Protein May Indicate Pancreatic Cancer Risk

A protein that dwindles in response to obesity and a sedentary lifestyle may one day help doctors predict which people are at increased risk for pancreas cancer, new research by Dana-Farber Cancer Institute and collaborating researchers indicates.

In a report in the Aug. 15 issue of Cancer Research, the researchers observed that, in a large study group, people with the lowest blood levels of a protein called IGFBP-1 were twice as likely to develop pancreas cancer as those with higher levels. Though much work remains to determine if the protein -- whose acronym stands for insulin-like growth factor binding protein-1 -- is a reliable indicator of pancreas cancer risk, the finding adds to the scientific understanding of how the disease develops.

"The levels of insulin and another circulating hormone, insulin-like growth factor or IGF, are modified by obesity and sedentary lifestyle, and there is evidence that these hormones may stimulate the growth of pancreas cancer cells," said the study's lead author, Brian Wolpin, MD, of Dana-Farber. "When IGF binds to proteins like IGFBP-1, there may be less IGF available to bind to pancreas cancer cells and promote their growth. We wanted to determine whether IGFBP-1 levels in the blood were linked to pancreas cancer risk".

The researchers measured circulating IGFBP-1 levels in a select group of participants in four large, ongoing health studies: the Health Professionals Follow-up Study, the Nurses' Health Study, the Physicians' Health Study, and the Women's Health Initiative. They collected blood samples from 573 participants and, four or more years later, checked IGFBP-1 levels in the samples of 144 people who developed pancreas cancer and 429 who did not.

They observed that the quarter of the group whose IGFBP-1 levels were lowest had twice the risk of developing pancreas cancer of those in the top three quarters. The connection became even stronger over time: Among cases diagnosed at least eight years after blood collection, those in the bottom quarter of IGFBP-1 levels had nearly three-and-a-half times the pancreas cancer risk of those in the upper quarters.

The risk may be elevated because higher amounts of IGFBP-1 are able to "soak up" more IGF, leaving less available to spur pancreas cancer cell growth, or because IGFBP-1 has some cancer-blocking properties of its own, said Wolpin, who is also an instructor in medicine at Harvard Medical School. Another possibility is that other molecules may be involved, for which IGFBP-1 acts as an intermediary.

"It's known that a variety of proteins are affected by obesity and sedentary lifestyle," he added. "Studies are exploring whether a subset of these may play a role in the risk of developing pancreas cancer. More research is also needed on how alterations in insulin and proteins in the IGF family alter the risk of this difficult disease".

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Treatment of pancreatic adenocarcinoma

Medicineworld.org: Treatment of pancreatic adenocarcinoma


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Pancreatic ductal adenocarcinoma (PDAC) is a highly cancerous digestive tumor with a very poor prognosis. Hypoxia-inducible transcription factor-1a (HIF-1a) is involved in cancerous progression in a number of solid tumors, including PDAC, upregulation of HIF-1a accelerates PDAC progression, but the exact regulatory mechanisms of HIF-1ain PDAC has not been unequivocally addressed. Recently, an increasing number of studies reported that toll-like receptors (TLRs) were upregulated in epithelial malignancies and involved in tumor progression, but whether TLRs, such as TLR4, is expressed on PDAC cells remains unknown. In immune-related cells, TLR signal pathway may induce expression of HIF-1a, but it is also still unclear whether there exists some association between TLR4 and HIF-1a in tumor microenviroment, such as PDAC.

A research article to be published on June 21, 2010 in the World Journal of Gastroenterology addresses this question. The research team led by He-Shui Wu, MD, from Department of Pancreatic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, used real time polymerase chain reaction and immunohistochemistry, to detect TLR4, NF-?B p65 and HIF-1a expression in 65 cases of PDAC tissues and 38 cases of corresponding adjacent tissues.

Their study revealed that TLR4, NF-?B p65 and HIF-1a were overexpressed in PDAC. The expression of TLR4 and HIF-1a was linked to tumor size, lymph node metastasis, venous invasion and pathological stage. Furthermore, the expression of TLR4 was positively correlated with expression of HIF-1a. Thus, TLR4 appears to be a novel marker for the progression and prognosis of PDAC, and may provide a new strategy for therapeutic intervention in the therapy of patients with PDAC in the future.

