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PubMedDate not supplied

[Gastrointestinal lymphomas].

Non-Hodgkin lymphomas affecting extranodal tissues can be primitive or secondary. The area most frequently involved is the gastrointestinal tract. MALT-type lymphomas are B-cell lymphomas characterized by small cells originating from the lymphoid tissue of the mucosa. The criteria for a correct diagnosis of extranodal lymphomas are morphological, but include immunophenotypic and immunogenotypic analysis. Gastrointestinal lymphomas consist of B-cell and T-cell lymphomas. B cell-lymphomas include: small cell B-lymphomas, large cell B-lymphomas, immunoproliferative small intestinal disease; multiple lymphomatous polyposis, follicular lymphomas, B-cell lymphomas centrocytic type. T-cell lymphomas include enteropathy-associated and non enteropathy-associated lymphomas.

Gastrointestinal Neoplasms↗
PubMed1996

[A rational surgical procedure in diffuse polyposis and multiple primary cancer against a background of polyps of the large intestine].

Under examination there were 292 patients. An analysis of results of treatment enabled the authors to conclude that surgical treatment of patients with diffuse polyposis of the colon is the method of choice. The method and volume of operations must be determined according to the involvement of the colon in polyposis, the age and state of the patients. The best method of surgery is a one-step radical operation-subtotal resection of the colon. Polyps concomitant to cancer of the colon should be ablated before the main operation since their histological analysis can change the volume of the planned radical operation. When choosing the method of surgical intervention for patients with primary-multiple cancer against the background of polyps the total portion of the colon with polyps should be ablated.

Colectomy↗
PubMed1988

Cell kinetics analysis of background colonic mucosa of patients with intestinal neoplasms by ex vivo autoradiography.

Studies of the cell kinetics of the colonic crypts could explain the morphogenesis of colonic adenomas and results suggest that a derangement of the proliferative zone of the colonic crypts takes place before adenoma development. This study was conducted to determine whether this is the case or not. The labelling distribution and labelling index (LI) of the colonic crypts was examined with ex vivo autoradiography. Eight patients with intestinal neoplasms, three with familial polyposis coli, four with ordinary colon cancer, and one with two colonic adenomas. Similar labelling distributions and absent upward shift of the active proliferative zone in crypts were observed in patients with familial polyposis and in those with non-polyposis cancer, or adenomas. The non-proliferative zone of the crypts was well preserved in all eight patients. The mean of the labelling index of the three patients with familial polyposis coli was 8.35% (3.17), values expressed as means (SD) and that of the five patients with non-polyposis cancer, or adenomas was 8.55% (3.20). None of the eight patients showed derangement of the proliferative zone of colonic crypts. This result is compatible with the hypothesis that adenomas are detected first as 'buds of adenomas', which sprout into the lamina propria mucosae in the middle part of normal crypts.

Adenocarcinoma↗
PubMed2001

Changes of E-cadherin and beta-catenin in human and mouse intestinal tumours.

An immunohistochemical analysis of E-cadherin and beta-catenin was performed in human colorectal cancer as well as in surrounding normal intestinal tissue. We also analysed the expression of these two cell adhesion proteins in transgenic Apc1638N mice as a model of human familial adenometous polyposis syndrome. In the normal intestinal mucosa of both species, E-cadherin and beta-catenin were localized along the lateral plasma membranes of epithelial cells. In intestinal tumour cells, however, they were also present in the cytoplasm. The expression of both proteins was reduced in human and mouse tumours. The pattern of their distribution was frequently heterogenous with strongly positive cells in a mosaic of negative ones. Further, E-cadherin and beta-catenin expression did not correlate to the Duke's staging of tumours and therefore neither can be used as prognostic criteria.

Adenocarcinoma↗
PubMed2001

A phenotypic change of small intestinal epithelium to colonocytes in small intestinal adenomas and adenocarcinomas.

