.00 and 3.00, the positivity rates of telomerase activity in pancreatic ductal carcinomas were 100 and 80%, respectively. Some of the adenoma samples displayed a weak telomerase ladder. However, when ...

Trichostatin A (TSA) possess histone deacetylase (HDAC) inhibitory potential, can reverse the deactivation of tumor suppressor genes and inhibit tumor cell proliferation. We evaluated the effect of TSA on HDAC expression, tumor cell proliferation, and cancer stem cells (CSCs) activities in pancreatic ductal adenocarnoma (PDAC) cells. The PDAC cell lines MiaPaCa-2 and PANC-1 were distinctly sensitive to TSA, with enhanced apoptosis, compared to SAHA. TSA or SAHA inhibited vimentin, HDACs 1, 7 and 8, upregulated E-cadherin mRNA and protein levels in the PDAC cells, and time-dependently downregulated Oct-4, Sox-2, and Nanog, as well as inhibited PDAC tumorsphere formation. TSA also induces accumulation of acetylated histones, while increasing histone 3 lysine 4 or 9 dimethylation levels in PDAC cellsand enhancing the epigenetic activity of SAHA. The anti-CSCs effect of TSA was like that obtained by silencing HDAC-1 or 7 using siRNA, and enhances Gemcitabine activity. Our study highlights the ...

Neuroendocrine pancreatic tumours grow slower and metastasise later than ductal and acinar carcinomas. The expression of the p53 tumour suppressor gene in pancreatic neuroendocrine tumour cells is unknown. Pancreatic neuroendocrine cell lines (n = 5) and human tumour tissues (n = 19) were studied for changed p53 coding sequence, transcription, and translation. Proliferative activity of tumour cells was determined analysing Ki-67 expression. No mutation in the p53 nucleotide sequence of neuroendocrine tumour cell was found. However, an overexpression of p53 could be detected in neuroendocrine pancreatic tumour cell lines at a protein level. As no p53 mutations were seen, it is suggested that post-translational events can also lead to an overexpression of p53.. ...

Pancreatic ductal adenocarcinoma (PDAC) shows great cellular heterogeneity, with pronounced epithelial and mesenchymal cancer cell populations. However, the cellular hierarchy underlying PDAC cell diversity is unknown. Here we identify the tetraspanin CD9 as a marker of PDAC tumour-initiating cells. CD9high cells had increased organoid formation capability, and generated tumour grafts in vivo at limiting dilutions. Tumours initiated from CD9high cells recapitulated the cellular heterogeneity of primary PDAC, whereas CD9low cells produced only duct-like epithelial progeny. CD9 knockdown decreased the growth of PDAC organoids, and heterozygous CD9 deletion in Pdx1-Cre; LSL-KRasG12D; p53F/F mice prolonged overall survival. Mechanistically, CD9 promoted the plasma membrane localization of the glutamine transporter ASCT2, enhancing glutamine uptake in PDAC cells. Thus, our study identifies a PDAC subpopulation capable of initiating PDAC and giving rise to PDAC heterogeneity, suggesting that the ...

Glycolytic cancer cells produce large quantities of lactate that must be removed to sustain metabolism in the absence of oxidative phosphorylation. The only venting mechanism described to do this at an adequate rate is H+-coupled lactate efflux on monocarboxylate transporters (MCTs). Outward MCT activity is, however, thermodynamically inhibited by extracellular acidity, a hallmark of solid tumours. This inhibition would feedback unfavourably on metabolism and growth, raising the possibility that other venting mechanisms become important in under-perfused tumours. We investigated connexin-assembled gap junctions as an alternative route for discharging lactate from pancreatic ductal adenocarcinoma (PDAC) cells. Diffusive coupling (calcein transmission) in vitro was strong between Colo357 cells, weaker yet hypoxia-inducible between BxPC3 cells, and very low between MiaPaCa2 cells. Coupling correlated with levels of connexin-43 (Cx43), a protein previously linked to late-stage disease. Evoked lactate

This research examines outcomes related to the use of neoadjuvant multi-agent chemotherapy and SBRT in borderline resectable pancreatic cancer.

