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Diffuse Gastric Cancer
Ann Framp, RGON, PG Cert
Gastric cancer is one of the leading causes of cancer deaths around the world. This article provides an
overview of gastric cancer using a unique case study involving a New Zealand Maori family genetically
predisposed to diffuse gastric cancer. The pathophysiology of diffuse gastric cancer, including prognosis,
diagnosis, and treatment, along with important patient considerations is highlighted.
G
astric cancer is still one of the major causes of
cancer deaths around the world, but its inci-
dence is slowly decreasing (Joo et al., 2001).
Most benign and malignant neoplasms of the
stomach arise from the epithelium. Although tumors of the
muscle, adipose, or lymphoid cells of the stomach do occur,
95% of malignant neoplasms of the stomach are adenocar-
cinomas. Adenocarcinomas have been divided histologically
into two types: the intestinal type and the diffuse type. The
aim of the endoscopy department is to diagnose the condi-
tion at the earliest possible stage to enable the patient to
take a course of treatment that will provide the best chances
of survival to beat this aggressive, life-threatening disease.
DM is a 33-year-old Maori woman. I first came into con-
tact with her in 1999 when she entered the endoscopic
screening program because she was a known E-cadherin
carrier. She has been having chromoendoscopy surveillance
for 4 years. This year she made a decision to have a pro-
phylactic gastrectomy; however, she requested a final chro-
moendoscopy, biopsy, and results prior to the procedure.
Background
DM is from a Maori family within the Tauranga region. The
family has a very aggressive form of familial diffuse gastric
cancer. Since the 1960s, 28 members of this family have died
of diffuse gastric cancer, many before the age of 40 and the
youngest being 14. In the early 1990s, the afflicted family met
to form a trust to try to find a reason for the cancer being
so prevalent among their close relatives. They traced their
whakapapa (family tree) using libraries, the registry of births,
Received December 12, 2005; accepted February 17, 2006.
About the author: Ann Framp, RGON, PG Cert, is a Nurse Lecturer,
School of Nursing, Bay of Plenty Polytechnic, Tauranga, New Zealand.
Correspondence to: Ann Framp, RGON, PG Cert, 77 James Cook Drive,
Welcome Bay, Tauranga, New Zealand (e-mail: annfra@actrix.co.nz).
232
deaths, and marriages, hospital records, and family members’
gravestones. This is not something Maori normally do. The
Maori family signed a kawenata (covenant) between the fam-
ily and God stating that the research was to be used only for
the cancer.
Through a chance telephone call, the family found a sci-
entist who had an interest in human genetics. Funding was
secured from the Health Research Council for the scientist to
attempt to identify an abnormal gene. Following 18 months
of research, the scientist found that the diffuse gastric cancer
was a result of an autosomal dominant genetic mutation—if
the person inherits the gene, it will be expressed.
Pathophysiology
In gastric cancer, the predisposing gene is mapped to an inter-
val on chromosome 16q22.1 containing the gene for the cell-
to-cell adhesion protein E-cadherin (CDH-1) (Keller et al.,
1999). The cadherins are a family of calcium-dependent
transmembrane linker proteins. The first three to be discov-
ered were named according to their tissue origin:
E-cadherin from epithelium, N-cadherin from neural tissue,
and P-cadherin from placenta. Studies show that the cadherins
are important intercellular adhesion receptors. E-cadherin
function is crucial for the establishment and maintenance of
epithelial tissue polarity and structural integrity (Keller et al.).
Thousands of cell adhesion molecules are found on almost
every cell in the body. One of the functions of the sticky glyco-
proteins (cadherins and integrins) is that they are the molecu-
lar “Velcro” that cells use to anchor themselves to molecules
in the extracellular space and to each other. The extracellular
portion of the E-cadherin molecule forms homophilic cellu-
lar bonds (the cells bind to each other). The intracellular
part provides a link to the actin cytoskeleton through an
association with the catenins, cytoplasmic plaque proteins
(Keller et al., 1999).
The cytoskeleton comprises rods that act as the cell’s
“bones” and “muscles” by supporting the cellular structures.
3566-05_GN2903-Framp.qxd 5/30/06 1:10 PM Page 233
The three types of rods are microtubules, microfilaments, and
intermediate filaments. The microfilaments are thin strands
of the contractile protein actin. Nearly all cells have a net-
work of microfilaments that brace and strengthen the cell
surface. Actin microfilaments interact with myosin, a motor
protein, to generate contractile forces within a muscle cell that
form a furrow that pinches a cell in two during cell division.
