National Cancer Institute®
Last Modified: November 21, 2001
1
UI - 21445668
AU - Waldum HL; Qvigstad G; Falkmer S
TI -
Indications for a neuroendocrine tumor-carcinoma sequence.
SO - Virchows Arch 2001 Aug;439(2):215-7
2
UI - 21441830
AU - Abrahams NA; Vesoulis Z; Petras RE
TI -
Angiogenic polypoid proliferation adjacent to ileal carcinoid tumors: a
nonspecific finding related to mucosal prolapse.
SO - Mod Pathol 2001 Sep;14(9):821-7
AD - Department of Anatomic Pathology, The Cleveland Clinic Foundation,
Cleveland, Ohio 44195, USA.
Case reports have highlighted angiogenic polypoid proliferation in the
mucosa adjacent to ileal carcinoid tumors, describing them as
granulation tissue polyposis and florid angiogenesis. Some authors have
proposed that the ileal carcinoid tumors themselves produce growth
factors that cause the change. The purpose of this study was to
determine the frequency of angiogenic polypoid proliferation in a large
cohort of resected ileal carcinoid tumors compared with control groups.
Search of the Cleveland Clinic and Summa Health System pathology files
(1985 to 1999) yielded 65 resected ileal carcinoid tumors. Mucosal
abnormalities adjacent to the ileal carcinoid tumors were graded 0 to
4+. Twenty ileal resection margins from colonic carcinoma cases served
as normal controls. Ileal mucosa adjacent to 22 noncarcinoid neoplasms
were also examined. The mucosa adjacent to 54/65 ileal carcinoid tumors
(83%) showed mucosal abnormalities (vs. 3/20 normal controls), including
mucosal edema, capillary ectasia, muscularis mucosae hypertrophy,
fibrosis/smooth muscle proliferation within the lamina propria,
club-shaped villi, and intramucosal capillary proliferation. Forty ileal
carcinoid tumor cases (61%) showed some degree of angiogenic polypoid
proliferation characterized by club-shaped villi and prominent
intramucosal capillaries, with 17 (26%) graded as 3+ or 4+. Angiogenic
polypoid proliferation was associated with hypertrophy of the muscularis
mucosae, lamina proprial fibrosis/smooth muscle proliferation, and
capillary ectasia similar to that described with gastrointestinal
mucosal trauma/prolapse. This trauma/prolapse change was identified in
45 cases (69%) and was graded 3+ or 4+ in 23 (35%). Seventeen (77%) of
the noncarcinoid neoplasms showed trauma/prolapse changes, with 7 (32%)
graded as 3+ or 4+. Angiogenic polypoid proliferation also correlated
with trauma/prolapse change in the noncarcinoid neoplasm controls.
Neither APP (P =.24) nor the prolapse changes (P =.33) were found to be
statistically different between the two tumor groups. Angiogenic
polypoid proliferation of the adjacent ileal mucosa is common in
patients with ileal carcinoid tumors and with noncarcinoid neoplasms.
Angiogenic polypoid proliferation almost invariably coexists with
fibromuscular change and capillary ectasia within the lamina propria,
suggesting that mucosal trauma/prolapse plays a role in the
histogenesis. The association of angiogenic polypoid proliferation with
a variety of different neoplasms makes it unlikely that the tumors
themselves secrete growth factors.
3
UI - 21443269
AU - Fujimori M; Ikeda S; Shimizu Y; Okajima M; Asahara T
TI -
Accumulation of beta-catenin protein and mutations in exon 3 of
beta-catenin gene in gastrointestinal carcinoid tumor.
SO - Cancer Res 2001 Sep 15;61(18):6656-9
AD - Second Department of Surgery, Hiroshima University Faculty of Medicine,
Hiroshima, Japan 734-8551.
The molecular basis of carcinogenesis in gastrointestinal carcinoid
tumors is not well understood. To clarify the contribution of the
Wnt/beta-catenin signaling to this type of carcinogenesis, we
investigated 72 cases of gastrointestinal carcinoid tumor both
immunohistochemically and by direct sequencing of beta-catenin.
Accumulation of beta-catenin in the cytoplasm and/or nucleus was
observed in 57 cases (79.2%). We also detected mutations in exon 3 of
beta-catenin in 27 cases (37.5%) and one mutation in APC (1.4%). Our
results suggest that alterations in the Wnt/beta-catenin signaling
pathway may be involved in the development of gastrointestinal carcinoid
tumors.
4
UI - 21452938
AU - Kema IP; Meijer WG; Meiborg G; Ooms B; Willemse PH; de Vries EG
TI -
Profiling of tryptophan-related plasma indoles in patients with
carcinoid tumors by automated, on-line, solid-phase extraction and HPLC
with fluorescence detection.