Avarol is a sesquiterpenoid hydroquinone with potent cytotoxicity. Although resolving endoplasmic reticulum (ER) stress is essential for intracellular homeostasis, erratic or excessive ER stress can lead to apoptosis. Here, we reported that avarol selectively induces cell death in pancreatic ductal adenocarcinomas (PDAC), which are difficult to treat owing to the availability of few chemotherapeutic agents. Analyses of the molecular mechanisms of avarol-induced apoptosis indicated upregulation of ER stress marker BiP and ER stress-dependent apoptosis inducer CHOP in PDAC cells but not in normal cells, suggesting that avarol selectively induces ER stress responses. We also showed that avarol activated the PERK-eIF2α pathway but did not affect the IRE1 and ATF6 pathways. Moreover, CHOP downregulation was significantly suppressed by avarol-induced apoptosis. Thus, the PERK-eIF2α-CHOP signaling pathway may be a novel molecular mechanism of avarol-induced apoptosis. The present data indicate that avarol

TY - JOUR. T1 - Colon and pancreas tumors enhance coagulation. T2 - Role of hemeoxygenase-1. AU - Nielsen, Vance G.. AU - Nfonsam, Valentine N.. AU - Matika, Ryan W.. AU - Ong, Evan S.. AU - Jie, Tun. AU - Warneke, James A.. AU - Steinbrenner, Evangelina B.. PY - 2014/7. Y1 - 2014/7. N2 - Colon and pancreatic cancer are associated with significant thrombophilia. Colon and pancreas tumor cells have an increase in hemeoxygenase-1 (HO-1) activity, the endogenous enzyme responsible for carbon monoxide production. Given that carbon monoxide enhances plasmatic coagulation, we determined if patients undergoing resection of colon and pancreatic tumors had an increase in endogenous carbon monoxide and plasmatic hypercoagulability. Patients with colon (n = 17) and pancreatic (n = 10) tumors were studied. Carbon monoxide was determined by the measurement of carboxyhemoglobin (COHb). A thrombelastographic method to assess plasma coagulation kinetics and formation of carboxyhemefibrinogen (COHF) was ...

Development of systems that reconstitute hallmark features of human pancreatic intraepithelial neoplasia (PanINs), the precursor to pancreatic ductal adenocarcinoma, could generate new strategies for early diagnosis and intervention. However, human cell-based PanIN models with defined mutations are unavailable. Here, we report that genetic modification of primary human pancreatic cells leads to development of lesions resembling native human PanINs. Primary human pancreas duct cells harbouring oncogenic KRAS and induced mutations in CDKN2A, SMAD4 and TP53 expand in vitro as epithelial spheres. After pancreatic transplantation, mutant clones form lesions histologically similar to native PanINs, including prominent stromal responses. Gene expression profiling reveals molecular similarities of mutant clones with native PanINs, and identifies potential PanIN biomarker candidates including Neuromedin U, a circulating peptide hormone. Prospective reconstitution of human PanIN development from primary cells

In February of this year the U.S. National Cancer Institute published an important overview of the state of the science and medicine of pancreatic cancer. We will comment on aspects of it from time to time in the future, but as it so comprehensive and precise, in a departure from our usual practice, we will show a copy it here (sans bibliography and figures) in our pancreatic cancer blog. The term Pancreatic Ductal Carcinoma is accurate and abbreviated PDAC in the original paper; here in the interests of a potential lay reader we will add in parentheses the term: pancreatic cancer.. Scientific Framework for Pancreatic Ductal Carcinoma Executive Summary Significant scientific progress has been made in the last decade in understanding the biology and natural history of pancreatic ductal adenocarcinoma (PDAC, pancreatic cancer); major clinical advances, however, have not occurred. Although PDAC (pancreatic cancer) shares some of the characteristics of other solid malignancies, such as mutations ...

TY - JOUR. T1 - CPI-613 rewires lipid metabolism to enhance pancreatic cancer apoptosis via the AMPK-ACC signaling. AU - Gao, Lixia. AU - Xu, Zhigang. AU - Huang, Zheng. AU - Tang, Yan. AU - Yang, Donglin. AU - Huang, Jiuhong. AU - He, Leilei. AU - Liu, Manran. AU - Chen, Zhongzhu. AU - Teng, Yong. N1 - Publisher Copyright: © 2020 The Author(s).. PY - 2020/4/28. Y1 - 2020/4/28. N2 - Background: Pancreatic cancer remains one of the most rapidly progressive and deadly malignancies worldwide. Current treatment regimens only result in small improvements in overall survival for patients with this cancer type. CPI-613 (Devimistat), a novel lipoate analog inhibiting mitochondrial metabolism, shows the new hope for pancreatic cancer treatment as an efficient and well-tolerated therapeutic option treated alone or in combination with chemotherapy. Methods: Pancreatic cancer cells growing in planar 2D cultures and 3D scaffold were used as research platforms. Cell viability was measured by MTT and ...