In diffuse gastric cancer, tumor cells have lost cell-to-cell
contacts and invade surrounding tissues as single cells (Keller
et al., 1999).
Alteration of intercellular adhesion will influence the
process of gastric cancer as metastatic cells break away from
the primary tumor, travel into the circulation, and then adhere
to secondary sites. The E-cadherin–catenin bond is essential
for maintaining intercellular adhesion and is thought to sup-
press epithelial tumor cell invasiveness and metastasis (Joo
et al., 2001).
In the diffuse type of gastric cancer, glandular structure is
often not present and cells are scattered as either solitary
cells or small clusters of cells. The diffuse type extends widely
with no distinct margins, and the cell cytoplasm often con-
tains mucus and is termed as signet ring cells. “Gastric
cancer with signet ring cell features is characterized by cells
containing a sufficient intracytoplasmic volume of mucin
to compress the nucleus against the periphery of the cell”
(Theuer, Nastanski, Brewster, Butler, & Anton-Culver, 1999,
p. 915). The E-cadherin–catenin complex is expressed in all
normal epithelial cells and is often reduced in early and
advanced gastric cancer as compared with normal epithelium
(Joo et al., 2001).
Prognosis
The penetrance of germline CDH-1 mutations is estimated
to be 70%; therefore, an E-cadherin gene mutation carrier in
a hereditary diffuse gastric cancer (HDGC) family has an
estimated 70% lifetime risk of developing gastric carcinoma.
Prognosis of diffuse gastric cancer is poor, with a 5-year sur-
vival of 10% (Chun et al., 2001). Detection of the cancer
is more difficult as it typically spreads submucosally and is
more extensive throughout the stomach than is evident from
any mucosal abnormalities observed either by endoscopy or
during operation. Clinical diagnosis therefore usually tends
to occur at an advanced and incurable stage.
There are four layers of the stomach lining: the mucosa,
the submucosa, the muscularis propria, and the serosa.
Advanced gastric cancer is the stage when the disease has
penetrated the muscular layer. It is usually associated with the
spread of tumor and as a result is rarely curable (Peckham,
Pinedo, & Veronesi, 1995).
The most common symptoms of diffuse gastric cancer are
weight loss (in 50% to 70% of patients) and epigastric pain
(in 45% to 65% of patients) followed by nausea and vom-
iting or anorexia. Other symptoms include early satiety,
belching, upper abdominal discomfort, pain when eating,
and dysphagia. Physical signs are late events and almost
always indicate that it is too late for curative surgery.
Gastric cancer metastasizes mainly by the lymphatic route
to regional lymph nodes of the lesser and greater curvature,
the porta hepatis, and the subpyloric region. Distant lym-
phatic metastases also occur, the most common being an
enlarged supraclavicular node, called Virchow’s (Sister Mary
VOLUME 29 • NUMBER 3
Joseph’s) node or sentinel node. Spread of the cancer may
affect any organ including the liver, lung, or brain. Direct inva-
sion to nearby organs is often encountered. Medical practi-
tioners also acknowledge that carcinoma of the stomach can
also spread to the ovary and it is termed a Krukenberg tumor
(Fuchs & Mayer, 1995).
Diagnosis and Treatment
Once diagnosed with the positive gene, the person has
knowledge of the huge risk associated with the development
of the cancer. In New Zealand, genetic counselling is offered
to people who are found to express the genetic mutation. It
is important as there are options for these people once the
gene is discovered. Early detection and early treatment are
believed to be effective in reducing mortality from gastric
cancer, especially in Japan where the incidence of this disease
is the highest in the world. (Tsukuma, Oshima, Narahara, &
Morii, 2000).
A literature review was undertaken at the Tauranga Hos-
pital Endoscopy Unit to find methods to enhance endoscopic
detection of early diffuse gastric cancer. Articles have been
published from other countries regarding vital dye staining,
which is used to detect early development of gastric cancer.
The main article used was the one written by Fennerty
(1994) that outlined the procedure of vital dye staining using
a combination of methylene blue and Congo red. This dye
is sprayed onto the surface of the stomach during a gastros-
copy to identify any early areas of abnormality.
Once the positive gene is discovered, a screening pro-
gram for gene carriers is offered that consists of an annual
chromoendoscopy. People can have the blood test for gene
identification from the age of 13 and screening can start
from 18 years of age.