Based on these results and prior reports, the authors speculated that active TLR4 signal pathway appears to be partly involved in up-regulating HIF-1a in PDAC tumor microenviroment via NF-?B pathway, and promoted progression of PDAC. These results demonstrated a new view of molecules involved in regulatory mechanism of HIF-1a and thus may provide new therapeutic targets for PDAC.

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Pancreatic ductal adenocarcinoma (PDAC) is a highly cancerous digestive tumor with a very poor prognosis. Hypoxia-inducible transcription factor-1and#945; (HIF-1and#945;) is involved in cancerous progression in a number of solid tumors, including PDAC, upregulation of HIF-1and#945; accelerates PDAC progression, but the exact regulatory mechanisms of HIF-1and#945;in PDAC has not been unequivocally addressed. Recently, an increasing number of studies reported that toll-like receptors (TLRs) were upregulated in epithelial malignancies and involved in tumor progression, but whether TLRs, such as TLR4, is expressed on PDAC cells remains unknown. In immune-related cells, TLR signal pathway may induce expression of HIF-1and#945;, but it is also still unclear whether there exists some association between TLR4 and HIF-1and#945; in tumor microenviroment, such as PDAC.
Medicineworld.org: Treatment of pancreatic adenocarcinoma

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The War on Cancer Continues

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Report finds progress has been made fighting some, but not all, malignancies

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Gene Mutation May Be Key to Familial Pancreatic Cancer

THURSDAY, Dec. 29 (HealthDay News) -- Individuals may face a higher hereditary risk for developing pancreatic cancer if they carry abnormalities in the so-called "ATM" gene, new research reveals.

The finding, reported in an upcoming issue of Cancer Discovery, stems from genetic-sequencing work conducted among 166 pancreatic cancer patients. For comparative purposes, 190 other individuals who did not have pancreatic cancer also underwent sequencing.

The study was led by Alison Klein, an associate professor of oncology at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins and director of the National Familial Pancreas Tumor Registry.

Noting that 10 percent of pancreatic cancer patients are from families in which more than one member has battled the disease, Klein pointed out in a news release from the American Association for Cancer Research that "there was significant reason to believe this clustering was due to genetics."

But she added that no previous effort had "been able to find the causative genes that explained the cluster of pancreatic cancer for a majority of these families."

Among the pancreatic cancer patients examined, four were found to have the ATM gene mutation. By contrast, none of the healthy individuals who were sequenced carried the abnormality, according to the report.

Ultimately, the finding could lead to the development of a new screening option for a disease that kills 95 percent of patients within five years of diagnosis, according to the release. Though endoscopy is under study as another possible screening tool, there are as yet no other recommended screening alternatives for the number four cause of cancer-related death.

More information

For more on pancreatic cancer, visit the U.S. National Library of Medicine.

SOURCE: American Association for Cancer Research, news release, Dec. 29, 2011

Copyright © 2011 HealthDay. All rights reserved.

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New Drug Developed To Target And Destroy Tumor Cells Successful In Mouse Model Of Pancreatic Cancer

Main Category: Pancreatic Cancer
Article Date: 21 Oct 2012 - 0:00 PDT Current ratings for:
New Drug Developed To Target And Destroy Tumor Cells Successful In Mouse Model Of Pancreatic Cancer

A new drug created at the University of Minnesota may hold the answer to defeating pancreatic cancer, according to results published in the prestigious journal Science Translational Medicine.

The study is based on successful outcomes in a mouse model - results researchers expect to carry over to human patients when the drug potentially begins human trials in 2013.

The drug, Minnelide, is a type of injectable chemotherapy designed to target tumor cells. The drug works by inhibiting a heat shock protein, HSP 70, which has been proven to aid the growth of tumor cells. By stopping HSP 70 from working, Minnelide disperses the cells integral to the tumor's growth and the cancer disintegrates.

The drug is based on patented technology designed in the labs of Ashok Saluja, Ph.D., professor and vice chair of research in the University of Minnesota Medical School's Department of Surgery, Selwyn Vickers, M.D., chairman of the Department of Surgery, and Gunda Georg, Ph.D., director of the Institute for Therapeutics Discovery and Development in the College of Pharmacy. Bruce Blazar, M.D., director of the Center for Translational Medicine, also partnered on this project.