TY - JOUR. T1 - Co-expression of mesothelin and CA125 correlates with unfavorable patient outcome in pancreatic ductal adenocarcinoma. AU - Einama, Takahiro. AU - Kamachi, Hirofumi. AU - Nishihara, Hiroshi. AU - Homma, Shigenori. AU - Kanno, Hiromi. AU - Takahashi, Kenta. AU - Sasaki, Ayami. AU - Tahara, Munenori. AU - Okada, Kuniaki. AU - Muraoka, Shunji. AU - Kamiyama, Toshiya. AU - Matsuno, Yoshihiro. AU - Ozaki, Michitaka. AU - Todo, Satoru. PY - 2011/11. Y1 - 2011/11. N2 - Objectives: Recent studies have shown that the high affinity of mesothelin-CA125 interaction might cause intracavitary tumor metastasis. We examined the clinicopathologic significance and prognostic implication of mesothelin and CA125 expression in pancreatic ductal adenocarcinoma. Methods: Tissue samples from 66 pancreatic ductal adenocarcinomas were immunohistochemically examined. Proportion and intensity of constituent tumor cells with mesothelin and CA125 expression were analyzed and classified as high-level ...

Pancreatic cancer is lethal, as it is often detected late. Thus, novel biomarkers of precursor lesions are needed to devise timely therapies. Pancreatic intraepithelial neoplasia (PanIN) and intraductal papillary mucinous neoplasm (IPMN) are major precursors of pancreatic cancer. In normal gastric mucosa, gastric gland mucin-specific O-glycans are unique in having α1,4-linked N-acetylglucosamine (αGlcNAc) residues attached to MUC6. Recently we reported that αGlcNAc functions as a tumor suppressor for differentiated-type gastric adenocarcinoma (Karasawa et al., J Clin Invest 122, 923, 2012). MUC6 is also expressed in pancreatic neoplasms, including PanIN and IPMN, but the role of αGlcNAc expression in pancreatic neoplasms remains unknown. Here, we analyze expression patterns of αGlcNAc, MUC6 and MUC5AC in pancreatic neoplasms and compare them with progression from PanIN to invasive ductal adenocarcinoma (IDAC) (the PanIN-IDAC sequence; 20 cases) and from IPMN to IPMN with associated invasive

TY - JOUR. T1 - Grading of well-differentiated pancreatic Neuroendocrine tumors is improved by the inclusion of both ki67 Proliferative index and mitotic rate. AU - McCall, Chad M.. AU - Shi, Chanjuan. AU - Cornish, Toby C.. AU - Klimstra, David S.. AU - Tang, Laura H.. AU - Basturk, Olca. AU - Mun, Liew Jun. AU - Ellison, Trevor A.. AU - Wolfgang, Christopher L.. AU - Choti, Michael A.. AU - Schulick, Richard D.. AU - Edil, Barish H.. AU - Hruban, Ralph H.. PY - 2013/11. Y1 - 2013/11. N2 - The grading system for pancreatic neuroendocrine tumors (PanNETs) adopted in 2010 by the World Health Organization (WHO) mandates the use of both mitotic rate and Ki67/MIB-1 index in defining the proliferative rate and assigning the grade. In cases when these measures are not concordant for grade, it is recommended to assign the higher grade, but specific data justifying this approach do not exist. Thus, we counted mitotic figures and immunolabeled, using the Ki67 antibody, 297 WHO mitotic grade 1 and 2 ...

BACKGROUND: Histologic characteristics have proven to be very useful for classifying different types of tumors of the pancreas. As a result, the major tumor types in the pancreas have long been classified based on their microscopic appearance. MAIN BODY: Recent advances in whole exome sequencing, gene expression profiling, and knowledge ... read more of tumorigenic pathways have deepened our understanding of the underlying biology of pancreatic neoplasia. These advances have not only confirmed the traditional histologic classification system, but also opened new doors to early diagnosis and targeted treatment. CONCLUSION: This review discusses the histopathology, genetic and epigenetic alterations and potential treatment targets of the five major malignant pancreatic tumors - pancreatic ductal adenocarcinoma, pancreatic neuroendocrine tumor, solid-pseudopapillary neoplasm, acinar cell carcinoma and pancreatoblastoma. show less ...