SO - Clin Chem 2001 Oct;47(10):1811-20
AD - Department of Pathology and Laboratory Medicine, University Hospital
Groningen, 9700 RB Groningen, The Netherlands. i.p.kema@lab.azg.nl
BACKGROUND: Profiling of the plasma indoles tryptophan,
5-hydroxytryptophan (5-HTP), serotonin, and 5-hydroxyindoleacetic acid
(5-HIAA) is useful in the diagnosis and follow-up of patients with
carcinoid tumors. We describe an automated method for the profiling of
these indoles in protein-containing matrices as well as the plasma
indole concentrations in healthy controls and patients with carcinoid
tumors. METHODS: Plasma, cerebrospinal fluid, and tissue homogenates
were prepurified by automated on-line solid-phase extraction (SPE) in
Hysphere Resin SH SPE cartridges containing strong hydrophobic
polystyrene resin. Analytes were eluted from the SPE cartridge by column
switching. Subsequent separation and detection were performed by
reversed-phase HPLC combined with fluorometric detection in a total
cycle time of 20 min. We obtained samples from 14 healthy controls and
17 patients with metastasized midgut carcinoid tumors for plasma indole
analysis. In the patient group, urinary excretion of 5-HIAA and
serotonin was compared with concentrations of plasma indoles. RESULTS:
Within- and between-series CVs for indoles in platelet-rich plasma were
0.6-6.2% and 3.7-12%, respectively. Results for platelet-rich plasma
serotonin compared favorably with those obtained by single-component
analysis. Plasma 5-HIAA, but not 5-HTP was detectable in 8 of 17
patients with carcinoid tumors. In the patient group, platelet-rich
plasma total tryptophan correlated negatively with platelet-rich plasma
serotonin (P = 0.021; r = -0.56), urinary 5-HIAA (P = 0.003; r = -0.68),
and urinary serotonin (P <0.0001; r = -0.80). CONCLUSIONS: The present
chromatographic approach reduces analytical variation and time needed
for analysis and gives more detailed information about metabolic
deviations in indole metabolism than do manual, single-component
analyses.
5
UI - 20307241
AU - Laine L; Ahnen D; McClain C; Solcia E; Walsh JH
TI -
Review article: potential gastrointestinal effects of long-term acid
suppression with proton pump inhibitors.
SO - Aliment Pharmacol Ther 2000 Jun;14(6):651-68
AD - University of Southern California School of Medicine, Los Angeles,
California 90033, USA. llaine@usc.edu
This review examines the evidence for the development of adverse effects
due to prolonged gastric acid suppression with proton pump inhibitors.
Potential areas of concern regarding long-term proton pump inhibitor use
have included: carcinoid formation; development of gastric
adenocarcinoma (especially in patients with Helicobacter pylori
infection); bacterial overgrowth; enteric infections; and malabsorption
of fat, minerals, and vitamins. Prolonged proton pump inhibitor use may
lead to enterochromaffin-like cell hyperplasia, but has not been
demonstrated to increase the risk of carcinoid formation. Long-term
proton pump inhibitor treatment has not been documented to hasten the
development or the progression of atrophic gastritis to intestinal
metaplasia and gastric cancer, although long-term studies are required
to allow definitive conclusions. At present, we do not recommend that
patients be tested routinely for H. pylori infection when using proton
pump inhibitors for prolonged periods. Gastric bacterial overgrowth does
increase with acid suppression, but important clinical sequelae, such a
higher rate of gastric adenocarcinoma, have not been seen. The risk of
enteric infection may increase with acid suppression, although this does
not seem to be a common clinical problem with prolonged proton pump
inhibitor use. The absorption of fats and minerals does not appear to be
significantly impaired with chronic acid suppression. However, vitamin
B12 concentration may be decreased when gastric acid is markedly
suppressed for prolonged periods (e.g. Zolllinger-Ellison syndrome), and
vitamin B12 levels should probably be assessed in patients taking
high-dose proton pump inhibitors for many years. Thus, current evidence
suggests that prolonged gastric acid suppression with proton pump
inhibitors rarely, if ever, produces adverse events. Nevertheless,
continued follow-up of patients taking proton pump inhibitors for
extended periods will provide greater experience regarding the potential
gastrointestinal adverse effects of long-term acid suppression.
6
UI - 21366204
AU - Nojiri T; Ikegami M
TI -
Multiple minute carcinoids in type A gastritis: attempt at 3-D
reconstruction.
SO - Pathol Int 2001 Jul;51(7):504-10
AD - Department of Pathology, Jikei University School of Medicine, Tokyo,
Japan. tac8@jikei.ac.jp
In type A gastritis, the numbers of endocrine cell micronests (ECM) and
carcinoids increase through the trophic action of gastrin. This study
examined the characteristics and growth of carcinoids in type A
gastritis. A total of 395 lesions in five surgically removed stomachs
with type A gastritis were investigated, in terms of number, size,
distribution and histological appearance, to clarify the tumorigenesis
and progression of carcinoids. 3-D reconstruction using serial paraffin
sections was used to study carcinoid progression. Our findings suggest
that in type A gastritis, carcinoids arise in areas where minute
carcinoids are present at a high density. They also suggest that early
stage carcinoids not only become large expansively, but also develop in
a very complex manner, by maintaining contact with surrounding minute
carcinoids.
7
UI - 21467940
AU - Danikas D; Sachs R; Dressner RM; Arvanitis ML
TI -
Testicular metastasis from ileal carcinoid: report of a case.