Pancreatic cancer is the most lethal of all cancers. This year alone, more than 44,000 Americans will be diagnosed with the disease and the median survival time following a pancreatic cancer diagnosis is just six months.

"A diagnosis of pancreatic cancer is incredibly grim. There is no good way to treat or cure this particular type of cancer," said Saluja, who holds the Eugene C. and Gail V. Sit Chair in Pancreatic and Gastrointestinal Cancer Research, "and the best options currently available offer just six weeks of added survival. It is far from tackling the real problem which is that pancreatic cancer tumor cells make survival proteins, rendering them increasingly difficult to defeat."

In 2007, Saluja and his collaborators discovered pancreatic cancer cells have too much HSP 70, which protects cells from dying. Because of this excess protein, pancreatic cancer cells are difficult to target with drugs, meaning the logical next step in fighting the cancer was to determine how to inhibit HSP 70 in these tumor cells.

Saluja found that triptolide, a compound derived from plants in China, worked to halt the development of HSP 70 in tumor cells, but because triptolide is not water soluble, it was still difficult to administer to patients. The Institute for Therapeutics Discovery and Development at the University of Minnesota, in collaboration with the Saluja lab, worked to make triptolide water soluble. They named their drug Minnelide as a nod to the compound from which it was derived, triptolide, and its discovery location, the University of Minnesota.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our pancreatic cancer section for the latest news on this subject.
The University of Minnesota holds the patent on the modifying factors that create Minnelide from triptolide. It has been licensed to Minneamrita Therapeutics LLC for production.

Funding for this research was provided by NIH grants R01CA124723 and R01 CA170496, as well as the Katherine and Robert Goodale Foundation and the Hirshberg Foundation.

University of Minnesota Academic Health Center

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Pancreatic Cancer Risk May Be Reduced By High Dietary Antioxidant Intake

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Main Category: Pancreatic Cancer
Also Included In: Cancer / Oncology;  Nutrition / Diet
Article Date: 23 Jul 2012 - 16:00 PDT Current ratings for:
Pancreatic Cancer Risk May Be Reduced By High Dietary Antioxidant Intake

Individuals can significantly reduce their risk of developing pancreatic cancer by increasing their dietary intake of the antioxidant vitamins C, E, and selenium, say researchers who are leading the Norfolk arm of the European Prospective Investigation of Cancer (EPIC) study.

The study, published in the journal Gut, states that 1 in 12 of these cancers might be prevented if the association turns out to be casual.

More than a 250,000 people die each year around the world due to pancreatic cancer. In the UK, 7,500 people are diagnosed with the disease each year.

Only 5% of patients with pancreatic cancer survive beyond 5 years, say the researchers. Risk factors of the disease include, smoking, type 2 diabetes, and diet.

The team analyzed the health of more than 23,500 adults who participated in the Norfolk arm of the EPIC study between 1993 and 1992. Patients were aged 40 to 74 years old.

?? All study participates filled out a food diary tracking the types and amounts of food the consumed during a 7 day period. In addition, they detailed the methods they used to prepare the food.

The team then matched each entry in the food diary to one of 11,00 food items. They then used a specially designed computer program called DINER in order to calculate the nutrient values.

According to the researchers, 49 people developed pancreatic cancer within 10 years of participating in the study, and this figure increased to 86 people by 2010. On average, they survived six months after being diagnosed with pancreatic cancer.
br> ?? The nutrient intakes of participants diagnosed with the disease were compared with those of almost 4,000 healthy individuals in order to see if there were any differences.

?? According to the researchers, weekly intake of selenium in the top 25% of consumption roughly reduced their risk of developing pancreatic cancer by 50% compared with those whose intake was in the bottom 25%.

In addition, patients were 67% less likely to develop the disease if their intake of vitamins C, Em and selenium was in the top 25% of consumption. ??

The researchers note that antioxidants may neutralize free radicals and curb genetically programmed influences, as well as stimulating the immune system response.

They explained:

"Other trials using antioxidant supplements have not produced such encouraging results, but this may be because food sources of these nutrients may behave differently from those found in supplements. If a causal association is confirmed by reporting consistent findings from other epidemiological studies, then population based dietary recommendations may help prevent pancreatic cancer."

