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What Research is Currently Being Done?
THE FOCUS IS ON PANCREATIC CANCER | Causes | Detection | Treatment
Research into the causes, prevention, detection, and treatment of pancreatic cancer is ongoing in the United States, and worldwide. 1
In 2001, the National Cancer Institute (NCI) convened a committee of scientists, clinicians, and advocates to review research
into pancreatic cancer and make recommendations regarding the most urgent needs and promising future directions. 2 The committee was named the Pancreatic Cancer Progress Review Group (PRG). As a result of the findings of the PRG, NCI funding
for pancreatic cancer research projects in all identified areas increased. The areas identified were:
- health of the field and overarching issues
- tumor biology
- risk, prevention, screening, and diagnosis
- therapy
- health services research
- scientific tool kit
Some of the 5-year funding results are shown in Table 13-1 .
Table 13-1 . Highlights of the National Cancer Institute Investment in Pancreatic Cancer Research 2
| |
2000 |
2005 |
Increase |
| Total funding for pancreatic cancer |
$21.8 million |
$66.7 million |
206% |
| Number of research projects |
85 |
204 |
140% |
| Number of investigators with NCI-funded grants |
34 |
82 |
141% |
| Number of scientific articlesacknowledging NCI support |
137 |
248 |
81% |
Additional highlights of the meeting include funding to 2:
- 3 Specialized Program of Research Excellence (SPORE) grants designed to create a flow of information from research to practice
- 129 active NCI-sponsored clinical trials relevant to pancreatic cancer
- 77 US institutions active in pancreatic cancer research
- 14 research projects that address three PRG priority areas: tumor biology; risk prevention, screening, and diagnosis; and
therapy
RESEARCH INTO CAUSES
Pancreatic cancer results from changes in DNA that cause cells to become cancerous. Researchers have identified genes that
may cause familial pancreatic cancer. These discoveries could lead to ways to predict which family members are at risk. 3-6 For example, recent studies have found that people who have two first-degree relatives (parent, child, sibling) with pancreatic
cancer have a greater risk of developing it. 7 The higher the number of family members who have been diagnosed with pancreatic cancer, the more that risk increases. In
2007, Wang and colleagues developed and made available to genetic counselors a computer program that can be used to calculate
a person’s risk of developing pancreatic cancer based on family history. 8
AT JEFFERSON we are developing a Pancreatic Tumor Registry.
Information about registering will be available soon.
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RESEARCH INTO DETECTION
Researchers are looking into tests to detect acquired genetic changes in pancreatic cancer. One of the most common DNA changes
affects the K-ras oncogene, which alters the regulation of cell growth. Endoscopic ultrasonography, endoscopic retrograde
cholangiopancreatography, and tests for K-ras changes are options currently being explored for people with a strong family
history of pancreatic cancer.1 (See Section 4 on Diagnosis.)
RESEARCH INTO TREATMENT
Research into various types of treatment are underway. Many clinical trials currently are being conducted to test new combinations
of chemotherapy drugs. The best ways to combine chemotherapy with radiation therapy or other therapies are being studied. 1 New drugs that are effective in other cancers are being tested to see if they work in patients with pancreatic cancer.One
of the main areas of research into the treatment of pancreatic cancer is targeted therapies. (See Section 7 on Treatment.) Targeted therapies are drugs that block the growth of cancer cells by interfering with specific molecules. Instead of destroying
all rapidly dividing cells, as traditional chemotherapy drugs do, targeted therapies kill only cancer cells. These treatments
are being developed and tested in clinical trials. The number of projects looking at targeted therapies has doubled in one
year. 2 Some of the therapies being investigated include 9:
- The K-ras oncogene by way of immunotherapy
- Matrix metalloproteinases (MMPs)
- Epidermal growth factor receptors (EGFRs)
- Angiogenesis factors
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AT JEFFERSON researchers are investigating various treatment options for pancreatic cancer, including:
- using anti-hypertensive drugs to halt progression of pancreatic cancer
- developing targeted therapies based on an individual's unique tumor cells
- evaluating the effectiveness of a particular combination of chemotherapy drugs
- comparing two surgical techniques to determine whether one leads to superior results
Learn more about our ongoing research efforts
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In active immunotherapy, which is a targeted therapy that works in the same way that vaccines work, the goal is for the immune system to recognize
abnormal chemicals present in pancreatic cancer cells. For example, the K-ras protein is altered in more than 90 percent of
pancreatic cancers. Researchers are testing ways to help the immune system attack cells that contain altered K-ras protein.
In passive immunotherapy, another targeted therapy, man-made antibodies to proteins are injected into patients. The goal is to have these antibodies
seek out pancreatic cancer cells that contain abnormal K-ras protein or other abnormal proteins such as carcinoembryonic antigen,
or CEA. The antibodies have radioactive atoms or toxins attached to destroy the abnormal protein.