OBJECTIVE: Using a novel monoclonal antibody (mAb Das-1) that specifically reacts with colon epithelium, we examined if there is a phenotypic change of small intestinal enterocytes toward colonocytes in small intestinal neoplastic tissue. METHODS: Tissue sections of the small intestine consisting of adenomas (n = 20, five with histories of familial polyposis), adenocarcinomas (eight primary and one metastatic from colon). carcinoids (n = 2), and hyperplastic polyps (n = 3) were examined by a sensitive immunoperoxidase assay using mAb Das-1 (IgM isotype). Normal jejunal (n = 10) and colonic (n = 10) biopsy specimens were also included as additional controls. RESULTS: mAb Das-1 reacted with normal colonic epithelium but not with jejunal mucosa. However, mAb Das-1 reacted strongly with each of the five adenomas (100%) from patients with histories of familial polyposis, but only five of 15 (33%) of the adenomas from nonfamilial polyposis patients, and each of the eight (100%) adenocarcinomas of the small intestine (p < 0.001). The reactivity with the adenomas from nonfamilial polyposis patients was very focal, whereas in the adenomas with familial polyposis the reactivity was more extensive. Each of the eight carcinomas reacted strongly with mAb Das-1. Adjacent normal small intestinal mucosa did not react. Hyperplastic polyps and the carcinoids did not react with mAb Das-1. CONCLUSION: These data demonstrate a phenotypic change in small intestinal epithelium toward the colonic phenotype, particularly in familial polyposis and in adenocarcinomas. mAb Das-1 may be clinically useful in identifying small intestinal adenomas with "high risk" for malignancy, such as in familial polyposis.

Adenocarcinoma↗
PubMedDate not supplied

Ileal polyposis as manifestation of neurofibromatosis syndrome.

A 13-year-old girl presented with features of intestinal obstruction. At surgery, the terminal 25 cm of ileum, which was resected along with the right colon, showed plexiform neurofibromatosis of the serosa and mesentery, hyperplastic submucosal and myenteric nerve plexuses and proliferation of neural tissue in the lamina propria, which manifested as diffuse polyposis of the ileal mucosa. The patient had a single inconspicuous external neurofibroma and a few café-au-lait spots on the back.

Adolescent↗
PubMed2000

Inhibition of intestinal tumors by curcumin is associated with changes in the intestinal immune cell profile.

BACKGROUND: The C57BL/6J-Min/+ (Min/+) mouse bears a germline mutation in Apc and is therefore a model for familial adenomatous polyposis and sporadic colorectal cancer. Min/+ intestinal mucosa exhibits a marked tendency for spontaneous adenoma formation. Curcumin is a phenolic antioxidant known for its antitumor and immune modulatory functions in vitro. Curcumin prevents adenoma formation in Min/+ mice, through a mechanism that may be related to its immunomodulatory properties. MATERIALS AND METHODS: To study the relationship between intestinal immunity and curcumin-induced antitumor response, we used immunohistochemistry to characterize the effect of curcumin treatment on resident intestinal immune effector cells in Min/+ mice. RESULTS/CONCLUSION: These results show that mucosal CD4(+) T cells and B cells increase in animals treated with curcumin, suggesting that curcumin modulates lymphocyte-mediated immune functions.

Adenomatous Polyposis Coli Protein↗
PubMed1984

Familial ganglioneuromatous polyposis of the large bowel. Report of a family with associated juvenile polyposis.

The unique familial occurrence of polypoid intestinal ganglioneuromatosis of the large bowel is reported. The lesions affected a 38-year-old father and three children aged 14, 12, and 10 years. In these cases, extensive diffuse and polypoid proliferation of nerve fibers and ganglion cells within the colonic mucosa was associated with pronounced epithelial changes resembling juvenile polyposis. None of the patients had any clinical evidence of the mucosal neuroma syndrome or Von Recklinghausen's neurofibromatosis, conditions in which intestinal ganglioneuromatosis can occur. The question of whether the juvenile-type polyps are hamartomatous or whether they represent a reactive process is addressed.

