Pancreatic Cancer and Crossing Roads of Metabolism
Curator: Demet Sag, PhD
PART I: Pancreatic Cancer
- Intro
- What is Pancreas cancer
- What are the current and possible applications for treatment and early diagnosis
- How pancreatic cancer is related to obesity, overweight, BMI, diabetes
- Genetics of Pancreatic Cancer
PART II : Translational Research on Molecular Genetics Studies at Immune Response Mechanism
- Natural Killer Cells
- IL-17
- Chemokines
search_result- pancreatic cancer clinical trial studies
https://clinicaltrials.gov/ct2/results?term=Pancreatic+Cancer&Search=Search
PART I: Pancreatic Cancer
Introduction:
Our body works a s a system even during complex diseases that is sometimes forgotten. From nutrition to basic immune responses since we are born we start to change how we respond and push the envelope to keep hemostasis in our body.
During this time additional factors also increase or decrease the rate of changes such as life style, environment, inherited as well acquired genetic make-up, types of infections, weight and stress only some of them. As a result we customized our body so deserve a personalized medicine for a treatment. Customized approach is its hype with developing technology to analyze data and compare functional genomics of individuals.
However, still we need the basic cell differentiation to solve the puzzle to respond well and connect the dots for physiological problems. At the stem of the changes there is a cell that respond and amplify its reaction to gain a support to defend at its best . Thus, in this review I like to make a possible connection for pancreatic cancer, obesity-diabetes and innate immune response through natural killer cells.
Pancreatic cancer is one of the most lethal malignancies. Pancreatic cancer is one of the most difficult cancers to treat. Fewer than 5% of patients survive more than 5 years after diagnosis. The 5-year survival rate is despite therapeutic improvements still only 6%. More than 80% of the pancreatic tumors are classified as pancreatic ductal adenocarcinoma (PDA).
When cells in the pancreas that secrete digestive enzymes (acinar cells) turn into duct-like structures, pancreatic cancer can develop. Oncogenic signaling – that which causes the development of tumors – can influence these duct-like cells to form lesions that are a cancer risk.
Crossing roads
The recent publication brought up the necessity to understand how pancreatic cancer and IL17 are connected.
Schematic diagram showing the central role of IL-17B–IL-17RB signaling in pancreatic cancer metastasis.
Adapted from an illustration by Heng-Hsiung Wu and colleagues
http://jem.rupress.org/content/212/3/284/F2.large.jpg
Simply, obesity and diabetes increases the risks of cancers, cardiovascular disease, hypertension, and type-2 DM. There is a very big public health concern as obesity epidemic, the incidence of diabetes is increasing globally, with an estimated 285 million people, or 6.6% of the population from 20 to 79 years of age, affected this is especially more alarming as child obesity is on the rise.
According to a World Health Organization (WHO) report showing that 400 million people are obese in the world, with a predicted increase to 700 million by 2015 and in the US, 30–35 percent of adults are obese. In addition, high BMI and increased risk of many common cancers, such as liver, endometrium, breast, pancreas, and colorectal cancers have a linear increasing relationship.
The BMI is calculated by dividing body weight in kilograms by height squared in meters kg/m2). The current standard categories of BMI are as follows: underweight, <18.5; normal weight, 18.5–24.9; overweight, 25.0–29.9; obese, 30.0–34.9; and severely obese, > or = 35.0).
Furthermore, natural killer cells not only control innate immune responses but have function in other immune responses that was not recognized well before.
Recently, there have been reports regarding Natural Killer cells on was about the function of IL17 that is produced by iNKT, a subtype of NK, for a possible drug target. In addition, regulation of receptors that are up or downregulated by NK cells for a precise determination between compromised cells and healthy cells.
Therefore, instead of sole reliance on SNPs, or GWAS for early diagnostics or only organ system base pathology, compiling the overall health of the system is necessary for a proper molecular diagnostics and targeted therapies.
SNAP SHOT:
Incidence
- It is a rare type of cancer.
- 20K to 200K US cases per year
Medically manageable
Treatment can help
Requires a medical diagnosis
- lab tests or imaging
- spreads rapidly and has a poor prognosis.
- treatments may include: removing the pancreas, radiation, and chemotherapy.
Ages affected; even though person may develop this cancer from age 0 to 60+ there is a high rate of incidence after age 40.
People may experience:
- Pain: in the abdomen or middle back
- Whole body: nausea, fatigue, or loss of appetite
- Also common: yellow skin and eyes, fluid in the abdomen, weight loss, or dark urine
- The pancreas secretes enzymes that aid digestion and hormones that help regulate the metabolism of sugars.
Prescription
- Chemotherapy regimen by injection: Irinotecan, Gemcitabine (Gemzar), Oxaliplatin (Eloxatin)
- Other treatments: Leucovorin by injection, Fluorouracil by injection (Adrucil)
Also common
- Chemotherapy regimen: Gemcitabine-Oxaliplatin regimen, Docetaxel-Gemcitabine regimen
- Procedures: Radiation therapy, Pancreatectomy, surgery to remove pancreatic tumors
Specialists
- Radiologist: Uses images to diagnose and treat disease within the body.
- Oncologist: Specializes in cancer.
- Palliative medicine: Focuses on improving quality of life for terminally ill patients.
- General surgeon: Performs a range of surgeries on the abdomen, skin, breast, and soft tissue.
- Gastroenterologist: Focuses on the digestive system and its disorders.
What are the current and possible applications for treatment and early diagnosis
Diagnostics
Several imaging techniques are employed in order to see if cancer exists and to find out how far it has spread. Common imaging tests include:
- Ultrasound – to visualize tumor
- Endoscopic ultrasound (EUS) – thin tube with a camera and light on one end
- Abdominal computerized tomography (CT) scans – to visualize tumor
- Endoscopic retrograde cholangiopancreatography (ERCP) – to x-ray the common bile duct
- Angiogram – to x-ray blood vessels
- Barium swallows to x-ray the upper gastrointestinal tract
- Magnetic resonance imaging (MRI) – to visualize tumor
- Positron emission tomography (PET) scans – useful to detect if disease has spread
New solutions in Diagnostics;
The study, published in Nature Communications, suggests that targeting the gene in question – protein kinase D1 (PKD1) – could lead to new ways of halting the development of one of the most difficult tumors to treat.
“As soon as pancreatic cancer develops, it begins to spread, and PKD1 is key to both processes. Given this finding, we are busy developing a PKD1 inhibitor that we can test further,” says the study’s co-lead investigator, Dr. Peter Storz.
Do we have new markers?
Is it possible check the cancer along with glucose levels or insulin at the point of care or companion diagnostics?
Therapy
New Solutions in Therapies
ABRAXANE (paclitaxel formulated as albumin bound nanoparticles; nab-paclitaxel), in combination with gemcitabine, has been recommended for use within NHS Scotland by the Scottish Medicines Consortium (SMC) for the treatment of metastatic adenocarcinoma of the pancreas.
The SMC decision is based on results from the MPACT (Metastatic Pancreatic Adenocarcinoma Clinical Trial) study, published in the October 2013 edition of the New England Journal of Medicine, which demonstrated an increase in median overall survival of 1.8 months when compared to gemcitabine alone [(8.5 months vs. 6.7 months respectively) (HR 0.72; 95% CI 0.62 to 0.83 P<0.001)].
Updated results from post-hoc analysis of the MPACT trial based on an extended data cut-off (8 months) at the time the trial was closed demonstrated an increase in the median overall survival benefit of 2.1 months when compared to gemcitabine alone [(8.7 months vs. 6.6 months respectively) (HR 0.72,95% CI = 0.62 to 0.83, P<.001)].
Using radioactive bacteria to stop the spread of pancreatic cancer – scientists from Albert Einstein College of Medicine of Yeshiva University used bacteria to carry radioisotopes commonly used in cancer treatment directly into pancreatic cancer cells. They found in animal experiments that the incidence of secondary tumors went down dramatically – i.e. the cancer was much less likely to spread (metastasize).
Targeting stroma is another approached that is followed by TGen to potentially extend patient survival in all cases including advanced cases based on a report at Clinical Cancer Research, published online by the American Association for Cancer Research. Thus this eliminates one of the limiting factor to reach tumor cells and destroying the accumulation of stroma — the supporting connective tissue that includes hyaluronan and few other collagen types.
One of the study leaders, Andrew Biankin, a Cancer Research UK scientist at the University of Glasgow in the UK said that “Being able to identify which patients would benefit from platinum-based treatments would be a game-changing moment for treating pancreatic cancer, potentially improving survival for a group of patients.”
In the journal Nature, the international team- including scientists from Cancer Research UK showed the evidence of large chunks of DNA being shuffled around, which they were able to classify according to the type of disruption they created in chromosomes.
The study concludes there are four subtypes of pancreatic cancer, depending on the frequency, location and types of DNA rearrangement. It terms the subtypes: stable, locally rearranged, scattered and unstable.
Can we develop an immunotherapy?
Genetics of Pancreatic Cancer
There are many ongoing studies to develop diagnostics technologies and treatments. However, the etiology of PC is not well understood. Pancreas has dual functions that include 2% of endocrine hormone secretion and 98% exocrine secretion, enzymes, to help digestion. As a result, pancreatic cancer is related to obesity, overweight, diabetes.
First, eliminating the risk factors can be the simplest path. Next approach is dropping the obesity and diabetes to prevent the occurrence of cancers since in the U.S. population, 50 percent are overweight, 30 percent are medically obese and 10 percent have diabetes mellitus (DM). Tobacco smoking, alcohol consumptions, chronic pancreatitis, and genetic risk factors, have been recognized as potential risk factors for the development and progression of PC.
Many studies showed that the administration of anti-diabetic drugs such as metformin and thiazolidinediones (TZD) class of PPAR-γ agonists decreases the risk of cancers. Thus, these agents are thought to be the target to diagnose or cure PC.
Type 2 diabetes mellitus has been associated with an increased risk of several human cancers, such as liver, pancreatic, endometrial, colorectal, breast, and bladder cancer. The majority of the data show that metformin therapy decreases, while insulin secretagog drugs slightly increase the risk of certain types of cancers in type 2 diabetes.
Metformin can decrease cell proliferation and induce apoptosis in certain cancer cell lines. Endogenous and exogenous (therapy induced) hyperinsulinemia may be mitogenic and may increase the risk of cancer in type 2 diabetes. Type 2 diabetes mellitus accounts for more than 95% of the cases.
In PDA these cells have been reported to express specific genes such as Aldh1 or CD133. To date, more than 20 case-control studies and cohort and nested case-control studies with information on the association between diabetes and pancreatic cancer, BMI and cancer, and obesity and cancer have been reported.
Meta analysis and cohort studies:
- Meta studies for Diabetes and PC
Most of the diabetes and PC studies were included in two meta-analyses, in 1995 and in 2005, investigating the risk of pancreatic cancer in relation to diabetes.
The first meta-analysis, conducted in 1995, included 20 of these 40 published case-control and cohort studies and reported an overall estimated relative risk (RR) of pancreatic cancer of 2.1 with a 95% confidence interval (CI) of 1.6-2.8. These values were relatively unchanged when the analyses were restricted to patients who had diabetes for at least 5 years (RR, 2.0 [95% CI, 1.2-3.2]).
The second meta-analysis, which was conducted in 2005, included 17 case-control and 19 cohort and nested case-control studies published from 1996 to 2005 and demonstrated an overall odds ratio (OR) for pancreatic cancer of 1.8 and 95% CI of 1.7-1.9 . Individuals diagnosed with diabetes within 4 years before their pancreatic cancer diagnosis had a 50% greater risk of pancreatic cancer than did those diagnosed with diabetes more than 5 years before their cancer diagnosis (OR, 2.1 [95% CI, 1.9-2.3] versus OR, 1.5 [95% CI, 1.3-1.8]; P = 0.005).
- In a recent pooled analysis of 2192 patients with pancreatic cancer and 5113 cancer-free controls in three large case-control studies conducted in the United States (results of two of the three studies were published after 2005),
- Risk estimates decreased as the number of years with diabetes increased.
- Individuals with diabetes for 2 or fewer, 3-5, 6-10, 11-15, or more than 15 years had ORs (95% CIs) of 2.9 (2.1-3.9), 1.9 (1.3-2.6), 1.6 (1.2-2.3), 1.3 (0.9-2.0), and 1.4 (1.0-2.0), respectively (P < 0.0001 for trend).
- Meta Studies between BMI and PC
Meta studies in 2003 and 2008 showed a week positive association between BMI and PC. In 2003, a meta-analysis of six case-control and eight prospective studies including 6,391 PC cases 2% increase in risk per 1 kg/m2 increase in BMI. In 2008, 221 datasets, including 282,137 incidence of cancer cases with 3,338,001 subjects the results were similar RR, 1.12; CI, 1.02–1.22.