Privacy for patients
Nurses involved with these patients must be aware of the
family’s cultural and privacy needs. A day is set aside for dye
testing and only those who are immediate family members
and know the gene status of one another attend the same
session. It is important that everything is very carefully
explained and the procedure is as comfortable and tolerable
as possible as these patients are going to return annually and
also tell other family members about their experiences. It
is very frightening for these individuals to undertake the
dye-testing procedure because of fear of the outcome of the
gastroscopy and the decision they may need to make if they
are found to have diffuse gastric cancer.
Maori do not view health in the same sense as non-Maori
do. Non-Maori like to be well in a physical sense, whereas
Maori see health as a concept of the whole person with four
cornerstones of health. These have been described by Durie
(1994) as Taha Wairua/spiritual well-being, Taha Hinengaro/
mental and emotional well-being, Taha Tinana/physical well-
being, and Taha Whanau/family and community well-being.
All four are considered by Maori to be the foundation of
good health and ensure strength and symmetry. Therefore on
dye-testing days, members from one family attend, and sup-
port people are also present.
All nurses who work in the endoscopy unit are aware of
the implications for these patients, the fears of the disease,
and how many family members they have lost from this
233
3566-05_GN2903-Framp.qxd 5/30/06 1:10 PM Page 234
aggressive cancer. The physician always spends time with the
patients postprocedure so that they may ask questions and
discuss implications of results.
Postprocedure Treatment
Dye testing involves the patient being fasted from midnight
because an empty stomach is required to enable a good view
of all of the stomach mucosa and for safety to prevent aspi-
ration due to the administration of sedation for the gastros-
copy. The patient is given Parvolex (acetylcysteine) orally, a
drug that removes the mucus from the lining of the stomach.
Acetylcysteine is a derivative of the amino acid cysteine
(Curel, Kumar, & Robinson, 2004). It has been used mostly
as a mucolytic agent for use in pulmonary diseases associated
with increased viscosity of bronchial secretions. Mucus is
composed of more than 95% water; however, its physical
characteristics are a result of glycoproteins. These glyco-
proteins bind to each other by ways of disulfide bonds and
give the mucus viscosity. Acetylcysteine ruptures the covalent
bond between sulfur atoms, which destroys the gel structure
of mucus, followed by disintegration of the epithelial mucoid
cap (Fennerty, 1994). This process allows the dye to come
into close contact with the epithelial lining.
The patient is taken into the endoscopy room and intra-
venous sedation is administered. In our unit, patients receive
hypnovel and fentanyl to sedate them so that they are able
to tolerate the procedure, and buscopan is administered to
inhibit peristalsis.
Drug Actions
Hypnovel is a hypnotic drug that has a very rapid sedative
and sleep-inducing effect. Following intravenous administra-
tion, amnesia of short duration occurs. Hypnovel binds to the
gamma-aminobutyric acid receptors in the brain. The gamma-
aminobutyric acid receptor consists of a multimolecular com-
plex that controls a chloride ion channel and contains specific
binding sites for benzodiazepines and barbiturates (Rang,
Dale, & Ritter, 1995).
Fentanyl is an opioid that is short acting and is used intra-
venously to treat pain. Fentanyl attaches to the mu and delta
receptors, which are specific membrane receptor proteins on
nerve cells. Mu receptors are thought to be responsible for
most of the analgesic effects of opioids, and the receptors
also trigger some unwanted side effects (e.g., respiratory
depression, euphoria, dependence). Opioids are known to
exert effects on ion channels through a direct G-protein cou-
pling to the channel, not involving any intracellular second
messenger. By this means, opioids promote the opening of
potassium channels and prevent the opening of calcium chan-
nels. These membrane effects reduce both neuronal excitabil-
ity (as the increased potassium conductance causes hyper-
polarization of the membrane) and transmitter release (due to
inhibition of calcium entry). The overall effect therefore
occurs at cellular level (Rang et al., 1995).
Buscopan exerts a spasmolytic action on the smooth mus-
cle of the gastrointestinal, biliary, and urinary tracts. It does
not enter the central nervous system. Peripheral anticholin-
ergic effects result from a ganglion-blocking action within
the visceral wall as well as from antimuscarinic activity
(Curel et al., 2004).