Adolescent↗
PubMed2004

[Diffuse colonic ganglioneuromatous polyposis].

Ganglioneuromatous polyposis is a very rare intestinal disease which differs from isolated polypoid ganglioneuroma and from diffuse ganglioneuromatosis. Its clinical, endoscopic, microscopic and evolutive features are poorly known. We report three cases of colonic ganglioneuromatous polyposis that illustrated an uncommon diffusion pattern in two men and one woman aged 63-72 who presented with chronic diarrhea. Endoscopic features suggesting the diagnosis were diffuse polyposis predominating in the cecum and right colon, with hyperhemic flat lesions enhanced after indigocarmin instillation. Histological study of the biopsies, and of colectomy specimens, showed a diffuse mucosal ganglioneuromatous proliferation with a few adenomatous polyps. Search for multiple endocrine neoplasia (MEN) type 2b was negative. In conclusion, this polypoid type of diffuse ganglioneuromatosis can be suspected in patients with chronic diarrhea by the special endoscopic aspect of the colonic polyposis. Pathologists should be aware of the distinctive features; diagnosis requires search for adenomas and/or neoplasia by total colopsy in addition to search for MEN 2b.

Adenomatous Polyposis Coli↗
PubMed2005

Age at exposure and Apc status influence the levels of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-DNA adducts in mouse intestine and liver.

We have previously shown that C57BL/6J-Min/+ (multiple intestinal neoplasia) mice, heterozygous for the Min mutation in the adenomatous polyposis coli gene, were more susceptible to intestinal tumorigenesis and had higher intestinal PhIP-DNA adduct levels after exposure to the food mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) on day 12 than on day 36 after birth [I.-L. Steffensen, H.A.J. Schut, J.E. Paulsen, A. Andreassen, J. Alexander, Intestinal tumorigenesis in multiple intestinal neoplasia mice induced by the food mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine: perinatal susceptibility, regional variation, and correlation with DNA adducts, Cancer Res. 61 (200l) 8689-8696]. In the present study, we have evaluated further whether this difference in susceptibility is related to adduct formation/removal, cell proliferation, apoptosis or expression of the nucleotide excision repair protein Xeroderma pigmentosum group A (XPA) in the intestines. Min/+ and +/+ (wild-type) mice were given a subcutaneous injection of 50 mg/kgbw PhIP on day 12 or 36, and the levels of PhIP-DNA adducts after 8, 12, 24 h, 3 or 7 days were quantified by use of 32P-postlabelling. In Min/+ mice, adduct levels were significantly higher after exposure on day 12 than on day 36 in the middle (1.5- to 8.5-fold) and distal (1.3- to 6.5-fold) small intestine from 8h to 3 days after administration of PhIP, but not in the colon and proximal small intestine. In the liver - a non-target organ for PhIP - adduct levels were 2.0- to 7.5-fold higher after exposure on day 12 than on day 36 from 8 to 24h after exposure. Adduct levels were generally higher in the middle (1.1- to 1.8-fold) and distal (1.1- to 2.0-fold) small intestines of Min/+ compared with +/+ mice after PhIP exposure on day 12, i.e. in the area of the intestines previously found also to have the highest number of tumors in Min/+ mice. PhIP increased cell proliferation and the number of apoptotic cells in the intestine and liver. However, the higher susceptibility to intestinal tumorigenesis in Min/+ mice exposed to PhIP at early age, or in Min/+ mice compared with +/+ mice, could not be explained by differences in cell proliferation, apoptosis or expression of the XPA repair protein.

Age Factors↗
PubMed2005

Connexin43 is overexpressed in Apc(Min/+)-mice adenomas and colocalises with COX-2 in myofibroblasts.