In 2007, 21 prospective studies handled , 10 were from the United States, 9 were from Europe, and 2 were from Asia and studies was conducted including 3,495,981 individuals and 8,062 PC cases. There was no significant difference between men and women and the estimated summary risk ratio (RR) per 5 kg/m2 increase in BMI was 1.12 (95% CI, 1.06–1.17) in men and women combined.
This study concluded that concluded that there was a positive association between BMI and risk of PC, per a 5 kg/m2 increase in BMI may be equal to a 12% increased risk of PC.
- The location and type of the obesity may also signal for a higher risk. The recent Women’s Health Initiative study in the United States among 138,503 postmenopausal showed that women central obesity in relation to PC (n=251) after average of 7.7 years of follow-up duration demonstrated that central adiposity is related to developing PC at a higher risk. Based on their result “women in the highest quintile of waist-to-hip ratio have a 70 percent (95% CI, 10–160%) greater risk of PC compared with women in the lowest quintile”
- Age of obesity or being overweight versus risk of developing PC was also examined.
- Regardless of their DM status they were at risk and decreased their survival even more so among men than women between age of 14-59.
overweight 14 to 39 years (highest odds ratio [OR], 1.67; 95% CI, 1.20–2.34) or
obese 20 to 49 years (highest OR, 2.58; 95% CI, 1.70–3.90) , independent of DM status.
- This association was different between men and women from the ages of 14 to 59:
stronger in men (adjusted OR, 1.80; 95% CI, 1.45–2.23)
weaker in women (adjusted OR, 1.32; 95% CI, 1.02–1.70).
- The effect of BMI , obesity and overweight had reduced overall survival of PC regardless of disease stage and tumor resection status
high BMI (= or > 25) 20 to 49 years , an earlier onset of PC by 2 to 6 years.
obese patients: hazard ratio, 1.86, 95% CI, 1.35–2.56).
overweight or obese 30 to 79 years, in the year prior to recruitment
overweight patients: hazard ratio, 1.26, 95% CI, 0.94–1.69;
Similarly, the authors concluded that:
- Being overweight or obese during early adulthood was associated with a greater risk of PC and a younger age of disease onset, whereas obesity at an older age was associated with a lower overall survival in patients diagnosed with PC.
- More recently, several large prospective cohort studies with a long duration of follow-up has been conducted in the U.S. showing a positive association between high BMI and the risk of PC (adjusted RR 1.13–1.54), suggesting the role of obesity and overweight with higher risk in the development and eventual death due to PC.
- Although the role of smoking and gender in the association of obesity and PC is not clear, the new evidence strongly supports a positive association of high BMI with increased risk of PC, consistent with the majority of early findings; however, all recent studies strongly suggest that obesity and overweight are independent risk factor of PC.
- Diabetes was associated with a 1.8-fold increase in risk of pancreatic cancer (95% CI, 1.5-2.1).
How pancreatic cancer is related to obesity, overweight, BMI, diabetes
Connections in Physiology and Pathology:
Altogether cumulative data suggest that DM has a three-fold increased risk for the development of PC and a two-fold risk for biliary cancer insulin resistance and abnormal glucose metabolism, even in the absence of diabetes, is associated with increased risk for the development of PC. Obesity alters the metabolism towards insulin resistance through affecting gene expression of inflammatory cytokines, adipose hormones such as adipokines, and PPAR-γ.
Furthermore, adiponectin also pointed out to be a negative link factor for cancers such as colon, breast, and PC. Therefore, insulin resistance is one of the earliest negative effects of obesity, early altered glucose metabolism, chronic inflammation, oxidative stress and decreased levels of adipose hormone adiponectin and PPAR-γ, key regulators for adipogenesis.
Potential pathways directly linking obesity and diabetes to pancreatic cancer. Obesity and diabetes cause mutiple alterations in glucose and lipid hemastasis, microenvironments, and immune responses, which result in the activation of several oncogenic signaling pathways.
These deregulations increase cell survival and proliferation, eventually leading to the development and progression of pancreatic cancer. ROS, reactive oxygen species; IGF-1, insulin-like growth factor-1; IR, insulin receptors; IGF-1R, insulin-like growth factor-1 receptors; TNFR, tumor necrosis factor receptors; TLR, Toll-like receptors; HIF-1α, hypoxia-inducible factor-α1; AMPK, AMP kinase; IKK, IκB kinase; PPAR-γ, peroxisome proliferator-activated receptor-γ; VEGF, vascular endothelial growth factor; MAPK, MAP kinase; mTOR, mammalian target of rapamycin; TSC, tuberous sclerosis complex; Akt, protein kinase B. PI3K, phosphoinositide-3-kinase; STAT3, activator of transcription-3; JNK, c-Jun NH2-terminal kinase.
Top six pathways interacting with obesity or diabetes in modifying the risk of pancreatic cancer are Chemokine Signaling, Pathways in cancer, Cytokine-cytokine receptor interaction, Calcium signaling pathway. MAPK signaling pathway.
This analysis showed
- GNGT2,
- RELA,
- TIAM1,
- CBLC,
- IFNA13,
- IL22RA1,
- IL2RA
- GNAS,
- MAP2K7,
- DAPK3,
- EPAS1 and
- FOS as contributor genes.
Furthermore, top overrepresented canonical pathways, including
- Role of RIG1-like Receptors in Antiviral Innate Immunity,
- Role of PI3K/AKT Signaling in the Pathogenesis of Influenza, and
- Molecular Mechanisms of Cancer
in genes interacting with risk factors (P < 10−8) are
- TRAF6,
- RELA,
- IFNA7,
- IFNA4,
- NFKB2,
- IFNA10,
- IFNA16,
- NFKB1,
- IFNA1/IFNA13,
- IFNA5,
- IFNA14,
- IFNA,
- GSK3B,
- IFNA16,
- IFNA14,
- TP53,
- FYN,
- ARHGEF4,
- GNAS,
- CYCS ,
- AXIN1,
- ADCY4,
- PRKAR2A,
- ARHGEF1 ,
- CDC42,
- RAC,3
- SIN3A,
- RB1,
- FOS ,
- CDH1,
- NFKBIA,
- GNAT1,
- PAK3,
- RHOA,
- RASGRP1,
- PIK3CD,
- BMP6,
- CHEK2, and
| KEGG code |
Pathway description |
Risk factor |
No. of genes/genes with marginal effecta |
No. of SNPs/eigenSNPs in the interaction analysisb |
PG x Ec |
Major contributing genesd |
| hsa04062e |
Chemokine Signalinge |
Obesity |
175/27 |
695/181 |
3.29 × 10−6 |
GNGT2 RELA TIAM1 |
| hsa05200 |
Pathways in cancer |
Obesity |
315/37 |
806/212 |
5.35 × 10−4 |
CBLC RELA |
| hsa04060 |
Cytokine-cytokine receptor interaction |
Obesity |
247/36 |
422/149 |
6.97 × 10−4 |
IFNA13 IL22RA1 IL2RA |
| hsa04020 |
Calcium signaling pathway |
Diabetes |
171/24 |
759/190 |
1.57 × 10−4 |
GNAS |
| hsa04010 |
MAPK signaling pathway |
Diabetes |
260/32 |
523/154 |
3.56 × 10−4 |
FOS MAP2K7 |
| hsa05200 |
Pathways in cancer |
Diabetes |
315/37 |
806/212 |
4.46 × 10−4 |
DAPK3 EPAS1 FOS |
aNumber of genes making up the pathway/ number of genes survived the PCA-LRT (P ≤ 0.10).
bNumber of SNPs in the “reconstructed” pathways/number of principal components for LRT.
cP value was estimated by LRT in logistic regression model with adjustment of age, sex, study site, pack years(continuous), obesity or diabetes as appropriate, and five principal components for population structure.
dGenes with PG x E ≤ 0.05 in logistic regression and P ≤ 0.10 in PCA-LRT.
ePathways remained significant after Bonferroni correction (P < 1.45 × 10−4)
Top overrepresented canonical pathways in genes interacting with risk factors (P < 10−8)
| Biological process |
Risk factor |
P Valuea |
Ratiob |
Contributing genes |
| Role of RIG1-like Receptors in Antiviral Innate Immunity |
Obesity |
6.71 × 10−11 |
12/49 (0.25) |
TRAF6 RELA IFNA7 IFNA4 NFKB2 IFNA10 IFNA16 NFKB1
IFNA1/IFNA13 IFNA5 IFNA14 IFNA6 |
| Role of PI3K/AKT Signaling in the Pathogenesis of Influenza |
Obesity |
8.64 × 10−9 |
12/74 (0.12) |
RELA IFNA7 IFNA4 NFKB2 GSK3B IFNA10 IFNA16 NFKB1
IFNA1/IFNA13 IFNA5 IFNA14 IFNA6 |
| Molecular Mechanisms of Cancer |
Diabetes |
1.03 × 10−9 |
24/378 (0.063) |
TP53 FYN ARHGEF4 GNAS CYCS AXIN1 ADCY4 PRKAR2A
ARHGEF1 CDC42 RAC3 SIN3A RB1 FOS CDH1 NFKBIA GNAT1
PAK3 RHOA RASGRP1 PIK3CD BMP6 CHEK2 E2F2 |
aCalculated using Fisher’s exact test (right-tailed).
bNumber of genes interacting with a risk factor of interest (P ≤ 0.05) in a given pathway divided by total number of genes making up that pathway.
Pancreatic Cancer and Diabetes:
We conclude that diabetes type II has a fundamental influence on pancreatic ductal adenocarcinoma by stimulating cancer cell proliferation, while metformin inhibits cancer cell proliferation. Chronic inflammation had only a minor effect on the pathophysiology of an established adenocarcinoma.
- Diabetes increases tumor size and proliferation of carcinoma cells
- Diabetes does not decrease cell death in carcinomas
- Diabetes II like syndrome reduces the number of Aldh1+cells within the tumor
- Metformin decreases tumor size and proliferation of carcinoma cells
Much is known about factors increasing the likelihood to develop PDA. Identified risk factors include among others chronic pancreatitis, long lasting diabetes, and obesity. Patients with chronic and especially hereditary pancreatitis have a very high relative risk of developing pancreatic cancer of 13.3 and 69.0, respectively. Patients with diabetes and obesity have a moderately increased relative risk of 1.8 and 1.3. These studies indicate that a substantial number of patients with PDA also suffer from local inflammation or diabetes.
http://www.biomedcentral.com/1471-2407/15/51/figure/F3?highres=y
http://www.biomedcentral.com/content/figures/s12885-015-1047-x-4.jpg
Potential mechanisms underlying the associations of diabetes and cancer.
- AdipoR1/R2, adiponectin receptor 1/2;
- AMPK, 5′-AMPactivated protein kinase;
- IGF-1, insulin-like growth factor-1;
- IGF-1R, insulin-like growth factor-1 receptor;
- IKK, IκA;B kinase; IR, insulin receptor;
- IRS-1, insulin receptor substrate-1;
- MAPK, mitogen-activated-protein-kinase;
- mTOR, mammalian target of rapamycin;
- NF-κA;B, nuclear factor-κA;B;
- ObR, leptin receptor;
- PAI-1, plasminogen activator inhibitor-1;
- PI3-K, phosphatidylinositol 3-kinase;
- ROS, Reactive oxygen species;
- TNF-α, tumor necrosis factor- α;
- TNF-R1, tumor necrosis factor-receptor 1;
- uPA, urokinase-type plasminogen activator;
- uPAR, urokinase-type plasminogen activator receptor;
- VEGF, vascular endothelial growth factor;
- VEGFR, vascular endothelial growth factor receptor.
http://www.ncbi.nlm.nih.gov/core/lw/2.0/html/tileshop_pmc/tileshop_pmc_inline.html?title=Click%20on%20image%20to%20zoom&p=PMC3&id=3238796_nihms-277874-f0001.jpg
Type 2 diabetes mellitus is likely the third modifiable risk factor for pancreatic cancer after cigarette smoking and obesity. The relationship between diabetes and pancreatic cancer is complex. Diabetes or impaired glucose tolerance is present in more than 2/3rd of pancreatic cancer patients.
Epidemiological investigations have found that long-term type 2 diabetes mellitus is associated with a 1.5-fold to 2.0-fold increase in the risk of pancreatic cancer. A causal relationship between diabetes and pancreatic cancer is also supported by findings from prediagnostic evaluations of glucose and insulin levels in prospective studies.
Insulin resistance and associated hyperglycemia, hyperinsulinemia, and inflammation have been suggested to be the underlying mechanisms contributing to development of diabetes-associated pancreatic cancer.