234
Procedure
The scope is inserted and the gastrointestinal tract is exam-
ined. If there is any sign of active ulcer disease, the dye-testing
procedure is not continued, as pentagastrin is contraindicated
in active ulcer disease. If there is no sign of ulcers, penta-
gastrin is given at a dose of 5 mcg/kg. Pentagastrin is a syn-
thetic pentapeptide that mimics the actions of natural gas-
trins. The most prominent action of pentagastrin is to
stimulate the secretion of gastric acid, pepsin, and intrinsic
factor (Rang et al., 1995).
The interior of the stomach is sprayed with a catheter
inserted into the biopsy channel of the endoscope. We begin
with methylene blue and then spray Congo red. Any cells that
are not secreting acid are abnormal cells. They will not react
with the blue or red dye and appear bleached. This combina-
tion staining with Congo red and methylene blue increases
the detection of early gastric cancer from 28% detected by
endoscopic examination alone to 89% (Fennerty, 1994). Any
white areas are biopsied for early gastric cancer. A water
pump is then used to wash the excess dye away.
Methylene blue is taken up by absorbing epithelium
actively. If there is any intestinal metaplasia in the stomach (a
precancerous condition), the area will take up the blue dye.
Any area that remains blue despite the washing is biopsied for
intestinal metaplasia. It is now becoming understood through
research that intestinal metaplasia is not a precursor for dif-
fuse gastric cancer but rather for the intestinal type of gastric
cancer. The intestinal type is strongly associated with Heli-
cobacter pylori and usually arises in an area of chronic gas-
tritis, gastric atrophy, and intestinal metaplasia; this finding
would be further supported with the work undertaken at the
Tauranga Hospital Endoscopy Unit (Shaw et al., 2005).
The dye-testing procedure was commenced at the Tau-
ranga Hospital Endoscopy Unit on February 3, 1999 and
74 chromoendoscopies were completed in the first 4 years.
During this period, five early gastric cancers have been
detected.
Early diagnosis is now a highly specialized, intensive, and
multidisciplinary undertaking, applicable both to early cancer
and to less advanced stages of invasive cancer. Early diagnosis
has an unequivocal life-saving impact (Fuchs & Mayer, 1995).
DM had a dye test in May 2002 that showed no abnor-
mality. Her mother died of gastric cancer at 42 years of age
and DM has tested positive for the CDH-1/E-cadherin gene.
DM’s brother, RM, is 30 years of age and had been to our
unit for dye testing. A bleached area was discovered, which
was proven to be gastric cancer. RM underwent a total
gastrectomy and his stomach was analyzed by a pathologist.
The stomach had extensive sampling from all areas of the
mucosa and 214 foci of intramucosal signet ring cell adeno-
carcinoma were discovered. The E-cadherin immunohisto-
chemistry on selected foci showed reduced E-cadherin
expression (Charlton et al., 2003).
DM was finding it increasingly difficult not to focus on
the thought that she would develop the gastric cancer and
was becoming stressed and unwell with the threat ever pres-
ent. She is from a family that has faced great sadness with the
loss of many of the family members. Once the test is positive,
it can be like a life sentence because the chance of develop-
ing the cancer is so high. The anxiety surrounding the impli-
cations of this alone can cause ill health. There are also con-
cerns around gaining medical insurance and employment if
GASTROENTEROLOGY NURSING
3566-05_GN2903-Framp.qxd 5/30/06 1:10 PM Page 235
the results are known, so the test results have to remain com-
pletely confidential. DM began to consider undergoing a
prophylactic total gastrectomy and visited a professor in
Auckland to discuss the possibility.
Prophylactic Total Gastrectomy
Lewis et al. (2001) state that penetrance of the gene is 70%
to 80%, and the average age of onset of gastric cancer is
37 years. These characteristics have led to the consideration
of prophylactic total gastrectomy in family members with
CDH-1 mutations. E-cadherin gene mutation in association
with familial gastric cancer is a new disease for which pro-
phylactic surgery must be considered. The morbidity of this
operation is much higher than that for other genetic diseases,
but the alternative is a mortality risk of more than 80% at a
young age.
Lewis et al. (2001) state that arranging genetic coun-
selling for these patients is essential, and any decision to pro-
ceed with surgery should be taken slowly, with maximal con-
sultation with family members and external counsellors and
advisers. It is particularly helpful to arrange counselling with
other patients who have undergone total gastrectomy so the
patient considering the procedure can ask questions from
someone with first-hand experience. These patients face a
difficult choice because failure to act means living with the
risk of developing cancer, whereas a decision to undergo a
prophylactic gastrectomy procedure poses significant risk
and lifestyle adjustment is also necessary.