Written by Grace Rattue ??
Copyright: Medical News Today
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Oral Bacteria Associated With Pancreatic Cancer Risk

Main Category: Pancreatic Cancer
Also Included In: Dentistry;  Infectious Diseases / Bacteria / Viruses
Article Date: 20 Sep 2012 - 1:00 PDT Current ratings for:
Oral Bacteria Associated With Pancreatic Cancer Risk

Pancreatic cancer is highly lethal and difficult to detect early. In a new study, researchers report that people who had high levels of antibodies for an infectious oral bacterium turned out to have double the risk for developing the cancer. High antibody levels for harmless oral bacteria, meanwhile, predicted a reduced pancreatic cancer risk.

A new study finds significant associations between antibodies for multiple oral bacteria and the risk of pancreatic cancer, adding support for the emerging idea that the ostensibly distant medical conditions are related.

The study of blood samples from more than 800 European adults, published in the journal Gut, found that high antibody levels for one of the more infectious periodontal bacterium strains of Porphyromonas gingivalis were associated with a two-fold risk for pancreatic cancer. Meanwhile, study subjects with high levels of antibodies for some kinds of harmless "commensal" oral bacteria were associated with a 45-percent lower risk of pancreatic cancer.

"The relative increase in risk from smoking is not much bigger than two," said Brown University epidemiologist Dominique Michaud, the paper's corresponding author. "If this is a real effect size of two, then potential impact of this finding is really significant."

Pancreatic cancer, which is difficult to detect and kills most patients within six months of diagnosis, is responsible for 40,000 deaths a year in the United States.

Several researchers, including Michaud, have found previous links between periodontal disease and pancreatic cancer. The Gut paper is the first study to test whether antibodies for oral bacteria are indicators of pancreatic cancer risk and the first study to associate the immune response to commensal bacteria with pancreatic cancer risk. The physiological mechanism linking oral bacteria and pancreatic cancer remains unknown, but the study strengthens the suggestion that there is one.

"This is not an established risk factor," said Michaud, who is also co-lead author with Jacques Izard, of the Forsyth Institute and Harvard University. "But I feel more confident that there is something going on. It's something we need to understand better."

Izard, a microbiologist, said the importance of bacteria in cancer is growing. "The impact of immune defense against both commensals and pathogenic bacteria undeniably plays a role," he said. "We need to further investigate the importance of bacteria in pancreatic cancer beyond the associated risk."

Prospective, controlled study

To conduct their research, Michaud and Izard drew on medical records and preserved blood samples collected by the Imperial College-led European Prospective Investigation into Cancer and Nutrition Study, a massive dataset of more than 500,000 adults in 10 countries. Detailed health histories and blood samples are available from more than 380,000 of the participants.

From that population, the researchers found 405 people who developed pancreatic cancer, but no other cancer, and who had blood samples available. The researchers also selected 416 demographically similar people who did not develop pancreatic cancer for comparison.

The researchers blinded themselves to which samples came from cancer patients and which didn't during their analysis of the blood, which consisted of measuring antibody concentrations for 25 pathogenic and commensal oral bacteria. In their study design and analysis they controlled for smoking, diabetes, body mass index, and other risk factors.

An important element of the study design was that date of the blood samples preceded the diagnosis of pancreatic cancer by as much as a decade, meaning that the significant difference in antibody levels were likely not a result of cancer.

Instead, the underlying mechanisms that link Porphyromonas gingivalis to pancreatic cancer could be causal, Michaud said, although much more research is needed to understand this association.

Meanwhile, the researchers speculate, the association of high levels of antibodies for commensal bacteria and pancreatic cancer, may indicate an innate, highly active immune response that is protective against cancer.

"Genetic determinants of immune surveillance clearly play a critical role in pancreatic cancer development," the authors wrote. "Consequently, it is plausible that elevated levels of antibodies to oral bacteria in individuals serve as a marker for a genetically stronger immune response, providing protection against carcinogenesis."

Michaud, who studies cancer risk factors generally, continues to investigate the association between oral bacteria and pancreatic cancer in collaboration with Izard.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our pancreatic cancer section for the latest news on this subject. Possible clue to a hard-to-diagnose cancer: http://news.brown.edu/files/imagecache/ursa_feature_image/article_images/Periodontic1.jpg
The National Cancer Institute was the primary funder of the study.
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