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[Familial polyposis of the colon (author's transl)].
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[Gastroduodenal adenomatous lesions in familial diffuse polyposis].
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[Familial polyposis of the colon].
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[Treatment of gastrointestinal polyposis. Endoscopico-surgical considerations].
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No effects of Smad2 (madh2) null mutation on malignant progression of intestinal polyps in Apc(delta716) knockout mice.
The loss of heterozygosity (LOH) in human chromosome 18q21 is found at high frequencies in advanced pancreatic and colorectal cancers. Several candidate tumor suppressor genes, such as SMAD2, SMAD4, and DCC, are located in this region. The homologues of these genes in the mouse are also clustered on chromosome 18. Mutations in the adenomatous polyposis coli (APC) gene are responsible for familial adenomatous polyposis, and we earlier constructed a mouse model for familial adenomatous polyposis, Apc(delta716). Although human APC is located on chromosome 5q, mouse Apc is on chromosome 18, 30 cM proximal to the Dcc-Smad4-Smad2 locus. Taking advantage of this fact, we constructed previously a cis-compound Apc(delta716) Smad4 mutant, the intestinal polyps of which progress to very invasive adenocarcinomas. To determine whether Smad2 mutations play similar roles in malignant progression, here we constructed compound mutant mice carrying Apc and Smad2 knockouts in the cis configuration. In contrast to the cis-compound Apc(delta716) Smad4 heterozygotes, the polyps in the cis-compound Apc(delta716) Smad2 heterozygotes showed no difference in the number, size, or histopathology from the polyps in the simple Apc(delta716) heterozygotes. These results suggest that, on human chromosome 18q21, the SMAD4 LOH plays a more significant role, and SMAD2 LOH is insufficient to cause malignant progression of colonic polyps.
Intestinal tumorigenesis in Min mice is enhanced by X-irradiation in an age-dependent manner.
We examined the effect of X-irradiation on intestinal tumorigenesis in Min (multiple intestinal neoplasia) mice. Single whole-body irradiation was given to mice of various ages from newborn to young adults. On the C57BL/6J (B6) background, X-irradiation increased tumor multiplicity of the small intestine exposed at ages from 2-3 days to 24-25 days, with a peak of 2.7-fold increase at 10-12 days of age; exposure at later ages resulted in only a slight increase. X-irradiation also increased colonic tumors; however, the susceptible age period appeared earlier than that of the small intestine; the peak value of 4.6-fold increase was observed in the exposure at around 2-3 days of age. Irradiation at 24 days or later ages showed almost no effect on the colonic tumor induction. On the (B6 x MSM)F1 background, X-irradiation resulted in 2.7-fold increase in the small intestinal tumors, but no increase in the colonic tumors, and besides, the age dependency observed in the small intestinal tumors was much attenuated. Collectively, we conclude that tumorigenic efficacy of X-irradiation in Min mice was determined by the combination of the target organ, the age at exposure, and the genetic background.
FAP with concurrent duodenal adenomatous polyposis and carcinoid tumor.
We report a patient with familial adenomatous polyposis (FAP) who developed duodenal adenomatosis with high-grade dysplasia and a periampullary carcinoid tumor several years after total colectomy. Only two prior case reports exist revealing carcinoid tumors in association with FAP. No genetic basis exists explaining the link between FAP and carcinoid tumors. However, the presence of two rare entities in the same patient might suggest an association and further research may be indicated.
Dynamics of glycoprotein metabolism in familial polyposis coli-derived colonic epithelial tissue.
Familial polyposis coli is a disease state that offers an opportunity to obtain colon tissue in a predictable manner in terms of identifying putative premalignant markers. Our results support the hypothesis that a sequential series of alterations occur in the dynamics of glycoprotein metabolism as normal colonic mucosa progresses to colon adenocarcinoma. Specifically, both nonmalignant polyps and colon adenocarcinoma tissue expressed diminished glycosylation of proteins, whereas an elevated level of activity for membrane-associated glycosyltransferases does not appear until colon cancer itself develops.