Stem Cells
http://www.ncbi.nlm.nih.gov/core/lw/2.0/html/tileshop_pmc/tileshop_pmc_inline.html?title=Click%20on%20image%20to%20zoom&p=PMC3&id=3410675_nihms295920f1.jpg
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3932318/
“A study by Permert et al.using glucose tolerance tests in patients with newly diagnosed pancreatic cancer showed that 75% of patients met criteria for diabetes. Pannala et al. used fasting blood glucose values or previous use of antidiabetic medications to define diabetes in patients with pancreatic cancer (N.=512) and age-matched control non-cancer subjects attending primary care clinics (N.=933) “
Distribution of fasting blood glucose among pancreatic cancer cases and controls. From Pannala et al.
“ They reported a nearly seven-fold higher prevalence of diabetes in pancreatic cancer patients compared to controls (47% vs. 7%). In a retrospective study using similar criteria, Chari et al. found the prevalence of diabetes in pancreatic cancer patients to be 40%. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3932318/”
Relationship between type 2 diabetes and risk of pancreatic cancer in case-control and nested case control studies. “Diamond: point estimate representing study-specific relative risks or summary relative risks with 95% CIs. Horizontal lines: represent 95% confidence intervals (CIs). Test for heterogeneity among studies: P<0.001, I2=93.6%. 1, cohort studies (N.=27) use incidence or mortality rate as the measurements of relative risk; 2, cohort studies (N.=8) use standardized incidence/mortality rate as the measurement of relative risk. From Benet al.”
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3932318/
Table II
Sensitivity and specificity for biomarkers for pancreatic cancer.
| Biomarker |
Study |
Sensitivity |
Specificity |
N. |
| CA19-9 |
Goonetilleke 68 |
79 |
82 |
Meta-analysis |
|
Steinberg 69 |
81 |
90 |
Meta-analysis |
| CA125 |
Duraker 85 |
57 |
78 |
123 |
|
Haguland 86 |
45 |
76 |
95 |
| CEA |
Ni 87 |
45 |
75 |
68 |
|
Haglund 86 |
54 |
76 |
95 |
|
Zhao 88 |
25 |
86 |
143 |
|
Duraker 85 |
39 |
91 |
123 |
| SPan-1 |
Kiriyama 74 |
81 |
76 |
64 |
|
Chung 89 |
92 |
83 |
67 |
|
Kobayashi 90 |
82 |
85 |
200 |
| Du-PAN 2 |
Satake 83 |
48 |
85 |
239 |
|
Sawabu 91 |
72 |
94 |
32 |
|
Kawa 92 |
64 |
– |
200 |
PART II: Targets for Immunomodulation to develop a therapy
Natural Killer Cells:
Natural Killer cells usually placed under non-specific immune response as a first defend mechanism during innate immunity. NKs responses to innate immune reactions but not only viruses but also bacteria and parasitic infections develop a new line of defense. These reactions involve amplification of many cytokines based on the specific infection or condition. Thus, these activities help NKs to evolve.
However, their functions proven to be more than innate immune response since from keeping the pregnancy term to prevent recurrent abortions to complex diseases such as cancer, diabetes and cardiovascular conditions they have roles thorough awakening chemokines and engaging them specifically with their receptors to activate other immune cells. For example, there is a signaling mechanism connection between NKs and DCs to respond attacks. Furthermore, there are interactions between various types of immune cells and they are specific for example between NK and Tregs.
During pregnancy there is a special kind of interaction between NK cells and Tregs.
- There can be several reasons such as to protect pregnancy from the immunosuppressive environment so then the successful implantation of the embryo and tolerance of the mother to the embryo can be established. In normal pregnancy, these cells are not killers, but rather provide a microenvironment that is pregnancy compatible and supports healthy placentation.
- During cancer development tumors want to build a microenvironment through an array of highly orchestrated immune elements to generate a new environment against the host. In normal pregnancy, decidua, the uterine endometrium, is critical for the development of placental vasculature.
- This is the region gets thicks and thin during female cycles to prevent or accept pregnancies. As a result, mother nature created that 70% of all human decidual lymphocytes are NK cells, defined as uterine or decidual NK (dNK) cells.
- The NK cell of decidua (dNK) and peripheral blood NK cells are different since dNK cells are characterized as CD56brightCD16−CD3−, express killer cell immunoglobulin-like receptors and exhibit low killing capacity despite the presence of cytolytic granules, and a higher frequency of CD4+CD25bright
The lesson learn here is that pregnancy and mammary tissue are great examples of controlling cellular differentiation and growth since after pregnancy all these cells go back to normal state.
Understanding these minute differences and relations to manipulate gene expression may help to:
- Develop better biomaterials to design long lasting medical devices and to deliver vaccines without side effects.
- Generate safer vaccines as NKcells are the secret weapons in DC vaccination and studying their behavior together with T-cell activation in vaccinated individuals might predict clinical outcome.
- Establish immunotherapies based on interactions between NK cells and Tregs for complex diseases not only cancer, but also many more such as autoimmune disorder, transplants, cardiovascular, diabetes.
Trascription factors are the silence players of the gene expression that matches input to output as a cellular response either good or bad but this can be monitored and corrected with a proper meical device or diagnostics tool to provide successful treatment regimen.
- Therefore, the effects of Tregs on NK during gene regulation analyzed and compared among other living organisms for concerved as well as signature sequence targets even though the study is on human.
- Unfortunatelly we can’t mutate the human for experimental purposes so comparative developmental studies now its widely called stem cell biology with a system biology approach may help to establish the pathway.
NK and T reg regulation share a common interest called T box proteins. These proteins are conserved and also play role in development of heart at very early development, embryology. What is shared among all T-box is simply lie behind the capacity for DNA binding through the T-box domain and transcriptional regulatory activity, which plays a role in controlling the expression of developmental gene in all animal species.
The Special T box protein: T-bet
The first identified T-box protein was Brachyury (T). in a nut shell
- The T-box domain is made up of about 180 amino-acid residues that includes a specific sequence of DNA
- called T-box domain, TCACACCT between residues 135 and 326 in mouse.
- However, T-bet which is the T-box protein expressed in T cells and also called as TBX21 is quite conserved in 18 members of the T-box protein (TBX) family
- since it has a crucial dual role during development and for coordination of both innate and adaptive immune responses.
T-Bet was originally cloned for its role in Th1 lineage, it has a role in Th2 development, too.
The whole mechanism based on direct activation and modulation mechanisms in that T-Bet directly activates IFN-γ gene transcription and enhances development of Th1 cells at the same time modulates IL-2 and Th2 cytokines in an IFN-γ-independent manner that creates an attenuation of Th2 cell development.
Thus, certain lipids ligands or markers can be utilized during vaccine design to steer the responses for immune therapies against autoimmune diseases. As a result, tumors can be removed and defeated by manipulating NKs action.
INKT:
NKT has functions in diabetes, asthma. One cell type that has been proposed to contribute immensely to the development of asthma is NKT cells, which constitute a small population of lymphocytes that express markers of both T cells (T-cell receptor, TCR) and NK cells (e.g., NK1.1, NKG2D). NKT cells can be subdivided into at least three subtypes, based on their TCR. Type I NKT cells or invariant NKT (iNKT) cells express invariant TCR chains (V14–J18 in mice and V24–J18 in humans) coupled with a limited repertoire of V chains (V8, V7 and V2 in mice and V11 in humans).
The studies in the past decade showed the protective mechanism of NKT cells during the development of Type 1 diabetes can be complex.
- First, NKT cells can impair the differentiation of anti-islet reactive T cells into Th1 effector cells in a cell–cell contact dependent manner, which did not require Th2 cytokine production or CD1d recognition.
- Second, NKT cells accumulating in the pancreas can indirectly suppress diabetogenic CD4+T cells via IFN-γ production.
- Last, anergic iNKT cells induced by protracted αGalCer stimulation can induce the production of noninflammatory DCs, which inhibit diabetes development in an Ag-specific fashion.
These findings point to an important protective role for NKT cells during autoimmune pathogenesis in the pancreas.
A crucial role has been suggested for invariant natural killer T cells (iNKT) in regulating the development of asthma, a complex and heterogeneous disease characterized by airway inflammation and airway hyperreactivity (AHR).
iNKT cells constitute a unique subset of T cells responding to endogenous and exogenous lipid antigens, rapidly secreting a large amount of cytokines, which amplify both innate and adaptive immunity.
IL17:
Terashima A et al (2008) identified a novel subset of natural killer T (NKT) cells that expresses the interleukin 17 receptor B (IL-17RB) for IL-25 (also known as IL-17E) and is essential for the induction of Airway hypersensitive reaction (AHR). IL-17RB is preferentially expressed on a fraction of CD4(+) NKT cells but not on other splenic leukocyte populations tested.
They strongly suggested that IL-17RB(+) CD4(+) NKT cells play a crucial role in the pathogenesis of asthma.
NKT connection can be established between through targeting IL17 and IL17RB. There is a functional specialization of interleukin-17 family members. Interleukin-17A (IL-17A) is the signature cytokine of the recently identified T helper 17 (Th17) cell subset. IL-17 has six family members (IL-17A to IL-17F).
Although IL-17A and IL-17F share the highest amino acid sequence homology, they perform distinct functions; IL-17A is involved in the development of autoimmunity, inflammation, and tumors, and also plays important roles in the host defenses against bacterial and fungal infections, whereas IL-17F is mainly involved in mucosal host defense mechanisms. IL-17E (IL-25) is an amplifier of Th2 immune responses.
There is no one easy answer for the role of IL-17 in pancreatic cancer as there are a number of unresolved issues and but it can be only suggested that pro-tumorigenic IL-17 activity is confined to specific subsets of patients with pancreatic cancer since there is a increased expression of IL-17RB in these patients about ∼40% of pancreatic cancers presented on their histochemical staining (IHC- immunohistochemistry.
IL17 and breast cancer:
In addition, during breast cancer there is an increased signaling of interleukin-17 receptor B (IL-17RB) and IL-17B. They promoted tumor formation in breast cancer cells in vivo and even created acinus formation in immortalized normal mammary epithelial cells in vitro cell culture assays.
- Furthermore, the elevated expression of IL-17RB not only present itself stronger than HER2 for a better prognosis but also brings the shortest survival rate if patients have increased IL-17RB and HER2 levels.
- However, decreased level of IL-17RB in trastuzumab-resistant breast cancer cells significantly reduced their tumor growth. This may prompt a different independent role for IL-17RB and HER2 in breast cancer development.
- In addition, treatment with antibodies specifically against IL-17RB or IL-17B effectively attenuated tumorigenicity of breast cancer cells.
These results suggest that the amplified IL-17RB/IL-17B signaling pathways may serve as a therapeutic target for developing treatment to manage IL-17RB-associated breast cancer.
IL 17 and Asthma:
A requirement for iNKT cells has also been shown in a model of asthma induced with air pollution, ozone and induced with respiratory viruses chronic asthma studied in detail. In these studies specific types of NKT cells found to that specific types of NK and receptors trigger of asthma symptoms. Taken together, these studies indicate that both Th2 cells (necessary for allergen-specific responses) and iNKT cells producing IL-4 and IL-13 are required for the development of allergen-induced AHR.
Although CD4+ IL-4/IL-13-producing iNKT cells (in concert with antigen-specific Th2 cells) are crucial in allergen-induced AHR, NK1.1–IL-17-producing iNKT cells have a major role in ozone-induced AHR.
A main question in iNKT cell biology involves the identification of lipid antigens that can activate iNKT cells since this allow to identify which microorganisms to attack as a result, the list of microorganisms that produce lipids that activate iNKT cells is rapidly growing.
Invariant natural killer T cells (iNKT) cell function in airway hyperreactivity (AHR). iNKT cells secrete various cytokines, including Th2 cytokines, which have direct effects on hematopoietic cells, airway smooth muscle cells, and goblet cells. Alternatively, iNKT cells could regulate other cell types that are known to be involved in asthma pathogenesis, e.g., neutrophils and alveolar macrophages.
http://www.nature.com/mi/journal/v2/n5/images/mi200996f1.jpg
Chemokines:
Chemokines have a crucial role in organogenesis of various organs including lymph nodes, arising from their key roles in stem cell migration. Moreover, most homeostatic chemokines can control the movement of lymphocytes and dendritic cells and eventually adaptive immunity. Chemokines are heparin-binding proteins with 4 cysteine residues in the conserved positions.
The human chemokine system has about 48 chemokines. They are subgrouped based on:
- Number of cysteines
- Number of amino acid separating cysteines
- Presence or absence of ELR motif includes, 3-amino acid sequence, glutamic acid-leucine-arginine
- functionally classified as inflammatory, homeostatic, or both, based on their expression patterns
Chemokines are structurally divided into 4 subgroups :CXC, CC, CX3C, and C. X represent an aminoacid so the first 2 cysteines are separated by 1 is grouped as CXC and 3 amino acids is called CX3C chemokines but in CC the first 2 cysteines are adjacent. In the C chemokines there is no second and fourth cysteines.
Various types of inflammatory stimuli induce abundantly the expression of inflammatory chemokines to induce the infiltration of inflammatory cells such as granulocytes and monocytes/macrophages.