SO - Dis Colon Rectum 2001 Sep;44(9):1365-6
AD - Department of Surgery, Monmouth Medical Center, Long Branch, New Jersey,
USA.
PURPOSE: This report presents a patient with testicular metastasis from
an ileal carcinoid. METHODS: This was a retrospective case review with
literature review. RESULTS: The patient underwent right orchiectomy for
a solid mass. Pathology revealed carcinoid tumor. Octreotide scan showed
increased concentration in the right lower quadrant of the abdomen.
Computerized tomography results were negative. Colonoscopy with biopsy
revealed carcinoid of the terminal ileum. The patient underwent an
elective resection of the terminal ileum and the right colon. Pathology
revealed carcinoid tumor with vascular and lymphatic invasion present,
and eight lymph nodes were positive. The patient had adjuvant treatment
with octreotide. CONCLUSION: Carcinoid tumors have been reported to
metastasize to numerous areas. This is the first report of testicular
metastasis from ileal carcinoid. Primary carcinoids of the testicle have
been reported also. The clinician should be aware of this rare
metastatic event. When pathology reveals carcinoid of the testicle,
metastatic disease should be excluded before the tumor is identified as
primary.
8
UI - 21289731
AU - Akahoshi K; Fujimaru T; Nakanishi K; Harada N; Nawata H
TI -
Endosonography probe-guided endoscopic resection of small flat rectal
carcinoid tumor using band ligation technique.
SO - Endoscopy 2001 May;33(5):471
AD - Dept. of Gastroenterology, Aso Iizuka Hospital, Japan.
akahoshi-kh1@aso-group.co.jp
9
UI - 20576718
AU - Habal N; Sims C; Bilchik AJ
TI -
Gastrointestinal carcinoid tumors and second primary malignancies.
SO - J Surg Oncol 2000 Dec;75(4):310-6
AD - Department of Surgical Oncology, John Wayne Cancer Institute, Santa
Monica, California, USA.
The development of second primary malignancies (SPM) in patients with
gastrointestinal carcinoid tumors is a well-described phenomenon, with
reported rates as high as 55%. There is a predilection for
gastrointestinal and genitourinary adenocarcinomas, but a variety of
other malignancies have been reported as well. The etiology of this
malignant predisposition may be rooted in the tumorigenic properties of
the various neuroendocrine peptides elaborated and secreted by
neuroendocrine cells. Peptides such as secretin, gastrin, bombesin,
cholecystokinin (CCK), and vasoactive intestinal peptide (VIP) are
believed to promote the growth of tumor cells. As many as 30 peptides
and amines identified in neuroendocrine cells may have similar
properties. This review of the literature on carcinoid-associated second
primary malignancies is accompanied by a case report of metastatic
carcinoid identified during surgical exploration for a perforating colon
adenocarcinoma. Copyright 2000 Wiley-Liss, Inc.
10
UI - 21486624
AU - Papotti M; Cassoni P; Volante M; Deghenghi R; Muccioli G; Ghigo E
TI -
Ghrelin-producing endocrine tumors of the stomach and intestine.
SO - J Clin Endocrinol Metab 2001 Oct;86(10):5052-9
AD - Department of Biomedical Sciences, University of Turin, Via Santena 7,
I-10126 Turin, Italy. mauro.papotti@unito.it
Ghrelin is a novel gastrointestinal hormone produced by about 20% of the
rat and human gastric neuroendocrine cell population, which possesses
strong GH-releasing activity, but also plays other central and
peripheral roles, including influence on food intake, gastric motility,
and acid secretion. The aim of the present study was to determine
whether gastrointestinal endocrine hyperplastic and neoplastic lesions
produce ghrelin, at both protein (immunohistochemistry) and mRNA (in
situ hybridization and/or RT-PCR) levels, and express the GH
secretagogue receptor mRNA by RT-PCR. Sixteen gastric and 20 intestinal
carcinoids as well as normal gastrointestinal mucosa and atrophic
gastritis-associated neuroendocrine cell hyperplasia were studied. The
majority (12 of 16, 75%) of gastric carcinoids and only 5 of 18 (27%) of
intestinal endocrine tumors were immunoreactive for ghrelin. In situ
hybridization confirmed the immunohistochemical data, but also showed
ghrelin mRNA in 1 gastric and 8 intestinal additional tumors. RT-PCR
showed ghrelin mRNA in 14 of 14 cases, indicating a low level of ghrelin
gene expression in all gastrointestinal endocrine tumors tested. Gastric
neuroendocrine hyperplastic cells were also strongly positive for
ghrelin. GH secretagogue receptor mRNA was absent in 3 gastric, but
present in 7 of 11 intestinal carcinoids studied by RT-PCR. These
findings demonstrate that most gastric carcinoids (and related
neuroendocrine cell hyperplasias) and some intestinal carcinoids produce
ghrelin. These hyperplastic/neoplastic conditions could represent the
clinical model to clarify the existence and impact of ghrelin
hypersecretion on endocrine and nonendocrine functions.
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.