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2003 Pancreas Cancer News at Johns Hopkins
Fundraisers to Benefit Hopkins Pancreas Cancer Research
November 9, 2003
Two fundraising events were held in different areas of the country to benefit pancreatic cancer research at John Hopkins. These fundraisers honored two very special men, helped to raise critical money to fight this dreadful disease, and celebrated November as Pancreas Cancer Awareness Month.
"The Second Annual Ride to Make a Difference for Pancreatic Cancer" was held in Atlanta, Georgia by the Joseph C. Monastra Foundation for Pancreatic Cancer Research. Held on a beautiful day with a full police escort of 5 motorcycle cops, the 75-mile ride was safe, smooth and enjoyable. The generosity shown by the biker community of Georgia was overwhelming with one auction item being donated back after being sold only to be sold again. To learn more about this remarkable family and their fundraising efforts, visit our Web site's overview of the Monastra family and Foundation.
The George Rubis Endowment for Pancreatic Cancer Research held "The First Annual Run for George" in Englewood Cliffs, New Jersey. The 5K race, silent auction, food and carnival games were enjoyed by the family, friends, and the local community in honor of George Rubis' memory and to support pancreatic cancer research at Johns Hopkins. Kieran Brune, Coordinator of the National Familial Pancreas Tumor Registry, ran the 5K event and spoke to those in attendance. To learn more about this remarkable family and their fundraising events, visit our web site section on Photos from "Run for George" 11/11/03.
New Pathway for Cancer Discovered in Hedgehog
September 17, 2003
Friends — I wanted to update you on a remarkable discovery from the
pancreatic cancer research team here at Johns Hopkins. Today the journal
Nature released an on-line version of a paper by Drs. Berman,
Maitra and Beachy in which they demonstrate the activation of the
"sonic hedgehog gene" in pancreatic and biliary cancers
(http://www.nature.com/nature).
The complete print version will appear
in a few weeks in Nature.
"Sonic hedgehog" is part of a cell pathway that plays an
important role in embryogenesis. Cell pathways are groups of proteins
within cells that interact/communicate with each other. Embryogenesis is
the formation of the embryo. Dr. Beachy discovered several of the key
components of this pathway, studying, of all things, fruit fly genetics.
It was shown that alterations in the sonic hedgehog pathway caused fruit
fly larva to look like, you guessed it, the computer game character
"sonic hedgehog". Dr. Beachy's team then went on to show that
this same pathway is important in human embryogenesis and that the sonic
hedgehog pathway plays a key role in maintaining stem cells in our bodies.
Dr. Beachy was elected to the National Academy of Science for this work.
Now, Drs. Beachy, Maitra and Berman team together to show that the sonic
hedgehog pathway is activated in human cancers, including cancers of the
pancreas and biliary tree. Furthermore, they show that when they block
the pathway using a drug called cyclopamine, that they completely block
tumor growth.
This paper is very exciting to me for several reasons. First, it helps
us understand the fundamental biology of pancreatic and biliary cancer.
Their data show that a pathway that regulates stem cells is altered in
these cancers (for scientists this is a very exciting idea). Second, the
discovery of this pathway's role in human pancreatic and biliary cancer
opens an entire new area for treating these cancers-- targeting pancreatic
and biliary cancers using drugs, such as cyclopamine, that specifically
inhibit the sonic hedgehog pathway. The team now plans to test a large
panel of blockers ("inhibitors") of the sonic hedgehog pathway
to determine which inhibitor provides the maximum anti-tumor effect and
the minimum side effects. Third, the study is an example of what, in my
opinion, makes Hopkins such a special place- the willingness of creative
scientists from very diverse fields to work together to tackle big
problems. Fourth, the creation of the cell lines and cancer xenografts
that were central to this research was made possible by private donations.
This is a wonderful example of how private philanthropy can support
cutting edge research and have a significant impact in the war on
cancer.
Ralph H. Hruban, M.D.
Professor of Pathology and of Oncology
Johns Hopkins Is Number One Again
July 18, 2003
For the 13th consecutive year, Johns Hopkins comes
in at the very top of the
list in the U.S. News & World Report's annual ranking of American
hospitals. Hopkins ranked in the top 10 in 16 of 17 specialties,
including cancer. Ratings are based on reputation (ranking by randomly
selected physicians), mortality rates, and hospital factors such as
discharges, ratio of nurses to beds, technology services,
hospice/palliative care services, and whether or not the hospital is an
NCI Cancer Center.