- inflammatory chemokines are CXC chemokines with ELR motif and CCL2.
- homeostatic chemokines are expressed constitutively in specific tissues or cells.
Chemokines exert their biological activities by binding their corresponding receptors, which belong to G-protein coupled receptor (GPCR) with 7-span transmembrane portions. Thus, the target cell specificity of each chemokine is determined by the expression pattern of its cognate receptor .
Moreover, chemokines can bind to proteoglycans and glycosaminoglycans with a high avidity, because the carboxyl-terminal region is capable of binding heparin.
Consequently, most chemokines are produced as secretory proteins, but upon their secretion, they are immobilized on endothelium cells and/or in extracellular matrix by interacting with proteoglycans and glycosaminoglycans. The immobilization facilitates the generation of a concentration gradient, which is important for inducing the target cells to migrate in a directed way.
The human chemokine system.
| Chemokine receptor |
Chemokines |
Receptor expression in |
| Leukocytes |
Epithelium |
Endothelium |
| CXCR1 |
CXCL6, 8 |
PMN |
+ |
− |
| CXCR2 |
CXCL1, 2, 3, 5, 6, 7, 8 |
PMN |
+ |
+ |
| CXCR3 |
CXCL4, 9, 10, 11 |
Th1, NK |
− |
+ |
| CXCR4 |
CXCL12 |
Widespread |
+ |
+ |
| CXCR5 |
CXCL13 |
B |
− |
− |
| CXCR6 |
CXCL16 |
Activated T |
+ |
− |
| CXCR7 (ACKR3) |
CXCL12, CXCL11 |
Widespread |
+ |
+ |
| Unknown |
CXCL14 (acts on monocytes) |
|
|
|
| CCR1 |
CCL3, 4, 5, 7, 14, 15, 16, 23 |
Mo, Mϕ, iDC, NK |
+ |
+ |
| CCR2 |
CCL2, 7, 8, 12, 13 |
Mo, Mϕ, iDC, NK
activated T, B |
+ |
+ |
| CCR3 |
CCL5, 7, 11, 13, 15, 24, 26, 28 |
Eo, Ba, Th2 |
− |
+ |
| CCR4 |
CCL2, 3, 5, 17, 22 |
iDC, Th2, NK, T, Mϕ |
− |
− |
| CCR5 |
CCL3, 4, 5, 8 |
Mo, Mϕ, NK, Th1
activated T |
+ |
− |
| CCR6 |
CCL20 |
iDC, activated T, B |
+ |
− |
| CCR7 |
CCL19, 21 |
mDC, Mϕ, naïve T
activated T |
+ |
− |
| CCR8 |
CCL1, 4, 17 |
Mo, iDC, Th2, Treg |
− |
− |
| CCR9 |
CCL25 |
T |
+ |
− |
| CCR10 |
CCL27, 28 |
Activated T, Treg |
+ |
− |
| Unknown |
CCL18 (acts on mDC and naïve T) |
|
|
|
| CX3CR1 |
CX3CL1 |
Mo, iDC, NK, Th1 |
+ |
− |
| XCR1 |
XCL1, 2 |
T, NK |
− |
− |
| Miscellaneous |
Scavenger receptors for chemokines |
|
|
|
| Duffy antigen (ACKR1) |
CCL2, 5, 11, 13, 14 |
|
|
|
|
CXCL1, 2, 3, 7, 8 |
|
|
|
| D6 (ACKR2) |
CCL2, 3, 4, 5, 7, 8, 12 |
|
|
|
|
CCL13, 14, 17, 22 |
|
|
|
| CCRRL1 (ACKR4) |
CCL19, CCL21, CCL25 |
|
|
|
Leukocyte anonyms are as follows. Ba: basophil, Eo: eosinophil, iDC: immature dendritic cell, mDC: mature dendritic cell, Mo: monocyte, Mϕ: macrophage, NK: natural killer cell, Th1: type I helper T cell, Th2: type II helper T cell, and Treg: regulatory T cell.
There are differences between human liver and peripheral NK cells. Regulation of NK cell functions by CD226, CD96 and TIGIT.close. CD226 binding to CD155 or CD112 at the cell surface of transformed or infected cells triggers cytotoxic granule exocytosis and target cell lysis by natural killer (NK) cells. TIGIT, CD226, CD96 and CRTAM ligand specificity and signalling.close.
Regulation of NK cell-mediated cancer immunosurveillance through CD155 expression.close. CD155 is frequently overexpressed by cancer cells.
pc10
|
Liver NK cells |
Circulating NK cells |
References |
| CD3-CD56+ |
30.6% (11.6–51.3%) |
12.8% (1–22%) |
17 |
| CD56bright/total NK cell |
~50% |
~10% |
18,19 |
| CD56dim/total NK cell |
~50% |
~90% |
18,19 |
| CD27 |
high |
low |
20,21 |
| CD16 |
− |
+ |
18,22 |
| CD69 |
+/−, higher |
+/− |
16 |
| Chemokine receptor |
CCR7 and CXCR3
(CD56bright) |
CXCR1, CX3CR1
(CD56dim) |
13,23 |
| Inhibitory receptor (NKG2A) |
high |
low |
24 |
| Natural cytotoxicity |
higher |
high |
18,19 |
| TRAIL |
high |
low |
1 |
| Perforin, Granzyme B |
high |
low |
2 |
| Cytokine production |
high
(MIP-1α/β, IL-10,
TNF-α, TNF-β, IFN-γ,
GM-CSF) |
low
(TNF-α, TNF-β, IFN-γ,
GM-CSF, IL-10) |
18 |
| ADCC |
– |
high |
25 |
- In conclusion, having to develop precise early diagnostics is about determining the overlapping genes as key among diabetes, obesity, overweight and pancreas functions even pregnancy can be suggested.
- It seems feasible to develop an immunotherapy for pancreatic cancer with the focus on chemokines and primary signaling between iNKT and Tregs such as one of the recent plausable target IL-17 and IL17 RB.
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Chan, C. J., Smyth, M. J. & Martinet, L. Molecular mechanisms of natural killer cell activation in response to cellular stress. Cell Death Differ. 21, 5–14 (2014).
Li, M. et al. T-cell immunoglobulin and ITIM domain (TIGIT) receptor/poliovirus receptor (PVR) ligand engagement suppresses interferon-γ production of natural killer cells via β-arrestin 2-mediated negative signaling. J. Biol. Chem. 289, 17647–17657 (2014).
Guma, M. et al. Imprint of human cytomegalovirus infection on the NK cell receptor repertoire. Blood 104, 3664–3671 (2004).
Sharma S. Natural killer cells and regulatory T cells in early pregnancy loss.
Int J Dev Biol. 2014;58(2-4):219-29. doi: 10.1387/ijdb.140109ss. Review.
Mukaida N, Sasaki S, Baba T. Chemokines in cancer development and progression and their potential as targeting molecules for cancer treatment. Mediators Inflamm. 2014;2014:170381. doi: 10.1155/2014/170381. Epub 2014 May 22. Review.
Van Elssen CH, Oth T, Germeraad WT, Bos GM, Vanderlocht J. Natural killer cells: the secret weapon in dendritic cell vaccination strategies.Clin Cancer Res. 2014 Mar 1;20(5):1095-103. doi: 10.1158/1078-0432.CCR-13-2302. Review.
Gardner AB, Lee SK, Woods EC, Acharya AP. Biomaterials-based modulation of the immune system. Biomed Res Int. 2013;2013:732182. doi: 10.1155/2013/732182. Epub 2013 Sep 22. Review.
Pedroza-Pacheco I, Madrigal A, Saudemont A. Interaction between natural killer cells and regulatory T cells: perspectives for immunotherapy. Cell Mol Immunol. 2013 May;10(3):222-9. doi: 10.1038/cmi.2013.2. Epub 2013 Mar 25. Review.
Lindau D, Gielen P, Kroesen M, Wesseling P, Adema GJ. The immunosuppressive tumour network: myeloid-derived suppressor cells, regulatory T cells and natural killer T cells. Immunology. 2013 Feb;138(2):105-15. doi: 10.1111/imm.12036. Review.
Tian Z, Chen Y, Gao B.Natural killer cells in liver disease. Hepatology. 2013 Apr;57(4):1654-62. doi: 10.1002/hep.26115. Review.
Joyce S, Girardi E, Zajonc DM. J NKT cell ligand recognition logic: molecular basis for a synaptic duet and transmission of inflammatory effectors. Immunol. 2011 Aug 1;187(3):1081-9. doi: 0.4049/jimmunol.1001910. Review.
Diana J, Gahzarian L, Simoni Y, Lehuen A. Innate immunity in type 1 diabetes. Discov Med. 2011 Jun;11(61):513-20. Review.
Wu L, Van Kaer L.Natural killer T cells in health and disease. Front Biosci (Schol Ed). 2011 Jan 1;3:236-51. Review.
Cantorna MT. Why do T cells express the vitamin D receptor? Ann N Y Acad Sci. 2011 Jan;1217:77-82. doi: 10.1111/j.1749-6632.2010.05823.x. Epub 2010 Nov 29. Review.
Key Papers:
These papers, Gilfian et all and Iguchi-Manaka et al, were the first to show the role of CD226 in NK cell- and CD8+ T cell-mediated tumour immunosurveillance using Cd226−/− mice.
- Gilfillan, S.et al. DNAM-1 promotes activation of cytotoxic lymphocytes by nonprofessional antigen-presenting cells and tumors. J. Exp. Med. 205, 2965–2973 (2008).
- Iguchi-Manaka, A.et al. Accelerated tumor growth in mice deficient in DNAM-1 receptor. Exp. Med. 205, 2959–2964 (2008).
Johnston, R. J. et al. The immunoreceptor TIGIT regulates antitumor and antiviral CD8+ T cell effector function. Cancer Cell 26, 923–937 (2014).
This study shows that TIGIT is expressed by PD1+ exhausted tumour-infiltrating T cells and that targeting these receptors with monoclonal antibodies represents a promising strategy to restore CD8+ T cell functions in cancer or in chronic infectious disease.
Khakoo, S. I. et al. HLA and NK cell inhibitory receptor genes in resolving hepatitis C virus infection. Science 305, 872–874 (2004).
Fang, M. et al. CD94 is essential for NK cell-mediated resistance to a lethal viral disease.Immunity 34, 579–589 (2011).
This study using CD94-deficient mice shows that the activating receptor formed by CD94 and NKG2E is essential for the resistance of C57BL/6 mice to mousepox.
Pradeu, T., Jaeger, S. & Vivier, E. The speed of change: towards a discontinuity theory of immunity? Nature Rev. Immunol. 13, 764–769 (2013).