Laparoscopic colorectal surgery: analysis of 140 cases.
BACKGROUND: This study was performed to prospectively assess the results of our first 140 consecutive patients who underwent laparoscopic or laparoscopic-assisted colorectal operations. METHODS: The parameters studied included the type and length of procedure, intra- and postoperative complications, conversion to open surgery, and length of ileus and hospitalization. RESULTS: 140 laparoscopic and laparoscopic-assisted procedures were performed between May 1991 and January 1995. The mean patient age was 48 (range 12-88) years; there were 78 males and 62 females. Indications for surgery included inflammatory bowel disease in 47, colorectal carcinoma in 19, diverticular disease in 17, polyps in 16, familial polyposis in 7, colonic inertia in 7, fecal incontinence in 11, sigmoidocele in 3, irradiation proctitis in 3, rectal prolapse in 2, intestinal lymphoma in 2, and miscellaneous conditions in 6. The procedures included 38 total abdominal colectomies (TAC) (ileoanal reservoir 28, ileorectal anastomosis 8 and end ileostomy 2); 70 segmental resections of the colon, small bowel, and rectum; 18 diverting stoma creations; 10 reversal of Hartmann's procedures; and 4 other procedures. In 15 cases, the laparoscopic procedure was converted to a laparotomy (11%); 31 patients (22%) sustained 37 complications, which included: enterotomies(7), hemorrhage(10), intraabdominal abscess(4), prolonged ileus(6), wound infection(4), intestinal obstruction(2), anastomotic leak(1), aspiration(1), cardiac arrhythmia(1), and upper intestinal bleeding(1); there was no mortality. The overall complication rate in TAC cases was significantly higher (42%) when compared to that of all other procedures (segmental resection 17%, others 9%), P < 0.05. The mean length of operating time was 4 (range 2.5-6.5) h for TAC, 2.6 (range 1.5-5.5) h for segmental colonic resections, and 1.7 (range 0.7-4) for all other procedures. The length of ileus was 3.5 (range 2-7) days after TAC, 3 (range 2-7) after the segmental resections and 2 (range 1-4) after the other procedures. The mean length of hospital stay was 6.8 (2-40) days (8.4, 6.5, and 6.3 days for the TAC, segmental resections, and other procedures, respectively). CONCLUSION: The feasibility of laparoscopic colorectal surgery has been well established. TAC is associated with a higher complication rate compared to other laparoscopic colorectal procedures.
Effect of increased calcium concentration on in vitro growth of human colonic mucosal lines.
The influences of different calcium concentrations in the culture medium on in vitro growth kinetics (generation time and saturation density) of established human colonic mucosal lines derived from subjects with and without familial adenomatosis of the colon and rectum were studied to test the hypothesis that hyperproliferation of colonic mucosal cells observed in some familial colon cancer can be reversed by increased extracellular calcium concentration. From the present studies, the genomic source of the adenomatous colonic lines appear to modify the effect of increased calcium on mucosal growth as demonstrated by differences in growth response in lines with and without the biomarker associated with genetic predisposition for some colon cancers, increased in vitro tetraploidy. Such observations suggested that other factors, including genomic differences, should be taken into consideration in the determination of the possible influences of calcium concentration on colonic mucosal proliferation.
The usefulness of severe combined immunodeficiency (SCID) mice to study human carcinogenesis.
In the present study, we engrafted normal colonic epithelial and histologically diagnosed colonic adenomas from a familial adenomatous polyposis (FAP) patient into severe combined immunodeficient (SCID) mice and subsequently examined them histologically and molecular biologically. Successful engraftment and metastasis was observed. The facts that human normal colonic epithelium and adenomatous polyps can take in SCID mice indicates the possibility that this human SCID mouse system will be useful for investigating the dynamics of human carcinogenesis in various tissues.
Cell proliferation and ultrastructural changes of the duodenal mucosa of patients affected by familial adenomatous polyposis.