The expression of gap junction proteins, connexins, in the intestine and their role in tumorigenesis are poorly characterised. Truncating mutations in the tumour suppressor gene adenomatous polyposis coli (APC) are early and important events, both in inheritable (familial adenomatous polyposis, FAP) and spontaneous forms of intestinal cancer. Multiple intestinal neoplasia (Min) mice, a FAP model with inherited heterozygous mutation in Apc, spontaneously develop numerous intestinal adenomas. We recently reported reduced expression of connexin32 in Paneth cells of Min-mice. We further examine the expression of connexin43 (Cx43) and other connexins as a function of heterozygous and homozygous Apc mutation in normal intestinal tissues and adenomas of Min-mice. Qualitative analysis of connexin mRNA in intestine revealed a similar expression pattern in Min- and wild-type (wt) mice. Connexin26 and connexin40 proteins were found in equal amounts in Min and wt epithelia of large and small intestine, respectively. Interestingly, the connexin43 level was increased in the stroma of Min-mice adenomas, in close proximity to epithelial cells with nuclear beta-catenin staining. Cx43 and COX-2 were located to the same areas of the adenomas, and immunostaining exhibited coexpression in the myofibroblasts. Prostaglandin E2 induces Cx43 expression and COX-2 is the rate-limiting enzyme in the prostaglandin synthesis. However, the COX-2-specific inhibitor, celecoxib, did not reduce Cx43 expression. Although both Cx43 and COX-2 are target genes for beta-catenin, they were overexpressed in stromal cells but not in epithelial tumour cells. We hypothesise that gap junctions may be of importance in the transfer of signals between epithelium and stroma.

Adenoma↗
PubMed2003

Extranodal diffuse follicular center lymphoma mimicking mantle cell lymphoma of the intestine.

We report a case of diffuse follicular center lymphoma (FCL), which is a morphological variant of follicular lymphoma, resembling multiple lymphomatous polyposis (mantle cell lymphoma of the intestine). The patient was a 48-year-old Japanese man who was found, by colonoscopy, to have numerous small polypoid lesions along the entire large intestine. Abdominal computed tomography revealed hepatosplenomegaly and enlargement of multiple mesenteric lymph nodes. Histologically, the lesion was characterized by diffuse proliferation of small- to medium-sized lymphocytes with cleaved nuclei in the mucosa and submucosa. Immunohistochemical studies showed that the tumor cells were CD20+, CD10+, BCL-2+, CD5-, surface IgM-, and cyclin D1-. Moreover, a cytogenetic study showed a translocation at (14;18)(q32;q21). Finally, this case was diagnosed as diffuse FCL, although the tumor was mimicking mantle cell lymphoma.

Chromosomes, Human, Pair 14↗
PubMed1999

[Early diagnosis of familial adenomatous polyposis based on multiple osteomas of the facial skull].

We describe a 21-year-old patient hospitalised because of a dislocated mandibular fracture and accidentally found to have multiple osteomas of the skull. A subsequent gastroenterological examination revealed the presence of multiple polyps in the large intestine, typical of familial adenomatous polyposis. A disease causing germline mutation in the adenomatous polyposis coli gene was identified by molecular genetic analysis. Although extracolonic features such as multiple osteomas, multiple epidermal cysts and desmoids are frequently found, most cases without a family history of familial adenomatous polyposis or colorectal cancer are only diagnosed because of colonic disease manifestations with colorectal cancer already present. This case report strikingly illustrates that in the absence of a family history the presence of extracolonic features allows presymptomatic diagnosis in familial adenomatous polyposis patients before colorectal cancer has developed.

Adenomatous Polyposis Coli↗
PubMed1997

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine increases the numbers of tumors, cystic crypts and aberrant crypt foci in multiple intestinal neoplasia mice.