This is an outstanding review on the formulation of a new immune paradigm ‘the discontinuity theory’
Further Reading:
| Vol 13, No 4 (2012): July – p. 330-469 |
Molecular Biology of Pancreatic Cancer: How Useful Is It in Clinical Practice? |
ABSTRACT HTML PDF |
| George H Sakorafas, Vasileios Smyrniotis |
|
| Vol 13, No 4 (2012): July – p. 330-469 |
Endoscopic Findings of Upper Gastrointestinal Lesions in Patients with Pancreatic Cancer |
ABSTRACT HTML PDF |
| Koushiro Ohtsubo, Hiroyuki Watanabe, Hisatsugu Mouri, Kaname Yamashita, Kazuo Yasumoto, Seiji Yano |
|
| Vol 13, No 5 (2012): September – p. 470-547 |
Two Avirulent, Lentogenic Strains of Newcastle Disease Virus Are Cytotoxic for Some Human Pancreatic Tumor Lines In Vitro |
ABSTRACT HTML PDF |
| Robert J Walter, Bashar M Attar, Asad Rafiq, Megan Delimata, Sooraj Tejaswi |
|
| Vol 14, No 3 (2013): May – p. 221-303 |
Duration of Diabetes and Pancreatic Cancer in a Case-Control Study in the Midwest and the Iowa Women’s Health Study (IWHS) Cohort |
ABSTRACT HTML PDF |
| Sarah A Henry, Anna E Prizment, Kristin E Anderson |
|
| Vol 16, No 1 (2015): January – p. 1-99 |
Endoscopic Management of Pain in Pancreatic Cancer |
ABSTRACT HTML PDF |
| Parit Mekaroonkamol, Field F Willingham, Saurabh Chawla |
|
| Vol 14, No 2 (2013): March – p. 109-220 |
Advancements in the Management of Pancreatic Cancer: 2013 |
ABSTRACT HTML PDF |
| Muhammad Wasif Saif |
|
| Vol 15, No 5 (2014): September – p. 413-540 |
New-onset Diabetes: A Clue to the Early Diagnosis of Pancreatic Cancer |
ABSTRACT HTML PDF |
| Suresh T Chari |
|
| Vol 13, No 5 (2012): September – p. 470-547 |
Effects of Porcine Pancreatic Enzymes on the Pancreas of Hamsters. Part 2: Carcinogenesis Studies |
ABSTRACT HTML PDF |
| Fumiaki Nozawa, Mehmet Yalniz, Murat Saruc, Jens Standop, Hiroshi Egami, Parviz M Pour |
|
| Vol 14, No 5 (2013): September – p. 475-527 |
Synchronous Triple Cancers of the Pancreas, Stomach, and Cecum Treated with S-1 Followed by Pancrelipase Treatment of Pancreatic Exocrine Insufficiency |
ABSTRACT HTML PDF |
| Koushiro Ohtsubo, Daisuke Ishikawa, Shigeki Nanjo, Shinji Takeuchi, Tadaaki Yamada, Hisatsugu Mouri, Kaname Yamashita, Kazuo Yasumoto, Toshifumi Gabata, Osamu Matsui, Hiroko Ikeda, Yasushi Takamatsu, Sakae Iwakami, Seiji Yano |
|
| Vol 13, No 1 (2012): January – p. 1-123 |
Newcastle Disease Virus LaSota Strain Kills Human Pancreatic Cancer Cells in Vitro with High Selectivity |
ABSTRACT HTML PDF |
| Robert J Walter, Bashar M Attar, Asad Rafiq, Sooraj Tejaswi, Megan Delimata |
|
| Vol 13, No 3 (2012): May – p. 252-329 |
Rare Solid Tumors of the Pancreas as Differential Diagnosis of Pancreatic Adenocarcinoma |
ABSTRACT HTML PDF |
| Sabine Kersting, Monika S Janot, Johanna Munding, Dominique Suelberg, Andrea Tannapfel, Ansgar M Chromik, Waldemar Uhl, Uwe Bergmann |
|
| Vol 14, No 4 (2013): July – p. 304-474 |
A Proteomic Comparison of Formalin-Fixed Paraffin-Embedded Pancreatic Tissue from Autoimmune Pancreatitis, Chronic Pancreatitis, and Pancreatic Cancer |
ABSTRACT HTML PDF SUPPL. TABLES 1-4 (PDF) |
| Joao A Paulo, Vivek Kadiyala, Scott Brizard, Peter A Banks, Hanno Steen, Darwin L Conwell |
|
| Vol 13, No 4 (2012): July – p. 330-469 |
Highlights on the First Line Treatment of Metastatic Pancreatic Cancer |
ABSTRACT HTML PDF |
| Krishna S Gunturu, Jamie Jarboe, Muhammad Wasif Saif |
|
| Vol 14, No 2 (2013): March – p. 109-220 |
Pancreatic Cancer: Updates on Translational Research and Future Applications |
ABSTRACT HTML PDF |
| Evangelos G Sarris, Konstantinos N Syrigos, Muhammad Wasif Saif |
|
| Vol 14, No 4 (2013): July – p. 304-474 |
Pancreatic Cancer: What About Screening and Detection? |
ABSTRACT HTML PDF |
| Froso Konstantinou, Kostas N Syrigos, Muhammad Wasif Saif |
|
| Vol 14, No 4 (2013): July – p. 304-474 |
Diabetes and Pancreatic Cancer |
ABSTRACT HTML PDF |
| Najla Hatem El-Jurdi, Muhammad Wasif Saif |
|
| Vol 13, No 5 (2012): September – p. 470-547 |
Effects of Porcine Pancreatic Enzymes on the Pancreas of Hamsters. Part 1: Basic Studies |
ABSTRACT HTML PDF |
| Murat Saruc, Fumiaki Nozawa, Mehmet Yalniz, Atsushi Itami, Parviz M Pour |
|
| Vol 14, No 2 (2013): March – p. 109-220 |
Analysis of Endoscopic Pancreatic Function Test (ePFT)-Collected Pancreatic Fluid Proteins Precipitated Via Ultracentrifugation |
ABSTRACT HTML PDF SUPPL.(XLS) SUPPL.(PDF) |
| Joao A Paulo, Vivek Kadiyala, Aleksandr Gaun, John F K Sauld, Ali Ghoulidi, Peter A Banks, Hanno Steen, Darwin L Conwell |
|
| Vol 16, No 1 (2015): January – p. 1-99 |
Regulation Mechanisms of the Hedgehog Pathway in Pancreatic Cancer: A Review |
ABSTRACT HTML PDF |
| Kim Christin Honselmann, Moritz Pross, Carlo Maria Felix Jung, Ulrich Friedrich Wellner, Steffen Deichmann, Tobias Keck, Dirk Bausch |
|
| Vol 14, No 5S (2013): September (Suppl.) – p. 528-602 |
History of Previous Cancer in Patients Undergoing Resection for Pancreatic Adenocarcinoma |
ABSTRACT PDF |
| Francesca Gavazzi, Maria Rachele Angiolini, Cristina Ridolfi, Maria Carla Tinti, Marco Madonini, Marco Montorsi, Alessandro Zerbi |
|
| Vol 13, No 4 (2012): July – p. 330-469 |
Molecular Biology of Pancreatic Cancer: How Useful Is It in Clinical Practice? |
ABSTRACT HTML PDF |
| George H Sakorafas, Vasileios Smyrniotis |
|
| Vol 13, No 4 (2012): July – p. 330-469 |
Endoscopic Findings of Upper Gastrointestinal Lesions in Patients with Pancreatic Cancer |
ABSTRACT HTML PDF |
| Koushiro Ohtsubo, Hiroyuki Watanabe, Hisatsugu Mouri, Kaname Yamashita, Kazuo Yasumoto, Seiji Yano |
|
| Vol 13, No 5 (2012): September – p. 470-547 |
Two Avirulent, Lentogenic Strains of Newcastle Disease Virus Are Cytotoxic for Some Human Pancreatic Tumor Lines In Vitro |
ABSTRACT HTML PDF |
| Robert J Walter, Bashar M Attar, Asad Rafiq, Megan Delimata, Sooraj Tejaswi |
|
| Vol 14, No 3 (2013): May – p. 221-303 |
Duration of Diabetes and Pancreatic Cancer in a Case-Control Study in the Midwest and the Iowa Women’s Health Study (IWHS) Cohort |
ABSTRACT HTML PDF |
| Sarah A Henry, Anna E Prizment, Kristin E Anderson |
|
| Vol 16, No 1 (2015): January – p. 1-99 |
Endoscopic Management of Pain in Pancreatic Cancer |
ABSTRACT HTML PDF |
| Parit Mekaroonkamol, Field F Willingham, Saurabh Chawla |
|
| Vol 14, No 2 (2013): March – p. 109-220 |
Advancements in the Management of Pancreatic Cancer: 2013 |
ABSTRACT HTML PDF |
| Muhammad Wasif Saif |
|
| Vol 15, No 5 (2014): September – p. 413-540 |
New-onset Diabetes: A Clue to the Early Diagnosis of Pancreatic Cancer |
ABSTRACT HTML PDF |
| Suresh T Chari |
|
| Vol 13, No 5 (2012): September – p. 470-547 |
Effects of Porcine Pancreatic Enzymes on the Pancreas of Hamsters. Part 2: Carcinogenesis Studies |
ABSTRACT HTML PDF |
| Fumiaki Nozawa, Mehmet Yalniz, Murat Saruc, Jens Standop, Hiroshi Egami, Parviz M Pour |
|
| Vol 14, No 5 (2013): September – p. 475-527 |
Synchronous Triple Cancers of the Pancreas, Stomach, and Cecum Treated with S-1 Followed by Pancrelipase Treatment of Pancreatic Exocrine Insufficiency |
ABSTRACT HTML PDF |
| Koushiro Ohtsubo, Daisuke Ishikawa, Shigeki Nanjo, Shinji Takeuchi, Tadaaki Yamada, Hisatsugu Mouri, Kaname Yamashita, Kazuo Yasumoto, Toshifumi Gabata, Osamu Matsui, Hiroko Ikeda, Yasushi Takamatsu, Sakae Iwakami, Seiji Yano |
|
| Vol 13, No 1 (2012): January – p. 1-123 |
Newcastle Disease Virus LaSota Strain Kills Human Pancreatic Cancer Cells in Vitro with High Selectivity |
ABSTRACT HTML PDF |
| Robert J Walter, Bashar M Attar, Asad Rafiq, Sooraj Tejaswi, Megan Delimata |
|
| Vol 13, No 3 (2012): May – p. 252-329 |
Rare Solid Tumors of the Pancreas as Differential Diagnosis of Pancreatic Adenocarcinoma |
ABSTRACT HTML PDF |
| Sabine Kersting, Monika S Janot, Johanna Munding, Dominique Suelberg, Andrea Tannapfel, Ansgar M Chromik, Waldemar Uhl, Uwe Bergmann |
|
| Vol 14, No 4 (2013): July – p. 304-474 |
A Proteomic Comparison of Formalin-Fixed Paraffin-Embedded Pancreatic Tissue from Autoimmune Pancreatitis, Chronic Pancreatitis, and Pancreatic Cancer |
ABSTRACT HTML PDF SUPPL. TABLES 1-4 (PDF) |
| Joao A Paulo, Vivek Kadiyala, Scott Brizard, Peter A Banks, Hanno Steen, Darwin L Conwell |
|
| Vol 13, No 4 (2012): July – p. 330-469 |
Highlights on the First Line Treatment of Metastatic Pancreatic Cancer |
ABSTRACT HTML PDF |
| Krishna S Gunturu, Jamie Jarboe, Muhammad Wasif Saif |
|
| Vol 14, No 2 (2013): March – p. 109-220 |
Pancreatic Cancer: Updates on Translational Research and Future Applications |
ABSTRACT HTML PDF |
| Evangelos G Sarris, Konstantinos N Syrigos, Muhammad Wasif Saif |
|
| Vol 14, No 4 (2013): July – p. 304-474 |
Pancreatic Cancer: What About Screening and Detection? |
ABSTRACT HTML PDF |
| Froso Konstantinou, Kostas N Syrigos, Muhammad Wasif Saif |
|
| Vol 14, No 4 (2013): July – p. 304-474 |
Diabetes and Pancreatic Cancer |
ABSTRACT HTML PDF |
| Najla Hatem El-Jurdi, Muhammad Wasif Saif |
|
| Vol 13, No 5 (2012): September – p. 470-547 |
Effects of Porcine Pancreatic Enzymes on the Pancreas of Hamsters. Part 1: Basic Studies |
ABSTRACT HTML PDF |
| Murat Saruc, Fumiaki Nozawa, Mehmet Yalniz, Atsushi Itami, Parviz M Pour |
|
| Vol 14, No 2 (2013): March – p. 109-220 |
Analysis of Endoscopic Pancreatic Function Test (ePFT)-Collected Pancreatic Fluid Proteins Precipitated Via Ultracentrifugation |
ABSTRACT HTML PDF SUPPL.(XLS) SUPPL.(PDF) |
| Joao A Paulo, Vivek Kadiyala, Aleksandr Gaun, John F K Sauld, Ali Ghoulidi, Peter A Banks, Hanno Steen, Darwin L Conwell |
|
| Vol 16, No 1 (2015): January – p. 1-99 |
Regulation Mechanisms of the Hedgehog Pathway in Pancreatic Cancer: A Review |
ABSTRACT HTML PDF |
| Kim Christin Honselmann, Moritz Pross, Carlo Maria Felix Jung, Ulrich Friedrich Wellner, Steffen Deichmann, Tobias Keck, Dirk Bausch |
|
| Vol 14, No 5S (2013): September (Suppl.) – p. 528-602 |
History of Previous Cancer in Patients Undergoing Resection for Pancreatic Adenocarcinoma |
ABSTRACT PDF |
| Francesca Gavazzi, Maria Rachele Angiolini, Cristina Ridolfi, Maria Carla Tinti, Marco Madonini, Marco Montorsi, Alessandro Zerbi |
Patents
http://www.uspto.gov/web/patents/patog/week10/OG/html/1412-2/US08974784-20150310.html
Anti-pancreatic cancer antibodies: David M. Goldenberg, Mendham, NJ (US); Hans J. Hansen, Picayune, MS (US); Chien-Hsing Chang, Downingtown, PA (US); …
http://www.uspto.gov/web/patents/patog/week42/OG/html/1407-3/US08865413-20141021.html
A method of diagnosing pancreatic cancer in a human, the method comprising detecting the level of golgi apparatus protein 1 in a sample from the …
http://www.uspto.gov/web/patents/patog/week10/OG/html/1412-2/US08974802-20150310.html
A method for the treatment of pancreatic cancer, which comprises the administration to a human patient with pancreatic cancer of an effective …