New Targets for Aberrant Methylation in Pancreas Cancer
July 10, 2003
Research by Norihiro Sato MD, PhD in the laboratory of Dr. Michael Goggins has led to the discovery of
multiple genes that undergo silencing by methylation in pancreatic cancer. Knowledge of these genes
provides us with a better understanding of the role of DNA methylation in pancreatic cancer development.
The authors also showed that these abnormally methylated genes can be detected in pancreatic juice from
patients with pancreatic cancer and raising hopes that their detection could aid in the early diagnosis of
pancreatic cancer.
Discovery of novel targets for aberrant methylation in pancreatic carcinoma using high-throughput microarrays.
Cancer Res. 2003 Jul 1;63(13):3735-42.
Anti-Cancer Drug Can Lead to Cancer Invasion
July 10, 2003
In the February 19th issue of the Journal of the National Cancer Institute, Sato and colleagues report an
unexpected adverse effect of an anti-cancer drug that is used to remove "methyl" groups (carbon-hydrogen)
from DNA. The authors find that this drug can switch on certain genes (matrix metalloproteinases) that lead
to cancer invasion. This effect is the result of the removal of methyl groups that function to keep these
genes switched off in pancreas cells.
Sato N, Maehara N, Su GH, Goggins M.
Effects of 5-aza-2'-deoxycytidine on matrix metalloproteinase expression and pancreatic cancer cell
invasiveness.
J Natl Cancer Inst. 2003 Feb 19;95(4):327-30.
Pancreatic Cancer Linked to Errant Reactivation of
Embryo Cell Pathway
June 25, 2003
Research by Johns Hopkins Kimmel Cancer Center specialists has uncovered a novel pathway in the origin of pancreatic
cancers. The Notch pathway, normally turned off in adults, can be
turned on after injury to the pancreas.
See the
Hopkins
news release for more details.
The findings of Dr. Steven Leach et al. are reported in the
June
23, 2003, issue of Cancer Cell.
Washington D.C. PanCAN Visits Johns Hopkins
June 22, 2003
On Saturday June 7, 2003 close to 25 members of the Washington D.C. PanCAN group visited Johns Hopkins. The
visit was organized by Mary Zapor from PanCAN and Sandy Markowitz from Hopkins. The visitors toured some of
the labs, spoke with the scientists, and listened to talks on the clinical treatment of pancreatic cancer from Drs.
Yeo and Laheru. In the end, the group had an informal lunch with the doctors and scientists. The morning was
educational, but most importantly it motivated the Hopkins docs to work that much harder in the battle against
pancreatic cancer, and it gave the PanCAN visitors a sense of the breadth and depth of research going on at Hopkins
and a sense of excitement that exists now in the research labs at Hopkins. To see pictures from this wonderful visit
go to: http://pathology2.jhu.edu/pancreas/pancanvisit/index.htm
The visit demonstrates the value of patient advocates, physicians and scientists working together.
If you would like to learn more about how you can support pancreatic cancer research at Johns Hopkins visit our Support Page.
Animation Explaining Mouse Models of Pancreatic Cancer
June 5, 2003
A number of you have asked us to explain the important, but very complex,
work that Gloria Su, PhD does in her lab developing mouse models of
pancreatic cancer. One of the Art as Applied to Medicine students here at
Johns Hopkins, Christian Rose, has developed a web animation to explain
Dr. Su's research. We have posted it on the
FAQ page of this
Web site. It is a big file, so you will have to be patient downloading
it. If you still have problems, try
downloading
the new Macromedia Flash Player 6.
We hope you find this animation interesting and educational.
Fanconi Gene Abnormalities in Pancreatic Cancer
May 8, 2003
Eight years ago while studying pancreatic cancers, the Kern Laboratory
found mutations of a new gene. Soon, this laboratory and others working in
other tumor systems found that mutations of the gene were often inherited,
raising the risk for pancreatic, ovarian, and breast cancer when an
individual inherits one bad copy of the gene. This was the second gene
found to cause inherited breast cancer, thus leading to the gene name,
BRCA2.