The multiple intestinal neoplasia (Min) mice have a mutation in the murine adenomatous polyposis coli (Apc) gene rendering them highly susceptible to spontaneous intestinal adenoma formation, similar to the familial adenomatous polyposis (FAP) syndrome in humans. We studied whether the most abundant mutagenic heterocyclic amine isolated from cooked food, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), could influence early intestinal neoplasia in C57BL/6J-Min/+ and C57BL/6J- +/+ (wild-type) mice of both sexes. PhIP was given in 4 weekly i.p. injections of 50 mg/kg. Ten weeks after the start of the experiment, PhIP had significantly increased the numbers of small tumors and cystic crypts in the proximal section of the small intestine in male Min/+ mice, and the numbers of aberrant crypt foci (ACF) in the large intestines of both males and females. The effects of PhIP were more pronounced in male than in female Min/+ mice. In +/+ mice, no tumors or cystic crypts in the small intestine, and no tumors and only a very few ACF in the large intestine, were induced by PhIP. These results show that a substance frequently present in the human diet is able to enhance the neoplastic process induced by a genetic lesion, which is also commonly found both in inherited and sporadic colon carcinomas in humans.

Animals↗
PubMed1985

[Diffuse familial polyposis].

Familial gastrointestinal polyposis constitutes a multiplication of the principle varieties of common polyps, not only in the colon but also in other parts of the gastrointestinal tract. These are hereditary and familial diseases with autosomal dominant transmission. The genetic defect can also be responsible for associated extra-gastrointestinal lesions. The classification of these familial polyposes is based on the histological features of the polyps. The adenomatous polyposes consist of familial recto-colonic polyposis (FRCP), which is the most frequent form, and Gardner's syndrome. This variety of polyposis selectively involves the recto-colon, but also presents gastric and duodenal lesions. The defining feature of Gardner's syndrome is the extra-gastrointestinal mesenchymal lesions, osteomas, skin tumours and, most importantly, mesenteric fibromatosis which may complicate abdominal operations. The prognosis of FRCP and Gardner's syndrome is determined by the almost obligatory and often multicentric malignant degeneration of the polyps, which justifies routine total proctocolectomy. Peutz-Jeghers' syndrome is syndrome is characterised by hamartomatous polyposis selectively involving the upper part of the small intestine. It generally has a benign course. Similarly, juvenile polyposis consists of benign inflammatory polyps and is accompanied by congenital anomalies in one third of cases. The diagnosis of familial polyposis should be proposed whenever polyps are detected, which appear to be unusual in terms of their number or their distribution. A family survey should be performed in such cases.

Colonic Polyps↗
PubMed2000

Loss of heterozygosity in spontaneous and X-ray-induced intestinal tumors arising in F1 hybrid min mice: evidence for sequential loss of APC(+) and Dpc4 in tumor development.

Min (multiple intestinal neoplasia) mice carry a mutant allele of the murine Apc (adenomatous polyposis coli) locus and are predisposed to intestinal adenoma formation in the intestinal tract. Early studies have shown complete loss of function of Apc by whole chromosome loss on the tumor-sensitive C57BL/6J genetic background and in AKR x B6 F1 hybrids. Gamma-radiation-induced chromosomal losses focus the critical region on wt Apc, but because of the limited number of polymorphic markers used, no other critical regions of loss on chromosome 18 were identified. Using intestinal tumors arising spontaneously and induced by X-rays in CBA/H x C57BL/6J F1 hybrid mice and high-resolution microsatellite loss of heterozygosity (LOH) techniques, we provide mapping data for wt Apc loss, which confirms and extends earlier observations. In addition, high-frequency loss events at the Dpc4 locus were found in both spontaneous and radiation-induced tumors. These data identified LOH of Dpc4 as a critical secondary event following complete functional loss of Apc. LOH across the Trp53 genomic region of chromosome 11 was not observed. No LOH was recorded for the Mom1 candidate gene Pla2g2a or for 9 out of 10 polymorphic markers from the Mom1 genomic region on murine chromosome 4. One marker mapping distal to Pla2g2a showed LOH in a small minority of spontaneous tumors. These data support the contention that Mom1 does not act as a classical tumor suppressor. Overall, our data indicates a significant role for Dpc4 mutation in intestinal tumor progression in the mouse and provides further evidence for the importance of interstitial chromosome losses in radiation tumorigenesis.