http://www.uspto.gov/web/patents/patog/week50/OG/html/1409-3/US08912191-20141216.html
A method of treatment of melanoma, colorectal cancer, or pancreatic cancerwherein the treatment inhibits the progress of, reduces the rate of …
http://www.uspto.gov/web/patents/patog/week10/OG/html/1412-2/US08975401-20150310.html
A method of treating a cancer selected from breast cancer, hepatocellular carcinoma … gastric carcinoma, leukemia and pancreatic cancer in a subject …
http://www.uspto.gov/web/patents/patog/week42/OG/html/1407-3/US08865173-20141021.html
Treatments for pancreatic cancer metastases: Suzanne M. Spong, San Francisco, CA (US); Thomas B. Neff, Atherton, CA (US); and Stephen J. Klaus, San …
http://www.uspto.gov/web/patents/patog/week48/OG/html/1409-1/US08901093-20141202.html
Custom vectors for treating and preventing pancreatic cancer: Dennis L. Panicali, Acton, MA (US); Gail P. Mazzara, Winchester, MA (US); Linda R. …
http://www.uspto.gov/web/patents/patog/week09/OG/html/1412-1/US08969366-20150303.html
A method for treating a disease selected from the group consisting of melanoma, stomach cancer, liver cancer, colorectal cancer, pancreatic …
http://www.uspto.gov/web/patents/patog/week13/OG/html/1401-1/US08685941-20140401.html
Drug composition cytotoxic for pancreatic cancer cells: James Turkson, Orlando, Fla. (US) Assigned to University of Central Florida Research …
http://www.uspto.gov/web/offices/com/sol/foia/tac/2.66/74713131.pdf
- John Shimazaki, Esq. 1539 Lincoln Way, Suite 204 … containing the Of fice Action because Applicant™s president™s father was ill withpancreatic…
http://www.uspto.gov/aia_implementation/gen_e_lsi_20130207.pdf
Page 5 of 23 extracolonic cancers of LS include liver cancer, pancreatic cancer, gall bladder duct cancer, prostate cancer, sarcomas, thyroid cancer …
http://www.uspto.gov/web/patents/patog/week02/OG/html/1410-2/US08932990-20150113.html
Detection of digestive organ cancer, gastric cancer, colorectal cancer, pancreatic cancer, and biliary tract cancer by gene expression profiling
http://www.uspto.gov/web/patents/patog/week06/OG/html/1399-2/US08648112-20140211.html
wherein said cancer is selected from the group consisting of a sarcoma, … a nervous system cancer, prostate cancer, pancreatic cancer, and colon can …
http://www.uspto.gov/web/patents/patog/week45/OG/html/1408-2/US08883775-20141111.html
A method of treating or ameliorating a hyperproliferative disorder selected from the group consisting of glioblastoma, lung cancer, breast cancer . …
http://www.uspto.gov/web/patents/patog/week30/OG/html/1404-5/US08791125-20140729.html
A method for treating a Weel kinase mediated cancer selected from the group consisting of breast cancer, lung cancer, pancreatic cancer, colon …
http://www.uspto.gov/web/patents/patog/week08/OG/html/1411-4/US08962891-20150224.html
wherein said proliferative disorder is breast cancer or pancreatic cancer. …
http://www.uspto.gov/web/patents/patog/week40/OG/html/1407-1/US08852599-20141007.html
A method for treating a cancer in a subject suffering from such cancer, … pancreatic cancer, ovarian cancer, lymphoma, colon cancer, mesothelioma, …
http://www.uspto.gov/web/patents/patog/week11/OG/html/1400-3/US08673898-20140318.html
A method of treating cancer, … lung cancer, melanoma, neuroblastomas, oral cancer, ovarian cancer, pancreatic cancer, prostate cancer , rectal cance …
http://www.uspto.gov/web/patents/patog/week43/OG/html/1407-4/US08871744-20141028.html
A method for treating a subject having breast cancer, ovarian cancer, or pancreatic cancer in need of therapy thereof comprising administering to …
http://www.uspto.gov/sites/default/files/aia_implementation/gene-comment-scudder.pdf
My daughter died of ovarian cancer. My other daughter and many … (mutation) is known to cause a higher incidence of pancreatic (for instance) cancer …
http://www.uspto.gov/web/patents/patog/week48/OG/html/1409-1/US08901137-20141202.html
A method of treating pancreatic cancer which method comprises administering to a patient a therapeutically effective amount of a compound that is:
http://www.uspto.gov/web/patents/patog/week02/OG/html/1410-2/US08933086-20150113.html
A method of treating pancreatic cancer in a patient, comprising administering to said patient a therapeutically effective amount of a compound …
http://www.uspto.gov/web/patents/patog/week49/OG/html/1409-2/US08906934-20141209.html
… wherein the cell proliferative disorder is selected from the group consisting of cervical cancer, colon cancer, ovarian cancer, pancreatic cancer, …
http://www.uspto.gov/web/patents/patog/week32/OG/html/1405-2/US08802703-20140812.html
A method of inhibiting MEK in a cancer cell selected from the group consisting of human melanoma cells and human pancreatic cancer cells …
http://www.uspto.gov/web/patents/patog/week08/OG/html/1399-4/US08658388-20140225.html
A method for performing a multiplex, high-throughput immunoassay for facilitating a cancer diagnosis, the method comprising:
http://www.uspto.gov/web/patents/patog/week48/OG/html/1409-1/US08901147-20141202.html
A method for the treatment of colorectal cancer, lung cancer, breast cancer, prostatecancer, urinary cancer, kidney cancer, and pancreatic …
http://www.uspto.gov/web/patents/patog/week16/OG/patentee/alphaY.htm
Yamaue, Hiroki; to Onco Therapy Science, Inc. Combination therapy for pancreatic cancer using an antigenic peptide and chemotherapeutic agent 08703713 …
http://www.uspto.gov/web/patents/patog/week48/OG/patentee/alphaP_Utility.htm
… The Custom vectors for treating and preventing pancreatic cancer … system and apparatus for control of pancreatic beta cell function to improve …
http://www.uspto.gov/web/patents/patog/week16/OG/patentee/alphaW.htm
Whatcott, Cliff; and Han, Haiyong, to Translational Genomics Research Institute, The Therapeutic target for pancreatic cancer cells 08703736 Cl. …
http://www.uspto.gov/web/patents/patog/week10/OG/patentee/alphaG.htm
Goldenberg, David M.; Hansen, Hans J.; Chang, Chien-Hsing; and Gold, David V., to Immunomedics, Inc. Anti-pancreatic cancer antibodies 08974784 Cl. …
http://www.uspto.gov/web/patents/patog/week42/OG/patentee/alphaD.htm
… Narayan, Vaibhav; and Patterson, Scott, to Celera Corporation Pancreatic cancertargets and uses thereof 08865413 Cl. 435-7.1. Domsch, Matthew L.; …
http://www.uspto.gov/web/trademarks/tmog/20050315_OG.pdf
15 March 2005 – United States Patent and Trademark Office
http://www.uspto.gov/web/patents/patog/week10/OG/html/1412-2/US08975248-20150310.html
Combinations of therapeutic agents for treating cancer: … myeloma, colorectal adenocarcinoma, cervical carcinoma and pancreatic carcinoma, …
http://www.uspto.gov/web/patents/patog/week05/OG/patentee/alphaG_Utility.htm
… Inc. Medium-chain length fatty acids, salts and triglycerides in combination with gemcitabine for treatment of pancreatic cancer 08946190 Cl. …
http://www.uspto.gov/web/patents/patog/week13/OG/patentee/alphaT_Utility.htm
Turkson, James; to University of Central Florida Research Foundation, Inc. Drug composition cytotoxic for pancreatic cancer cells 08685941 Cl. 514-49.
http://www.uspto.gov/web/patents/patog/week31/OG/patentee/alphaG_Utility.htm
… David M., to Immunomedics, Inc. Anti-mucin antibodies for early detection and treatment of pancreatic cancer 08795662 Cl. 424-130.1. Gold, …
http://www.uspto.gov/web/trademarks/tmog/20110816_OG.pdf
http://www.uspto.gov
http://www.uspto.gov/web/patents/patog/week29/OG/patentee/alphaG.htm
Goggins, Michael G.; and Sato, Norihiro, to Johns Hopkins University, The Aberrantly methylated genes in pancreatic cancer 08785614 Cl. 536-24.3. …
http://www.uspto.gov/web/patents/patog/week46/OG/html/1408-3/US08889697-20141118.html
wherein said cancer is pancreatic cnacer, chronic myelogenous leukemia (CML), acute myelogenous leukemia (AML), acute lymphoblastic leukemia (ALL …
http://www.uspto.gov/web/patents/patog/week39/OG/patentee/alphaM_Utility.htm
Malafa, Mokenge P.; and Sebti, Said M., to University of South Florida Delta-tocotrienol treatment and prevention of pancreatic cancer 08846653 Cl. …
http://www.uspto.gov/web/patents/patog/week02/OG/patentee/alphaK_Utility.htm
… Taro, to National University Corporation Kanazawa University Detection of digestive organ cancer, gastric cancer, colorectal cancer, pancreatic …
http://www.uspto.gov/web/patents/patog/week11/OG/patentee/alphaK_Utility.htm
Kirn, David; to Sillajen Biotherapeutics, Inc. Oncolytic vaccinia virus cancer therapy 08980246 Cl. 424-93.2. Kirn, Larry J.; …
http://www.uspto.gov/web/patents/patog/week39/OG/patentee/alphaM_Utility.htm
Malafa, Mokenge P.; and Sebti, Said M., to University of South Florida Delta-tocotrienol treatment and prevention of pancreatic cancer 08846653 Cl. …
http://www.uspto.gov/web/patents/patog/week35/OG/patentee/alphaS_Utility.htm
list of patentees to whom patents were issued on the 2nd day of september, 2014 and to whom reexamination certificates were issued during the week …
http://www.uspto.gov/web/patents/patog/week42/OG/patentee/alphaS.htm
… Therapeutics Inc. Compounds and compositions for stabilizing hypoxia inducible factor-2 alpha as a method for treating cancer 08865748 Cl. …
http://www.uspto.gov/sites/default/files/ip/boards/bpai/decisions/prec/bhide.pdf
high incidence of ras involvement, such as colon and pancreatic tumors. By … withcancer or pre-cancerous states will serve to treat or palliate the …
http://www.uspto.gov/web/patents/classification/cpc/html/cpc-C07K.html
PEPTIDES (peptides in … Cancer-associated SCM-recognition factor, CRISPP} [2013‑01] … Kazal type inhibitors, e.g. pancreatic secretory inhibitor, …
http://www.uspto.gov/web/patents/classification/uspc514/defs514.htm
… compound X useful as an anti-cancer … certain rules as to patent … Cystic fibrosis is manifested by faulty digestion due to a deficiency of pa …
http://www.uspto.gov/web/patents/classification/cpc/html/cpc-G01N_3.html
Cancer-associated SCM-recognition factor, CRISPP . G01N 2333/4748. . . . . … Bovine/basic pancreatic trypsin inhibitor (BPTI, aprotinin) G01N …
http://www.uspto.gov/web/patents/classification/uspc530/defs530.htm
CLASS 530 , CHEMISTRY: NATURAL … Typically the processes of this subclass include solvent extraction of pancreatic … as well as with some forms of …
http://www.uspto.gov/web/patents/classification/cpc/html/defA61K.html
PREPARATIONS FOR MEDICAL, DENTAL, OR TOILET PURPOSES … i.e. Pancreatic stem cells are classified in A61K 35/39, … preparations containing cancer a …
http://www.uspto.gov/web/offices/ac/ido/oeip/taf/def/530.htm
Typically the processes of this subclass include solvent extraction of pancreatic … 828 for cancer -associated proteins … provided for in Class …
http://www.uspto.gov/web/patents/classification/cpc/html/cpc-G01N_1.html
