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PubMed1996

Common deleted region on the long arm of chromosome 5 in esophageal carcinoma.

BACKGROUND & AIMS: The existence of an unknown tumor-suppressor gene on 5q for esophageal carcinoma other than the APC gene has been suggested. The location of the putative tumor-suppressor gene on 5q, distinct from the APC gene, was examined. METHODS: Sixty-one primary esophageal carcinomas were examined for nine microsatellite loci by the polymerase chain reaction followed by polyacrylamide gel electorophoresis. Loss of heterozygosity at the APC gene locus also was examined by the polymerase chain reaction-restriction fragment length polymorphisms. RESULTS: Thirty-five of 61 esophageal carcinomas (57%) showed loss of heterozygosity at single or multiple loci on 5q, and the smallest common deleted region was identified at 5q31.1, the location of the IRF-1 gene locus. All tumors showing loss of heterozygosity at the APC gene locus showed complete or large interstitial deletions on 5q. CONCLUSIONS: Deletion at the APC gene locus may just be the result of large deletions on 5q and may not be important in esophageal carcinogenesis, and the IRF-1 gene or other gene(s) on 5q31.1 may be the true target of frequent deletions on 5q that may play an important role in the pathogenesis of the majority of esophageal carcinomas.

Carcinoma↗
PubMed2000

Hypermethylated APC DNA in plasma and prognosis of patients with esophageal adenocarcinoma.

BACKGROUND: The adenomatous polyposis coli (APC) locus on chromosome 5q21-22 shows frequent loss of heterozygosity (LOH) in esophageal carcinomas. However, the prevalence of truncating mutations in the APC gene in esophageal carcinomas is low. Because hypermethylation of promoter regions is known to affect several other tumor suppressor genes, we investigated whether the APC promoter region is hypermethylated in esophageal cancer patients and whether this abnormality could serve as a prognostic plasma biomarker. METHODS: We assayed DNA from tumor tissue and matched plasma from esophageal cancer patients for hypermethylation of the promoter region of the APC gene. We used the maximal chi-square statistic to identify a discriminatory cutoff value for hypermethylated APC DNA levels in plasma and used bootstrap-like simulations to determine the P: value to test for the strength of this association. This cutoff value was used to generate Kaplan-Meier survival curves. All P values were based on two-sided tests. RESULTS: Hypermethylation of the promoter region of the APC gene occurred in abnormal esophageal tissue in 48 (92%) of 52 patients with esophageal adenocarcinoma, in 16 (50%) of 32 patients with esophageal squamous cell carcinoma, and in 17 (39.5%) of 43 patients with Barrett's metaplasia but not in matching normal esophageal tissues. Hypermethylated APC DNA was observed in the plasma of 13 (25%) of 52 adenocarcinoma patients and in two (6.3%) of 32 squamous carcinoma patients. High plasma levels of methylated APC DNA were statistically significantly associated with reduced patient survival (P =.016). CONCLUSION: The APC promoter region was hypermethylated in tumors of the majority of patients with primary esophageal adenocarcinomas. Levels of hypermethylated APC gene DNA in the plasma may be a useful biomarker of biologically aggressive disease in esophageal adenocarcinoma patients and should be evaluated as a potential biomarker in additional tumor types.

Adenocarcinoma↗
PubMed2001

Upstream stimulating factor-1 (USF1) and USF2 bind to and activate the promoter of the adenomatous polyposis coli (APC) tumor suppressor gene.

The adenomatous polyposis coli (APC) gene product is involved in cell cycle arrest and apoptosis, and loss of function is associated with the development of colorectal carcinogenesis. Although it has been demonstrated that the APC gene is inducible, its transcriptional regulation has not been elucidated. Therefore, we characterized the promoter region of the APC gene and transcription factors required for basal expression. The APC gene has a TATA-less promoter and contains consensus binding sites for Octamer, AP2, Sp1, a CAAT-box, and three nucleotide sequences for E-box A, B, and M. The E-boxes are functional in several cancer cell lines and upstream stimulating factor-1 (USF1) and USF2 interact with these sites, with a preferred sequence-specificity for the B site. Analysis of activation of the cloned APC promoter by USF1 and USF2 in transient transfection assays in HCT-116 cells demonstrated that mutation of the E-box B site completely abolished the basal promoter activity. Further, the ectopic USF1 and USF2 expression in HCT-116 cells with deletion mutations of E-box A, B, and M sites showed that these E-boxes contribute to USF1- and USF2-mediated transcriptional activation of the APC promoter, with maximum promoter activity being associated with the E-box B site. Thus, USF1 and USF2 transcription factors are critical for APC gene expression.