Patients affected by familial adenomatous polyposis (FAP) are at risk of developing duodenal neoplasia. Our objective was to detect early abnormalities of the epithelial cell proliferation and ultrastructure of apparently normal duodenal mucosa of FAP patients. Biopsy specimens were taken from the duodenal mucosa. Cell proliferation was studied by immunohistochemistry with proliferating cell nuclear antigen (PCNA), and ultrastructure, by transmission electron microscopy. We found that the PCNA labeling index for duodenal mucosa of patients with FAP was higher in comparison to the case of hospital controls without cancer risk (P = 0.019). Moreover, ultrastructural changes related to an impairment of cell adhesion function were found in all biopsies of FAP patients but not in the duodenal mucosa of the controls. We conclude that alterations of cell proliferation kinetics and epithelial adherens junction structures were phenotypic characteristics of histologically normal duodenal mucosa of FAP patients. These abnormalities may be considered as intermediate biomarkers of neoplasia and potential surrogate endpoints in chemoprevention studies.
Cell proliferation and differentiation in familial adenomatous polyposis (FAP).
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Colonic late-onset familial adenomatous polyposis combined with severe duodenal polyposis and familial endometrial cancer.
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Spontaneous aberrant crypt foci in Apc1638N mice with a mutant Apc allele.
The Apc1638N/+ mouse has a chain-terminating mutation in one allele of the adenomatous polyposis coli (Apc) gene that is similar to most mutations observed in the human familial adenomatous polyposis syndrome. Aberrant crypt foci (ACF), the earliest identified neoplastic lesions in the colon, are morphologically abnormal structures that are identifiedmicroscopically in the grossly normal colonic mucosas of rodents treated with colon carcinogens and of human patients. The colons and cecums of 62 Apc1638N/+ mice were evaluated for the spontaneous occurrence of ACF and tumors. Both male and female mice were killed at different times between 5 and 28 weeks of age. Wild-type littermates, ie, Apc(+/+) mice, at 22 to 26 weeks of age served as controls. ACF were identified in 97% of the Apc1638N/+ mice starting at 5 weeks of age and not in any wild-type littermates. Although the number of ACF increased with age (P < 0.0001), the average number of crypts per focus of the ACF did not increase significantly. In addition, wild-type Apc protein was detected by immunohistochemistry in all 22 ACF evaluated. Together these data suggest that heterozygous loss of Apc may be sufficient to initiate ACF in these mice and that these mice may be suitable models to study the interaction of environmental factors with an inherited mutation of the Apc gene that is associated with colon cancer.
Introduction of human adenomatous polyposis coli gene into Min mice via cationic liposomes.
BACKGROUND: The adenomatous polyposis coli (APC) gene is a tumor-suppressor gene involved in familial polyposis coli (FAP), a hereditary disease heralded by the development of hundreds of colorectal adenomas. A mouse model for FAP, the multiple intestinal neoplasia (Min) mouse, develops multiple adenomatous polyps of the large and small intestine similar to their human counterparts. To test the feasibility of introducing normal human APC as a means of either preventing or reversing polyp formation, we describe a method of in vivo transfection of APC into colonic epithelium of the Min mouse. METHODS: Anesthetized young (4 weeks) Min mice were treated with enemas containing lipofectant and a normal human APC cDNA plasmid every 72 hours for 2 months and then euthanized at 24, 48, and 72 hours after the last treatment. Polymerase chain reaction (PCR) was used to detect the presence of the plasmid DNA. RESULTS: PCR on the extracted colonic epithelial DNA showed the presence of plasmid DNA up to 72 hours after the last treatment. Expression of the plasmid construct was confirmed by reverse transcriptase-PCR. CONCLUSIONS: We have demonstrated the repeated introduction and detection of normal human APC in the colonic epithelium of the Min Mouse in vivo during an extended period of time with no toxic side effects by means of our prolonged therapy.
Linking colorectal cancer to Wnt signaling.
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