Brennan (2003) states the mortality rate at his institution
is currently 3%, but there are series reported in the year 2000
that describe an operative mortality rate for total gastrectomy
of 7% to 15%. Early postoperative complications include
anastomotic failure, bleeding, ileus, transit failure at the anas-
tomosis, cholecystitis, pancreatitis, pulmonary infections, and
thromboembolism.
Chun et al. (2001) state that although total gastrectomy
for benign disease does not substantially alter nutritional
status, total gastrectomy for known gastric cancer results in
weight loss, malabsorption, disturbed eating habits, and post-
prandial symptoms. Studies on total gastrectomy for gastric
cancer suggest an average weight loss of 4–7 kg. Weight loss
after total gastrectomy with Roux-enY esophagojejunostomy
is partly due to changes in the rate and pathway of enteric
flow of chyme. Rapid intestinal transit time results in short-
ened contact of chyme with absorptive epithelium, causing
malabsorption of nutrients normally digested by mucosal
enzymes, including lactase.
Bypassing the duodenum and alterations in secretin and
cholecystokinin secretion after total gastrectomy result in rel-
ative pancreatic insufficiency and a 66–100% incidence of fat
malabsorption and steatorrhea. Dumping occurs in 20% to
30% of patents and is caused by rapid emptying of hyper-
osmolar carbohydrates into the small bowel and release in
enteric hormones. In addition, patients may have malabsorp-
tion from bacterial overgrowth, postprandial fullness from
loss of the stomach’s reservoir function, and iron and vitamin
B12 deficiencies (Fitzgerald & Caldas, 2004).
After much consideration, DM felt strongly about going
ahead with the prophylactic gastrectomy. It was decided
that she would come into the endoscopy department for one
last gastroscopy and dye test prior to the surgery. During the
dye testing, a very small bleached patch was noted, the size
VOLUME 29 • NUMBER 3
of biopsy forceps (3 mm); but it was in the transitional zone
where the other bleached areas had been detected in other
family members. A biopsy was taken and it showed diffuse
gastric cancer.
This was the affirmation DM required. She underwent
a Roux-en Y total gastrectomy 4 weeks later. She had no
immediate postoperative complications, but 3 weeks later
she began to suffer from early satiety, difficulty swallowing,
and postprandial abdominal cramps. She had a gastroscopy
and was found to have an anastomotic stricture. This was
dilated and she was then able to be discharged home and is
now doing very well.
Other Risks
An epidemiological study of 11 different HDGC families
undertaken by Pharoah, Guilford, and Caldas (2001) indi-
cates that lobular breast carcinoma might be associated with
E-cadherin germline mutations. Women have a 39% lifetime
risk of developing breast cancer with a mean age at diagnosis
of 53 years. DM is also possibly at risk of developing lobular
breast cancer, despite the fact that no female mutation carri-
ers in her particular HDGC family have had a histological
diagnosis of lobular breast cancer. Because most have died of
gastric cancer, DM will go onto a trial breast-screening pro-
gram and in due course, hopefully it will become clearer
whether there is a risk in her family or not.
Evaluation
DM has had to make a very difficult decision regarding her
treatment and future. I believe the treatment for her diffuse
gastric cancer has been life saving and appropriate. It was
fortunate that she had the final gastroscopy that confirmed
that she was making the correct choice. The surgeon spent
time with DM prior to her decision to proceed with the total
gastrectomy and informed her of the procedural risks, but her
decision was made because of the high risk of development of
the diffuse gastric cancer. DM was able to see the progress her
brother had made following his total gastrectomy and had
spent a lot of time discussing her decision with family mem-
bers and the genetic counsellors associated with this family.
Lewis et al. (2001) state that the consideration that must
be made in comparing total gastrectomy with other prophy-
lactic surgical procedures for genetically determined disease is
that total gastrectomy has much greater risk than mastec-
tomy or thyroidectomy, with higher immediate and late
morbidity and major lifelong consequences. Considering the
alternatives and what is known at this stage, however, total
gastrectomy appears to be a rational choice for individuals
with E-cadherin mutations who otherwise have a high risk of
death at an early age.
Conclusions
I believe the work undertaken in the endoscopy department
with chromoendoscopy is offering this family a chance of sur-
vival because endoscopy alone is not sufficient for identifying
the cancer soon enough to ensure a good chance of survival.