Image via Wikipedia A new drug combination tested in mice may target the cells responsible for driving some pancreatic tumors. The combination of gemcitabi

View details of top pancreatic neuroendocrine tumor hospitals in Navi Mumbai. Get guidance from medical experts to select best pancreatic neuroendocrine tumor hospital in Navi Mumbai

The combination of Afinitor® (everolimus) and Temodar® (temozolomide) appears to be active against advanced pancreatic neuroendocrine tumors. The details of this Phase I/II study were presented at the 2010 American Society of Clinical Oncology (ASCO) Gastrointestinal Cancers Symposium.[1]. Neuroendocrine tumors form from cells that release hormones in response to a signal from the nervous system. These tumors include carcinoid tumors, islet cell tumors, medullary thyroid carcinomas, pheochromocytomas, and Merkel cell carcinomas. Although they can occur in many different parts of the body, neuroendocrine tumors often develop in the digestive system.. Afinitor is an oral targeted therapy that works by inhibiting a protein known as the mammalian target of rapamycin (mTOR). The mTOR protein plays an important role in regulating cancer cell division and blood vessel growth. It was approved in 2009 for the treatment of selected patients with advanced renal cell (kidney) cancer.. The combination of ...

The tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) is a specific and potent inducer of apoptosis in cancer cells, but the resistance of many tumour cells to TRAIL still represents a major hurdle for the clinical treatment of tumours with TRAIL. As apoptosis is regulated by the balance of activities of several anti-apoptotic factors and pro-apoptotic factors, we analysed the relative contribution of the two sides and found that down-regulation of Bcl-x L and in particular XIAP, but not c-Flip, sensitised the TRAIL resistant pancreatic cancer cell line Panc-1. A combination of both XIAP and Bcl-x L knock-downs showed no substantial added benefit indicating that both act in the same pathway. Notably, the degree of sensitisation by silencing of anti-apoptotic genes was further elevated by concomitantly increasing the pro-apoptotic potential in Panc-1 cells through over-expression of TRAIL-R1 or IFN-γ-mediated increases in caspase-8 levels. Similar sensitisation effects were ...

BONITA, CA--(Marketwired - October 09, 2015) - The combination of PharmaCyte Biotechs (OTCQB: PMCB) signature live-cell encapsulation technology, Cell-in-a-Box® with low doses of ifosfamide has already won the FDAs Orphan Drug status here in the U.S

TY - JOUR. T1 - SIRT1-Activating compounds (STAC) negatively regulate pancreatic cancer cell growth and viability through a SIRT1 lysosomal-dependent pathway. AU - Chini, Claudia C.S.. AU - Espindola-Netto, Jair M.. AU - Mondal, Gourish. AU - Guerrico, Anatilde M.Gonzalez. AU - Nin, Veronica. AU - Escande, Carlos. AU - Sola-Penna, Mauro. AU - Zhang, Jin San. AU - Billadeau, Daniel D.. AU - Chini, Eduardo N.. N1 - Funding Information: Grant Support This work was supported by the Pancreatic Cancer SPORE project from NIH/ NCIto E.N. Chini (grant: CA102701-08) and the Mayo Clinic Center for Cell Signaling in Gastroenterology (NIDDK P30DK084567). J.M. Espindola-Netto is a recipient of a grant from Coordenac?o de Aperfeicoamento de Pessoal de N?vel Superior (CAPES) and Conselho Nacional de Desenvolvimento Cient?fico e Tecnologico (CNPq). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in ...

BAG3 Directly Stabilizes Hexokinase 2 mRNA and Promotes Aerobic Glycolysis in Pancreatic Cancer Cells Scientists showed that aberrant expression of BAG3 significantly contributes to the reprogramming of glucose metabolism in pancreatic ductal adenocarcinoma cells. [J Cell Biol] Abstract Long Noncoding RNA NORAD, a Novel Competing Endogenous RNA, Enhances the Hypoxia-Induced Epithelial-Mesenchymal Transition to Promote Metastasis in Pancreatic Cancer NORAD expression was measured in 33 paired cancerous and noncancerous tissue samples by real-time PCR. The effects of NORAD on pancreatic cancer cells were studied by overexpression and knockdown in vitro. [Mol Cancer] Full Article A New Panel of Pancreatic Cancer Biomarkers Discovered Using a Mass Spectrometry-Based Pipeline Scientists developed a coherent, high-throughput and non-discriminatory pipeline for the novel clinical biomarker discovery of pancreatic carcinoma. [Br J Cancer] Abstract Alternative Polyadenylation of ZEB1 Promotes Its ...