Matrix metalloproteinase (MMP) inhibitors are a new class of drugs under study. Cancer cells make enzymes that dissolve the
surrounding substance and allow cancer cells to spread. MMP inhibitors work by blocking these enzymes.
Epidermal growth factor receptors (EGFRs) are molecules on the surface of cancer cells that may stimulate the growth of many
types of cancers, including pancreatic cancer. Researchers are studying different drugs that block these and other receptors.
Angiogenesis factors are blood vessel growth factors. To block the growth of new vessels that tumors depend on, and thereby
starve the tumor of nourishment, anti-angiogenesis drugs have been developed. These drugs are being studied in clinical trials.
In 2007 results of another exciting avenue in pancreatic cancer research were reported. Researchers at the University of Michigan
Comprehensive Cancer Center identified cancer stem cells in pancreatic tumors. Cancer stem cells are believed to replicate to drive tumor growth. Current cancer treatments do not attack these cells. By identifying cancer
stem cells, researchers may be able to develop drugs to target and kill them. This is a radically different approach compared
with current treatments, which shrink tumors by killing as many cells as possible, including healthy cells. Stem cells also
have been identified in breast, brain, central nervous system, and colon cancers, and in leukemia. 10
In 2008, Jefferson researchers found that metastatic cancer cells in the lymph nodes of patients with pancreatic cancer produce enough of the protein, IDO, to essentially
wall-off the immune system’s T-cells and recruit cells that suppress the immune system’s response to the tumor. The findings
might mean not only a better way to detect pancreatic cancer spreading to lymph nodes, but also could enhance tumor immune
therapy strategies against the fast-moving, deadly disease.
Read the news release |
This extensive research and these new developments offer hope for the thousands of people who will be diagnosed with pancreatic
cancer. 2
THE LUSTGARTEN FOUNDATION FOR PANCREATIC CANCER RESEARCH
The Lustgarten Foundation for Pancreatic Cancer Research is the nation’s largest private supporter of pancreatic cancer research.
Encouraged by the remarkable potential of genomics for the future of pancreatic cancer research and treatment, in 2007 The
Lustgarten Foundation initiated a multi-million dollar project to sequence the genome of pancreatic cancers. It is anticipated
that this endeavor will revolutionize the ways in which pancreatic cancer is diagnosed and treated for decades to come.
World-class investigator Bert Vogelstein, MD, and his team of collaborators at The Sidney Kimmel Comprehensive Cancer Center
of The Johns Hopkins University Medical Institutions, including Kenneth W. Kinzler, PhD, Victor E. Velculescu, MD, and Scott
E. Kern, MD, have been selected for the project. Dr. Vogelstein and his team have developed novel technologies that enable
rapid analysis of the different genomes of cancers. The team completed the first sequencing of the breast and colorectal cancer
genomes, identifying a treasure trove of genes whose involvement in those cancers was not previously known.
For more information about research and the latest in pancreatic cancer, visit
http://www.lustgarten.org.
REFERENCES ! Click reference number to return to text.
1. American Cancer Society. Pancreatic cancer. http://documents.cancer.org/116.00. Accessed April 25, 2007.
2. National Cancer Institute. Pancreatic cancer: five years of research projects. December 2006. http://planning.cancer.gov/disease/2006PancreaticProgRpt.pdf.
Accessed April 18, 2007.
3. Arnold MA, Goggins M. BRCA2 and predisposition to pancreatic and other cancers. Expert Rev Mol Med. 2001;3:1-10.
4. Izeradjene K, Combs C, Best M, et al. Kras(G12D) and Smad4/Dpc4 haploinsufficiency cooperate to induce mucinous cystic neoplasms
and invasive adenocarcinoma of the pancreas. Cancer Cell. 2007;11:229-43.
5. Klein AP, Beaty TH, Bailey-Wilson JE, et al. Evidence for major gene influencing risk of pancreatic cancer. Genet Epidemiol.
2002;23:133-49.
6. Lynch HT, Brand RE, Deters CA, et al. Hereditary pancreatic cancer. Pancreatology. 2001;1:466-71.
7. Klein AP, Brune KA, Petersen GM, et al. Prospective risk of pancreatic cancer in familial pancreatic cancer kindreds. Cancer
Res. 2004;64:2634-8.
8. Wang W, Chen S, Brune KA, et al. PancPRO: risk assessment for individuals with a family history of pancreatic cancer. J Clin
Oncol. 2007;25:1717-22.
9. McKenna S, Eatock M. The medical management of pancreatic cancer: a review. The Oncologist. 2003;8:149-60.
10. Li C, Heidt DG, Dalerba P, et al. Identification of pancreatic cancer stem cells. Cancer Res. 2007;567:1030-7.
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