Home page of the United States Patent and … Pancreatic cells} G01N 33/5073 … – relevant features relating to a specifically defined cancer are …
http://www.uspto.gov/web/patents/classification/shadowFiles/defs514sf.htm?514_971&S&10E&10F
class 514, drug, bio-affecting and body treating compositions …
http://www.uspto.gov/web/patents/patog/week47/OG/patentee/alphaN_Utility.htm
… Dale E., to Buck Institute for Age Research, The Reagents and methods for cancertreatment and … useful for diagnosis and treatment of pancreati …
http://www.uspto.gov/web/patents/classification/cpc/html/cpc-C12Y_2.html
Pancreatic ribonuclease (3.1.27.5) C12Y 301/27006. . Enterobacter ribonuclease (3.1.27.6) C12Y 301/27007. . Ribonuclease F (3.1.27.7) C12Y 301/27008. …
http://www.uspto.gov/web/patents/patog/week01/OG/patentee/alphaI_Utility.htm
Institute for Cancer Research: See … and Segev, Hanna, to Technion Research & Development Foundation Limited Populations of pancreatic …
http://www.uspto.gov/web/patents/patog/week53/OG/patentee/alphaC.htm
Cancer Research Technology Limited: See–Collins, Ian; Reader, John Charles; Klair, Suki; Scanlon, Jane; Addison, Glynn; and Cherry, Michael 08618121 …
http://www.uspto.gov/web/patents/patog/week12/OG/patentee/alphaP_Utility.htm
… to University Health Network Cyclic inhibitors of carnitine palmitoyltransferase and treating cancer … progenitor cells and pancreatic endocrine …
http://www.uspto.gov/web/patents/patog/week47/OG/patentee/alphaI.htm
… to King Fahd University of Petroleum and Minerals Cytotoxic compounds for treatingcancer … or preventing a pancreatic dysfunction 08894972 Cl …
http://www.uspto.gov/web/patents/patog/week50/OG/patentee/alphaC.htm
… and Taylor-Papadimitriou, Joyce, to Københavns Universitet Generation of a cancer-specific … to CuRNA, Inc. Treatment of pancreatic …
http://www.uspto.gov/web/patents/patog/week29/OG/patentee/alphaP_Utility.htm
… to Cedars-Sinai Medical Center Drug delivery of temozolomide for systemic based treatment of cancer … Pancreatic enzyme compositions and …
http://www.uspto.gov/web/offices/ac/ido/oeip/taf/def/424.htm
… a disclosed or even specifically claimed utility (i.e., compound X having an attached radionuclide useful as an anti-cancer diagnostic or …
http://www.uspto.gov/web/patents/patog/week25/OG/patentee/alphaT_Utility.htm
… Chang-Jer, to Gold Nanotech Inc. Physical nano-complexes for preventing and treating cancer and … and protective solution for protecting pancrea …
http://www.uspto.gov/web/patents/patog/week27/OG/patentee/alphaA_Utility.htm
… Thomas T., to Penn State Research Foundation, The In vivo photodynamic therapy ofcancer via a near infrared … of pancreatic beta-cells by …
http://www.uspto.gov/web/patents/patog/week32/OG/patentee/alphaB_Utility.htm
Birnie, Richard; to University of York, The Cancer vaccine 08802619 Cl. 514-1. Birtwhistle, Daniel P.; Long, James R.; and Reinke, Robert E., …
http://www.uspto.gov/web/patents/patog/week20/OG/patentee/alphaC_Utility.htm
… to Cornell University Method for treating cancer 08729133 Cl. 514-673 … methods for promoting the generation of PDX1+ pancreatic cells …
http://www.uspto.gov/web/patents/patog/week49/OG/patentee/alphaL_Utility.htm
… Kurt, to Abbvie Biotherapeutics Inc. Compositions against cancer antigen LIV-1 and uses … H., to Amylin Pharmaceuticals, LLC Pancreatic …
http://www.uspto.gov/web/patents/patog/week11/OG/patentee/alphaS_Utility.htm
… Kenji; and Matsuda, Hirokazu, to Kyoto University Molecular probe for imaging ofpancreatic islets and use … use in the treatment of cancer …
http://www.uspto.gov/web/patents/patog/week36/OG/patentee/alphaK.htm
… Emi; Matsumi, Chiemi; and Saitoh, Yukie, to Actgen Inc Antibody having anti-cancer … The Plectin-1 targeted agents for detection and treatment …
http://www.uspto.gov/web/patents/patog/week53/OG/patentee/alphaK.htm
list of patentees to whom patents were issued on the 31th day of december, 2013 and to whom reexamination certificates were issued during the week …
http://www.uspto.gov/web/patents/patog/week40/OG/patentee/alphaK_Utility.htm
… Uemoto, Shinji; and Kawaguchi, Yoshiya, to Kyoto University Method of culturingpancreatic islet-like tissues by a … of breast cancer 08853183 …
Clinical Trials:
| Region Name |
Number of Studies |
| World |
1824 |
|
| Africa [map] |
10 |
|
| Central America [map] |
4 |
|
| East Asia [map] |
179 |
|
| Japan |
40 |
[studies] |
| Europe [map] |
444 |
|
| Middle East [map] |
46 |
|
| North America |
1189 |
|
| Canada [map] |
102 |
[studies] |
| Mexico |
11 |
[studies] |
| United States [map] |
1144 |
[studies] |
|
|
|
|
| North Asia [map] |
24 |
|
| Pacifica [map] |
39 |
|
| South America [map] |
30 |
|
| South Asia [map] |
23 |
|
| Southeast Asia [map] |
25 |
|
Search Results for ‘pancreas cancer’
Genomics and Epigenetics: Genetic Errors and Methodologies – Cancer and Other Diseases on March 25, 2015 | Read Full Post »
@Mayo Clinic: Inhibiting the gene, protein kinase D1 (PKD1), and its protein could stop spread of this form of Pancreatic Cancer on February 24, 2015 Read Full Post »
The Changing Economics of Cancer Medicine: Causes for the Vanishing of Independent Oncology Groups in the US on November 26, 2014 | Read Full Post »
Autophagy-Modulating Proteins and Small Molecules Candidate Targets for Cancer Therapy: Commentary of Bioinformatics Approaches on September 18, 2014 | Read Full Post »
New Immunotherapy Could Fight a Range of Cancers on June 4, 2014 Read Full Post »
Locally Advanced Pancreatic Cancer: Efficacy of FOLFIRINOX on June 1, 2014 Read Full Post »
ipilimumab, a Drug that blocks CTLA-4 Freeing T cells to Attack Tumors @DM Anderson Cancer Center on May 28, 2014 | Read Full Post »
NIH Study Demonstrates that a New Cancer Immunotherapy Method could be Effective against a wide range of Cancers on May 12, 2014 |
Cancer Research: Curations and Reporting Posted in on May 6, 2014 | Read Full Post »
Cancer Research: Curations and Reporting: Aviva Lev-Ari, PhD, RN on April 20, 2014 | Read Full Post »
Prologue to Cancer – e-book Volume One – Where are we in this journey? on April 13, 2014 | Read Full Post »
Epilogue: Envisioning New Insights in Cancer Translational Biology on April 4, 2014 | Read Full Post »
A Synthesis of the Beauty and Complexity of How We View Cancer
on March 26, 2014 Read Full Post »
Pancreatic Cancer Diagnosis: Four Novel Histo-pathologies Screening Characteristics offers more Reliable Identification of Cellular Features associated with Cancer
on November 13, 2013 | Read Full Post »
What`s new in pancreatic cancer research and treatment?
on October 21, 2013 | Read Full Post »
Family History of Cancer may increase the Risk of Close Relatives developing the Same Type of Cancer as well as Different Types
on July 25, 2013 Read Full Post »
2013 Perspective on “War on Cancer” on December 23, 1971
on July 5, 2013 Read Full Post »
Mesothelin: An early detection biomarker for cancer (By Jack Andraka) on April 21, 2013 | Read Full Post »
Pancreatic Cancer: Genetics, Genomics and Immunotherapy
on April 11, 2013 | Read Full Post »
New methods for Study of Cellular Replication, Growth, and Regulation on March 25, 2015 Read Full Post »
Diet and Diabetes on March 2, 2015 | Read Full Post »
Neonatal Pathophysiology on February 22, 2015 | Read Full Post »
Endocrine Action on Midbrain on February 12, 2015 | Read Full Post »
Gastrointestinal Endocrinology on February 10, 2015 | Read Full Post »
Parathyroids and Bone Metabolism on February 10, 2015 | Read Full Post »
Pancreatic Islets on February 8, 2015 | Read Full Post »
Pituitary Neuroendocrine Axis on February 4, 2015 |Read Full Post »
Highlights in the History of Physiology on December 28, 2014 | Read Full Post »
Outline of Medical Discoveries between 1880 and 1980 on December 3, 2014 | Read Full Post »
Diagnostics Industry and Drug Development in the Genomics Era: Mid 80s to Present on November 21, 2014 Read Full Post »
Implantable Medical Devices to 2015 – Industry Market Research, Market Share, Market Size, Sales, Demand Forecast, Market Leaders, Company Profiles, Industry Trends on November 17, 2014 | Read Full Post »
Pharmacological Action of Steroid Hormones on October 27, 2014 | Read Full Post »
Metabolomics Summary and Perspective on October 16, 2014 | Read Full Post »
Pancreatic Tumors take nearly 20 years to become Lethal after the first Genetic Perturbations – Discovery @ The Johns Hopkins University on October 15, 2014 |Read Full Post »
Isoenzymes in cell metabolic pathways on October 6, 2014 | Read Full Post »
Metformin, thyroid-pituitary axis, diabetes mellitus, and metabolism on September 28, 2014 | Read Full Post »
Carbohydrate Metabolism on August 13, 2014 | Read Full Post »
A Primer on DNA and DNA Replication on July 29, 2014 | Read Full Post »
The Discovery and Properties of Avemar – Fermented Wheat Germ Extract: Carcinogenesis Suppressor on June 7, 2014 | Read Full Post »
Previous Articles posted on Prostate Cancer
| @Mayo Clinic: Inhibiting the gene, protein kinase D1 (PKD1), and its protein could stop spread of this form of Pancreatic Cancer |
2012pharmaceutical |
2015/02/24
Published |
| Thymoquinone, an extract of nigella sativa seed oil, blocked pancreatic cancer cell growth and killed the cells by enhancing the process of programmed cell death. |
larryhbern |
2014/07/15
Published |
| Moringa Oleifera Kills 97% of Pancreatic Cancer Cells in Vitro |
larryhbern |
2014/06/21
Published |
| The Gonzalez protocol: Worse than useless for pancreatic cancer |
sjwilliamspa |
2014/06/17
Published |
| An alternative approach to overcoming the apoptotic resistance of pancreatic cancer |
2012pharmaceutical |
2014/06/03
Published |
| Locally Advanced Pancreatic Cancer: Efficacy of FOLFIRINOX |
2012pharmaceutical |
2014/06/01
Published |
| Consortium of European Research Institutions and Private Partners will develop a microfluidics-based lab-on-a-chip device to identify Pancreatic Cancer Circulating Tumor Cells (CTC) in blood |
2012pharmaceutical |
2014/04/10
Published |
| Pancreatic Cancer Diagnosis: Four Novel Histo-pathologies Screening Characteristics offers more Reliable Identification of Cellular Features associated with Cancer |
2012pharmaceutical |
2013/11/13
Published |
| What`s new in pancreatic cancer research and treatment? |
2012pharmaceutical |
2013/10/21
Published |
| Pancreatic Cancer: Genetics, Genomics and Immunotherapy |
tildabarliya |
2013/04/11
Published |
| Pancreatic cancer genomes: Axon guidance pathway genes – aberrations revealed |
2012pharmaceutical |
2012/10/24
Published |
| Biomarker tool development for Early Diagnosis of Pancreatic Cancer: Van Andel Institute and Emory University |
2012pharmaceutical |
2012/10/24