In a paper published in the May 15, 2003 issue of the journal Cancer
Research, Dr. Michiel van der Heijden and colleagues, also working in
the Kern Laboratory, is following up on that earlier discovery. They knew
that BRCA2 was one of the genes that gives rise to a rare syndrome,
Fanconi anemia, when two bad copies are inherited by an individual.
Fanconi anemia causes skeletal abnormalities and progressive bone marrow
failure, and genes other than BRCA2 are responsible for most cases of the
syndrome. In each case, one needed to inherit two bad copies in order to
develop the syndrome. But what if an individual only inherited one bad
copy, a condition that was previously thought to be lacking any
association with disease? Was it possible that some of these other Fanconi
genes might play a role in pancreatic cancer? Dr. van der Heijden found
the answer to be "Yes!"
The scientists studied two of the Fanconi genes, FANCC and FANCG.
Inherited and new mutations were found in a number of pancreatic cancers.
Some of these mutations are inherited, meaning that individuals were
inheriting a risk for pancreatic cancer. Fanconi anemia gene mutations are
found in about 1 in 300 persons in the general population, and in 1 in
about 75 Ashkenazi Jews. It remains to be determined how much the risk of
cancer increases for such persons, and whether cancers other than
pancreatic cancer would be included in the higher risk. Dr. van der
Heijden and colleagues had another interesting finding; three of the nine
persons whose pancreas cancer had young onset (less than 50 years of age)
had such mutations. He perhaps had discovered a fairly common cause of
young-onset pancreatic cancer.
There are no easy tests for the kinds of Fanconi gene mutations now
being studied, but such tests may become available in the future. Such
testing is likely to be of clinical importance. Cells that are defective
in the Fanconi genes are known from other research to be highly sensitive
to certain chemicals. If may be possible in the future to recommend a
different therapeutic regimen for patients with these mutations. More
research in this exciting new area is needed.
Read Press
Release
Activin Abnormalities in Pancreatic Cancer
February 15, 2003
Two years ago while studying pancreatic cancers in the Kern Laboratory,
Dr. Gloria Su and colleagues identified mutations in a gene that allows
cells to respond to the presence of the extracellular protein, activin.
Activin is part of a major system that vertebrate cells use to control
populations of cells during development. It now appeared that the adult
tissues also used activin for a similar purpose. The cancer cells had
lost this form of control by activin by evolving dysfunctional mutations
in the type IB receptor for activin that would normally be present on the
surface of cells.
In a paper to be published in the March 1, 2003 issue of the journal
Cancer Research, Dr. Paula Hempen and colleagues, also working in the Kern
Laboratory, have followed up on that earlier discovery. They find
additional mutations of another form of the activin receptor, extending
the numbers of tumors known to have abnormalities in the activin system.
The newly discovered mutations are in the ACVR2 gene, the activin type 2
receptor. The ACVR2 gene mutations were found in nearly all
gastrointestinal tumors that had defects in a DNA-repair pathway involved
in familial forms of cancer, including families at high risk of
colorectal, pancreatic, and endometrial cancers.
These activin receptor mutations seem to be a fundamental change,
without which the tumors perhaps could not occur. Dr. Byungwoo Ryu and
colleagues in the Kern Laboratory therefore studied the genes that respond
to activin signals to uncover the ways in which the cells are regulated by
activin. Using a high-density gene expression screen, they studied gene
expression changes characteristic of activin. Some of the genes regulated
include genes that directly control cell division. This work is currently
in press at the journal Cancer Biology & Therapy, and represents the
largest study of gene responses to activin published to date.
Recent Publication Describes Pancreatic Cancer
 Current Problems in Cancer:
Pancreatic Cancer
July/August 2002 • Volume 26 • Number 4
Theresa Pluth Yeo, MSN, MPH, et al.
Written by Johns Hopkins physicians and researchers involved in
pancreas cancer treatment and study, this article provides a comprehensive
overview of pancreas cancer.
New Animation Details Anti-PC Vaccine
January 27, 2003
We've added an animation to our Website to describe the pancreas cancer
vaccine being developed by Dr. Liz Jaffee here at Johns Hopkins. Created
by a Medical Arts student, Helen MacFarlane, the animation helps the
layperson understand how the vaccine is made and how it works. The vaccine
is currently in a Phase 2 trial and is still enrolling participants. Click here to view the animation
and learn more about this vaccine.
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