Animals↗
PubMed1999

Neonatal exposure to the food mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine via breast milk or directly induces intestinal tumors in multiple intestinal neoplasia mice.

We examined whether the food mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) could increase intestinal tumorigenesis in neonatal C57BL/6J-Min/+ mice, a murine model for familial adenomatous polyposis. Min/+ mice are heterozygous for a nonsense mutation in the adenomatous polyposis coli gene and spontaneously develop multiple intestinal adenomas, primarily in the small intestine. Neonatal Min/+ mice (3-6 days old) were exposed to PhIP via breast milk from lactating dams given 8 s.c. injections of 50 mg/kg PhIP three times a week or to 8 s.c. injections of 25 or 50 mg/kg PhIP directly, over the same period. At the age of 11 weeks, the number, diameter and location of the intestinal tumors were scored. Remarkably, a 2- to 4-fold increase in the number of small intestinal tumors was seen in Min/+ mice exposed to PhIP via breast milk (P < 0.001). To our knowledge, this is the first time PhIP has been reported to induce tumors following exposure via breast milk from PhIP-exposed dams. Upon direct exposure to 50 mg/kg PhIP, a 6- to 9-fold increase in the number of small intestinal tumors was observed (P < 0.001). The diameter of the PhIP-induced small intestinal tumors was slightly increased (P < 0.001). In the colon, a 3- to 4-fold increase in the number of tumors was seen in Min/+ mice exposed to PhIP via breast milk (P = 0. 004). Direct exposure to 50 mg/kg PhIP caused a 2- to 6-fold increase in the number of colonic tumors (P = 0.014). The PhIP-induced colonic tumors were located more distally and displayed a smaller diameter than the tumors from the controls (P < 0.05). In contrast to a previous study, where PhIP showed only a moderate tumorigenic effect in adult Min/+ mice, the present study demonstrates a strong tumorigenic effect of PhIP in neonatally exposed Min/+ mice, even after exposure via breast milk from PhIP-exposed dams.

Animals↗
PubMed2005

Macrophage migration inhibitory factor promotes intestinal tumorigenesis.

BACKGROUND & AIMS: The cytokine macrophage migration inhibitory factor (MIF) is expressed throughout the human gastrointestinal tract. Recently, protumorigenic activity of MIF has been described in several cancer models. Therefore, we investigated the expression and function of MIF during the early stages of intestinal tumorigenesis. METHODS: MIF messenger RNA, protein, and tautomerase activity were measured in normal intestinal mucosa and adenomas from patients with sporadic colorectal adenomas and in the adenomatous polyposis coli (Apc)Min/+ mouse model of intestinal tumorigenesis. MIF function was investigated by using VACO-235 human colorectal adenoma cells in vitro and by testing the effect of genetic deletion of Mif on ApcMin/+ mouse intestinal tumorigenesis. RESULTS: MIF expression and tautomerase activity were increased in human and ApcMin/+ mouse intestinal adenomas compared with adjacent normal mucosa. Up-regulation of MIF occurred mainly in epithelial cells (associated with an increasing grade of dysplasia), but also in stromal plasma cells. Exogenous MIF inhibited apoptosis and promoted anchorage-independent growth of VACO-235 cells (maximal at 100 ng/mL). Homozygous deletion of Mif was associated with a reduction in the number and size of ApcMin/+ mouse adenomas (P = .025 for the difference in large [>7-mm] tumors) and decreased angiogenesis (43% decrease in mean tumor microvessel density), but there was no alteration in epithelial cell apoptosis or proliferation. CONCLUSIONS: MIF expression is increased in sporadic human colorectal adenomas, and exogenous MIF drives tumorigenic behavior of epithelial cells in vitro. Mif also promotes intestinal tumorigenesis (predominantly via angiogenesis) in the ApcMin/+ mouse. Therefore, MIF is a potential colorectal cancer chemoprevention target.

Adenoma↗