Despite advances in surgery, radiotherapy, and chemotherapy, pancreatic adenocarcinoma often progresses rapidly and causes death. The physical decline of these patients is expected to impact their quality of life (QoL). Therefore, in addition to objective measures of effectiveness, the evaluation of health-related QoL should be considered a matter of major concern when assessing therapy outcomes. Observational, prospective, multicenter study including patients with metastatic pancreatic adenocarcinoma who started first-line chemotherapy in 12 Spanish centers. Treatment and clinical characteristics were recorded at baseline. Patients health-related quality of life, ECOG, and Karnofsky index were measured at baseline, at Days 15 and 30, and every four weeks up to 6 months of chemotherapy. Health-related quality of life was measured using the EORTC-QLQ-C30 and EQ-5D questionnaires. Other endpoints included overall survival and progression-free survival. The study sample included 116 patients (median age

Growing tumors are hypoxic and respond to microenvironmental stress through increased expression of the hypoxia inducible factor-1α (HIF-1α) transcription factor, resulting in an adaptive switch to glycolytic metabolism, angiogenic signaling, survival, and metastasis. HIF-1α expression is associated with tumor resistance to cytotoxic therapy and inferior patient outcomes. Pancreatic cancer is the most hypoxic of all solid tumors and remains refractory to current chemoradiotherapy. We have seen nuclear HIF-1α in 88% of human pancreatic ductal carcinoma but in only 16% of normal pancreas. Stroma adjacent to the pancreatic ductal carcinoma also showed HIF-1α in 43% of cases. We investigated the novel selective HIF-1α inhibitor PX-478 on in vitro and in vivo radiation response of human pancreatic cancer models. Inhibition of HIF-1α by PX-478 increased cell killing by radiation. In mice with Panc-1, CF-PAC-1, or SU.86.86 pancreatic xenografts, concurrent administration of PX-478 potentiated ...

Cancer stem cells (CSCs) have been studied for their self-renewal capacity and pluripotency, as well as their resistance to anticancer therapy and their ability to metastasize to distant organs. CSCs are difficult to study because their population is quite low in tumor specimens. To overcome this problem, we established a culture method to induce a pancreatic cancer stem-like cell (P-CSLC)-enriched population from human pancreatic cancer cell lines. Human pancreatic cancer cell lines established at our department were cultured in CSC-inducing media containing epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), leukemia inhibitory factor (LIF), neural cell survivor factor-1 (NSF-1), and N-acetylcysteine. Sphere cells were obtained and then transferred to a laminin-coated dish and cultured for approximately two months. The surface markers, gene expression, aldehyde dehydrogenase (ALDH) activity, cell cycle, and tumorigenicity of these induced cells were examined for their stem ...

TY - JOUR. T1 - Palliative care in advanced pancreatic cancer. AU - Muircroft, Wendy. AU - Currow, David. PY - 2016/3. Y1 - 2016/3. N2 - The management of patients with advanced pancreatic cancer often requires a multi-disciplinary approach with individualised therapy. Addressing the underlying causes of several of the troublesome symptoms that are relatively unique to the pathophysiology of pancreatic cancer is crucial in order to optimise the function and comfort of people diagnosed with this poor prognosis cancer. Early recognition and response is likely to improve outcomes later in the course of the disease, but more work needs to be done to compare expectant and reactive approaches to the most troublesome symptoms in advanced pancreatic cancer. Given such a poor outlook, referral to a palliative care service that has an active, team-based approach that includes dietetics, gastroenterology, interventional pain expertise and liaison psychiatry is likely to deliver the best possible outcomes. ...

Cystic pancreatic tumors are detected with increasing frequency and remain a clinical problem. Since they have different potential of malignancy the management and decision making process is a hard task. Guidelines, concerning pancreatic cystic tumors indicate the management with mucinous, serous cystic pancreatic neoplasms and solid pseudopappilary tumor, while the management with pancreatic cystic neuroendocrine tumors is not included into these standards. This review tries to answer the question are the cystic pancreatic neuroendocrine tumors different entity from solid tumors of neuroendocrine origin.The management and differential diagnosis of these neoplasms with special focus on features on imaging studies allowing preoperative diagnosis are discussed ...

Less than 5% of pancreatic tumors are Pancreatic Neuroendocrine Tumors (also called PNETs or islet cell tumors). Learn about PNETs and our patient services.

A carbohydrate, mannose-binding lectin or MBL, carried on the surface of a species of acne-causing fungi, Malassezia, has been shown to cause carcinogenesis and an increase in Pancreatic Ductal Adenocarcinoma (PDA); the fungus levels increase significantly in the pancreas prior to the disease.. Furthermore, when researchers(1) ablated the mycobiome (the fungal or yeast microbiome) of the pancreas, slow to moderate cancers stopped progressing. But when they introduced Malassezia strains - but not Candida Saccharomyces or Aspergillus strains - the cancer accelerated. Malassezia is a species of fungi (funghi) or yeast naturally found on the skin of most animals and humans. It is thought to lie behind fungal acne.. At CANCERactive, we have covered several studies showing that bacteria from the mouth associated with gum disease were linked to Pancreatic Cancer, and that a sudden rush of bacteria from the gut to the pancreas caused a 1000-fold increase in bacteria in the pancreatic microbiome and ...