Fennerty (1994) states in his summary that tissue staining has
broad clinical and research application in gastroenterology
but remains underused. The work and research undertaken
235
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within New Zealand may be now utilized in other countries
as articles are being published and presentations given on dis-
covery of the gene and management.
Despite the possible risk of breast cancer, DM is able to
carry on her life with less stress and look forward to the
future. In the endoscopy department, we feel excited about
the research being undertaken and privileged to be part of
the program to aid early detection of this condition. We
feel that the undertaking of the genetic screening and dye
testing has offered new hope to this family while being a
unique opportunity for endoscopy staff to learn about dif-
fuse gastric cancer.
References
Brennan, M. F. (2003). Pre-emptive surgery and increasing
demands for technical perfection. British Journal of
Surgery, 90, 3–4.
Charleton, A., Blair, V., Shoaw, D., Parry, S., Guilford, P., &
Martin, I. (2004). Hereditary diffuse gastric cancer: Pre-
dominance of multiple foci of signet-ring cell carcinoma in
distal stomach and transitional zone. Gut, 53, 814–820.
Chun, Y. S., Lindor, N. M., Smyrk, T. C., Peterson, B. T.,
Burgart, L. J., Guilford, P., et al. (2001). Germline
E-cadherin gene mutations: Is prophylactic total
gastrectomy indicated? Cancer, 92(1), 181–187.
Curel, P., Kumar, N., & Robinson, B. (Eds.). (2004). New
ethical compendium. Auckland: Adis International Ltd.
Durie, M. (1994). Whaiora Maori health development (2nd
ed.). Auckland: Oxford University Press.
Fennerty, M. B. (1994). Tissue staining. Gastrointestinal
Endoscopy Clinics of North America, 4(2), 297–310.
Fitzgerald, R. C., & Caldas, C. (2004). Clinical implications
of E-cadherin associated hereditary diffuse gastric cancer.
Gut, 53, 775–778.
Fuchs, C. S., & Mayer, R. J. (1995). Gastric carcinoma.
New English Journal of Medicine, 333(1), 32–41.
Joo, Y., Rew, J., Kim, H., Choi, S., Park, C., & Kim, S.
(2001). Change in the E-cadherin-catenin complex
expression in early and advanced gastric cancers. Diges-
tion, 64(2), 111–118.
Keller, G., Vogelsang, H., Becker, I., Hutter, J., Ott, K., Can-
didus, S., et al. (1999). Diffuse type gastric and lobular
breast carcinoma in a familial gastric cancer patient with
an E-cadherin germline Mutation. American Journal of
Pathology, 155(2), 337–342.
Lewis, F. R., Mellinger, J. D., Hayashi, A., Lorelli, D., Mon-
aghan, K. G., Carneiro, F., et al. (2001). Prophylactic total
gastrectomy for familial gastric cancer. Surgery, 130(4),
612–617.
Peckham, M., Pinedo, H., &Veronesi, U. (Eds.). (1995).
Oxford textbook of oncology (Vol. 1). New York: Oxford
University.
Pharoah, P., Guilford, P., & Caldas, C. (2001). Incidence of
gastric cancer and breast cancer in CDH-1 (E-Cadherin)
mutation carriers from hereditary diffuse gastric cancer
families. Gastroenterology, 121, 1348–1353.
Rang, H. P., Dale, M. M., & Ritter, J. M. (1995). Pharma-
cology (3rd ed.). Edinburgh: Churchill Livingstone.
Shaw, D., Blair, V., Framp, A., Harawira, P., McLeod, M.,
& Guilford, P., et al. (2005). Chromoendoscoic surveil-
lance in hereditary diffuse gastric cancer: An alternative
to prophylactic gastrectomy? Gut, 54(4), 461–468.
Theuer, C. P., Nastanski, F., Brewster, W. R., Butler, J. A., &
Anton-Culver, H. (1999). Signet ring cell histology is asso-
ciated with unique clinical features but does not affect gas-
tric cancer survival. American Surgeon, 65(10), 915–921.
Tsukuma, H., Oshima, A., Narahara, H., & Morii, T. (2000).
Natural history of early gastric cancer: A non-concurrent,
long term, follow up study. Gut, 47(5), 618–624.

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Diffuse Gastric Cancer

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236 GASTROENTEROLOGY NURSING