Published |
| Personalized Pancreatic Cancer Treatment Option |
2012pharmaceutical |
2012/10/16
Published |
| Battle of Steve Jobs and Ralph Steinman with Pancreatic cancer: How we lost |
ritusaxena |
2012/05/21
Published |
| Early Biomarker for Pancreatic Cancer Identified |
pkandala |
2012/05/17
Published |
| Usp9x: Promising therapeutic target for pancreatic cancer |
ritusaxena |
2012/05/14
Published |
| War on Cancer Needs to Refocus to Stay Ahead of Disease Says Cancer Expert |
sjwilliamspa |
2015/03/27
Published |
| Antibiotics that target mitochondria effectively eradicate cancer stem cells, across multiple tumor types: Treating cancer like an infectious disease |
2012pharmaceutical |
2015/02/15
Published |
| Pancreatic Islets |
larryhbern |
2015/02/08
Publ |
|
|
|
|
| Vol 13, No 4 (2012): July – p. 330-469 |
Molecular Biology of Pancreatic Cancer: How Useful Is It in Clinical Practice? |
ABSTRACT HTML PDF |
| George H Sakorafas, Vasileios Smyrniotis |
|
| Vol 13, No 4 (2012): July – p. 330-469 |
Endoscopic Findings of Upper Gastrointestinal Lesions in Patients with Pancreatic Cancer |
ABSTRACT HTML PDF |
| Koushiro Ohtsubo, Hiroyuki Watanabe, Hisatsugu Mouri, Kaname Yamashita, Kazuo Yasumoto, Seiji Yano |
|
| Vol 13, No 5 (2012): September – p. 470-547 |
Two Avirulent, Lentogenic Strains of Newcastle Disease Virus Are Cytotoxic for Some Human Pancreatic Tumor Lines In Vitro |
ABSTRACT HTML PDF |
| Robert J Walter, Bashar M Attar, Asad Rafiq, Megan Delimata, Sooraj Tejaswi |
|
| Vol 14, No 3 (2013): May – p. 221-303 |
Duration of Diabetes and Pancreatic Cancer in a Case-Control Study in the Midwest and the Iowa Women’s Health Study (IWHS) Cohort |
ABSTRACT HTML PDF |
| Sarah A Henry, Anna E Prizment, Kristin E Anderson |
|
| Vol 16, No 1 (2015): January – p. 1-99 |
Endoscopic Management of Pain in Pancreatic Cancer |
ABSTRACT HTML PDF |
| Parit Mekaroonkamol, Field F Willingham, Saurabh Chawla |
|
| Vol 14, No 2 (2013): March – p. 109-220 |
Advancements in the Management of Pancreatic Cancer: 2013 |
ABSTRACT HTML PDF |
| Muhammad Wasif Saif |
|
| Vol 15, No 5 (2014): September – p. 413-540 |
New-onset Diabetes: A Clue to the Early Diagnosis of Pancreatic Cancer |
ABSTRACT HTML PDF |
| Suresh T Chari |
|
| Vol 13, No 5 (2012): September – p. 470-547 |
Effects of Porcine Pancreatic Enzymes on the Pancreas of Hamsters. Part 2: Carcinogenesis Studies |
ABSTRACT HTML PDF |
| Fumiaki Nozawa, Mehmet Yalniz, Murat Saruc, Jens Standop, Hiroshi Egami, Parviz M Pour |
|
| Vol 14, No 5 (2013): September – p. 475-527 |
Synchronous Triple Cancers of the Pancreas, Stomach, and Cecum Treated with S-1 Followed by Pancrelipase Treatment of Pancreatic Exocrine Insufficiency |
ABSTRACT HTML PDF |
| Koushiro Ohtsubo, Daisuke Ishikawa, Shigeki Nanjo, Shinji Takeuchi, Tadaaki Yamada, Hisatsugu Mouri, Kaname Yamashita, Kazuo Yasumoto, Toshifumi Gabata, Osamu Matsui, Hiroko Ikeda, Yasushi Takamatsu, Sakae Iwakami, Seiji Yano |
|
| Vol 13, No 1 (2012): January – p. 1-123 |
Newcastle Disease Virus LaSota Strain Kills Human Pancreatic Cancer Cells in Vitro with High Selectivity |
ABSTRACT HTML PDF |
| Robert J Walter, Bashar M Attar, Asad Rafiq, Sooraj Tejaswi, Megan Delimata |
|
| Vol 13, No 3 (2012): May – p. 252-329 |
Rare Solid Tumors of the Pancreas as Differential Diagnosis of Pancreatic Adenocarcinoma |
ABSTRACT HTML PDF |
| Sabine Kersting, Monika S Janot, Johanna Munding, Dominique Suelberg, Andrea Tannapfel, Ansgar M Chromik, Waldemar Uhl, Uwe Bergmann |
|
| Vol 14, No 4 (2013): July – p. 304-474 |
A Proteomic Comparison of Formalin-Fixed Paraffin-Embedded Pancreatic Tissue from Autoimmune Pancreatitis, Chronic Pancreatitis, and Pancreatic Cancer |
ABSTRACT HTML PDF SUPPL. TABLES 1-4 (PDF) |
| Joao A Paulo, Vivek Kadiyala, Scott Brizard, Peter A Banks, Hanno Steen, Darwin L Conwell |
|
| Vol 13, No 4 (2012): July – p. 330-469 |
Highlights on the First Line Treatment of Metastatic Pancreatic Cancer |
ABSTRACT HTML PDF |
| Krishna S Gunturu, Jamie Jarboe, Muhammad Wasif Saif |
|
| Vol 14, No 2 (2013): March – p. 109-220 |
Pancreatic Cancer: Updates on Translational Research and Future Applications |
ABSTRACT HTML PDF |
| Evangelos G Sarris, Konstantinos N Syrigos, Muhammad Wasif Saif |
|
| Vol 14, No 4 (2013): July – p. 304-474 |
Pancreatic Cancer: What About Screening and Detection? |
ABSTRACT HTML PDF |
| Froso Konstantinou, Kostas N Syrigos, Muhammad Wasif Saif |
|
| Vol 14, No 4 (2013): July – p. 304-474 |
Diabetes and Pancreatic Cancer |
ABSTRACT HTML PDF |
| Najla Hatem El-Jurdi, Muhammad Wasif Saif |
|
| Vol 13, No 5 (2012): September – p. 470-547 |
Effects of Porcine Pancreatic Enzymes on the Pancreas of Hamsters. Part 1: Basic Studies |
ABSTRACT HTML PDF |
| Murat Saruc, Fumiaki Nozawa, Mehmet Yalniz, Atsushi Itami, Parviz M Pour |
|
| Vol 14, No 2 (2013): March – p. 109-220 |
Analysis of Endoscopic Pancreatic Function Test (ePFT)-Collected Pancreatic Fluid Proteins Precipitated Via Ultracentrifugation |
ABSTRACT HTML PDF SUPPL.(XLS) SUPPL.(PDF) |
| Joao A Paulo, Vivek Kadiyala, Aleksandr Gaun, John F K Sauld, Ali Ghoulidi, Peter A Banks, Hanno Steen, Darwin L Conwell |
|
| Vol 16, No 1 (2015): January – p. 1-99 |
Regulation Mechanisms of the Hedgehog Pathway in Pancreatic Cancer: A Review |
ABSTRACT HTML PDF |
| Kim Christin Honselmann, Moritz Pross, Carlo Maria Felix Jung, Ulrich Friedrich Wellner, Steffen Deichmann, Tobias Keck, Dirk Bausch |
|
| Vol 14, No 5S (2013): September (Suppl.) – p. 528-602 |
History of Previous Cancer in Patients Undergoing Resection for Pancreatic Adenocarcinoma |
ABSTRACT PDF |
| Francesca Gavazzi, Maria Rachele Angiolini, Cristina Ridolfi, Maria Carla Tinti, Marco Madonini, Marco Montorsi, Alessandro Zerbi |
|
| Vol 13, No 4 (2012): July – p. 330-469 |
Molecular Biology of Pancreatic Cancer: How Useful Is It in Clinical Practice? |
ABSTRACT HTML PDF |
| George H Sakorafas, Vasileios Smyrniotis |
|
| Vol 13, No 4 (2012): July – p. 330-469 |
Endoscopic Findings of Upper Gastrointestinal Lesions in Patients with Pancreatic Cancer |
ABSTRACT HTML PDF |
| Koushiro Ohtsubo, Hiroyuki Watanabe, Hisatsugu Mouri, Kaname Yamashita, Kazuo Yasumoto, Seiji Yano |
|
| Vol 13, No 5 (2012): September – p. 470-547 |
Two Avirulent, Lentogenic Strains of Newcastle Disease Virus Are Cytotoxic for Some Human Pancreatic Tumor Lines In Vitro |
ABSTRACT HTML PDF |
| Robert J Walter, Bashar M Attar, Asad Rafiq, Megan Delimata, Sooraj Tejaswi |
|
| Vol 14, No 3 (2013): May – p. 221-303 |
Duration of Diabetes and Pancreatic Cancer in a Case-Control Study in the Midwest and the Iowa Women’s Health Study (IWHS) Cohort |
ABSTRACT HTML PDF |
| Sarah A Henry, Anna E Prizment, Kristin E Anderson |
|
| Vol 16, No 1 (2015): January – p. 1-99 |
Endoscopic Management of Pain in Pancreatic Cancer |
ABSTRACT HTML PDF |
| Parit Mekaroonkamol, Field F Willingham, Saurabh Chawla |
|
| Vol 14, No 2 (2013): March – p. 109-220 |
Advancements in the Management of Pancreatic Cancer: 2013 |
ABSTRACT HTML PDF |
| Muhammad Wasif Saif |
|
| Vol 15, No 5 (2014): September – p. 413-540 |
New-onset Diabetes: A Clue to the Early Diagnosis of Pancreatic Cancer |
ABSTRACT HTML PDF |
| Suresh T Chari |
|
| Vol 13, No 5 (2012): September – p. 470-547 |
Effects of Porcine Pancreatic Enzymes on the Pancreas of Hamsters. Part 2: Carcinogenesis Studies |
ABSTRACT HTML PDF |
| Fumiaki Nozawa, Mehmet Yalniz, Murat Saruc, Jens Standop, Hiroshi Egami, Parviz M Pour |
|
| Vol 14, No 5 (2013): September – p. 475-527 |
Synchronous Triple Cancers of the Pancreas, Stomach, and Cecum Treated with S-1 Followed by Pancrelipase Treatment of Pancreatic Exocrine Insufficiency |
ABSTRACT HTML PDF |
| Koushiro Ohtsubo, Daisuke Ishikawa, Shigeki Nanjo, Shinji Takeuchi, Tadaaki Yamada, Hisatsugu Mouri, Kaname Yamashita, Kazuo Yasumoto, Toshifumi Gabata, Osamu Matsui, Hiroko Ikeda, Yasushi Takamatsu, Sakae Iwakami, Seiji Yano |
|
| Vol 13, No 1 (2012): January – p. 1-123 |
Newcastle Disease Virus LaSota Strain Kills Human Pancreatic Cancer Cells in Vitro with High Selectivity |
ABSTRACT HTML PDF |
| Robert J Walter, Bashar M Attar, Asad Rafiq, Sooraj Tejaswi, Megan Delimata |
|
| Vol 13, No 3 (2012): May – p. 252-329 |
Rare Solid Tumors of the Pancreas as Differential Diagnosis of Pancreatic Adenocarcinoma |
ABSTRACT HTML PDF |
| Sabine Kersting, Monika S Janot, Johanna Munding, Dominique Suelberg, Andrea Tannapfel, Ansgar M Chromik, Waldemar Uhl, Uwe Bergmann |
|
| Vol 14, No 4 (2013): July – p. 304-474 |
A Proteomic Comparison of Formalin-Fixed Paraffin-Embedded Pancreatic Tissue from Autoimmune Pancreatitis, Chronic Pancreatitis, and Pancreatic Cancer |
ABSTRACT HTML PDF SUPPL. TABLES 1-4 (PDF) |
| Joao A Paulo, Vivek Kadiyala, Scott Brizard, Peter A Banks, Hanno Steen, Darwin L Conwell |
|
| Vol 13, No 4 (2012): July – p. 330-469 |
Highlights on the First Line Treatment of Metastatic Pancreatic Cancer |
ABSTRACT HTML PDF |
| Krishna S Gunturu, Jamie Jarboe, Muhammad Wasif Saif |
|
| Vol 14, No 2 (2013): March – p. 109-220 |
Pancreatic Cancer: Updates on Translational Research and Future Applications |
ABSTRACT HTML PDF |
| Evangelos G Sarris, Konstantinos N Syrigos, Muhammad Wasif Saif |
|
| Vol 14, No 4 (2013): July – p. 304-474 |
Pancreatic Cancer: What About Screening and Detection? |
ABSTRACT HTML PDF |
| Froso Konstantinou, Kostas N Syrigos, Muhammad Wasif Saif |
|
| Vol 14, No 4 (2013): July – p. 304-474 |
Diabetes and Pancreatic Cancer |
ABSTRACT HTML PDF |
| Najla Hatem El-Jurdi, Muhammad Wasif Saif |
|
| Vol 13, No 5 (2012): September – p. 470-547 |
Effects of Porcine Pancreatic Enzymes on the Pancreas of Hamsters. Part 1: Basic Studies |
ABSTRACT HTML PDF |
| Murat Saruc, Fumiaki Nozawa, Mehmet Yalniz, Atsushi Itami, Parviz M Pour |
|
| Vol 14, No 2 (2013): March – p. 109-220 |
Analysis of Endoscopic Pancreatic Function Test (ePFT)-Collected Pancreatic Fluid Proteins Precipitated Via Ultracentrifugation |
ABSTRACT HTML PDF SUPPL.(XLS) SUPPL.(PDF) |
| Joao A Paulo, Vivek Kadiyala, Aleksandr Gaun, John F K Sauld, Ali Ghoulidi, Peter A Banks, Hanno Steen, Darwin L Conwell |
|
| Vol 16, No 1 (2015): January – p. 1-99 |
Regulation Mechanisms of the Hedgehog Pathway in Pancreatic Cancer: A Review |
ABSTRACT HTML PDF |
| Kim Christin Honselmann, Moritz Pross, Carlo Maria Felix Jung, Ulrich Friedrich Wellner, Steffen Deichmann, Tobias Keck, Dirk Bausch |
|
| Vol 14, No 5S (2013): September (Suppl.) – p. 528-602 |
History of Previous Cancer in Patients Undergoing Resection for Pancreatic Adenocarcinoma |
ABSTRACT PDF |
| Francesca Gavazzi, Maria Rachele Angiolini, Cristina Ridolfi, Maria Carla Tinti, Marco Madonini, Marco Montorsi, Alessandro Zerbi |
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