Adenomatous Polyposis Coli Protein↗
PubMed2002

APC germline mutations identified in Czech patients with familial adenomatous polyposis.

Familial adenomatous polyposis (FAP) is an autosomal dominantly inherited predisposition to colorectal cancer, which is caused by germline mutations in the adenomatous polyposis coli (APC) gene. The APC mutations have been investigated in 46 Czech unrelated FAP families and 9 suspected FAP families using DGGE analysis and direct DNA sequencing. We found 25 germline APC mutations and identified 11 which were not previously reported. Of the identified mutations, 10 were 1 to 5 bp deletions, four were 1 bp insertions and six were nonsense, all leading to the formation of premature stop codon. In addition, we detected two mutations in the splice-donor region of APC intron 11, one missense and two samesense mutations. Phenotypes of patients with known and novel types of mutations are presented and discussed.

Adenomatous Polyposis Coli↗
PubMed1994

Molecular genetic profiles of colitis-associated neoplasms.

BACKGROUND/AIMS: A major long-term risk for patients with chronic idiopathic colitis is the development of colorectal dysplasia and adenocarcinoma. The presence or absence of specific genetic changes in these lesions will provide important insights into the relationship of colitis-associated dysplasia and the development of carcinoma. METHODS: A case-study approach was used to develop detailed molecular genetic profiles of advanced dysplasias and carcinomas from six patients with ulcerative colitis or Crohn's colitis. RESULTS: Numerous genetic alterations were identified in each of the dysplasias and carcinomas profiled. These genetic alterations involved many of the same targets found in sporadic colorectal tumors and included multiple sites of allelic deletion, microsatellite instabilities, and mutations of the K-ras, p53, and APC genes. The progression of dysplasia to carcinoma was often accompanied by an accumulation of these mutations. CONCLUSIONS: Genetic alterations are common in colitis-associated neoplasia, just as in sporadic colorectal neoplasia. This could have important implications for the evaluation and treatment of patients with colitis.

Adenocarcinoma↗
PubMed1995

Colorectal adenoma progression and genetic change: is there a link?

Focal neoplastic change occurs frequently within the colorectum. Yet, of the several hundreds of microadenomas that are likely to be present within an individual colorectum, only one or two will develop into a clinically diagnosable adenoma. In turn, only a fraction of adenomas will progress to malignancy. The risk that a particular microadenoma will end its natural history as a carcinoma varies according to clinical context. The risk is very low in familial adenomatous polyposis (FAP), but relatively high in hereditary non-polyposis colorectal cancer (HNPCC). This variation is governed by the timing and ordering of the underlying mutational events. In FAP, inactivation of the wild-type APC gene occurs early, whereas K-ras mutations are late events. The converse appears to apply in the case of sporadic adenomas. In flat adenomas, which are known to be relatively aggressive, K-ras mutations may not occur at all. In HNPCC, mutational events are accelerated as a result of defective DNA mismatch repair. The evolution of colorectal adenoma occurs through a variety of quite distinct genetic pathways.

Adenocarcinoma↗
PubMed1999

Histological and genetic changes in malignant transformation of gallbladder adenoma.

DESIGN: Elucidate the histological and genetic changes in malignant transformation of adenoma of the gallbladder. MATERIALS AND METHODS: Forty-three adenomas and 20 intramucosal tumors of carcinoma-in-adenomas were studied for histological and genetic changes (particularly K-ras mutation and p53 protein overexpression by immunohistochemistry) in malignant transformation. The genetic changes were compared with those of 164 carcinomas without anomalous union and 17 carcinomas with anomalous union of pancreatico-biliary duct. RESULTS: Atypical cell foci, i.e. spindle cell foci, were observed only in the adenoma area, with a frequency of 23% in 39 adenomas, and of 45% in 20 tumors of carcinoma-in-adenoma. 129 of 130 spindle cell foci examined were negative for Ki-67 staining and all the spindle cell foci were negative for p53 stain. K-ras mutation and p53 overexpression were not found in all adenomas, pure and with carcinoma i.s., and only one carcinoma (1/16, 6%) with adenoma showed p53 overexpression. K-ras mutation was low (10%, 4/40) in carcinomas without adenoma, but high in carcinomas with anomalous union of pancreatico-biliary duct. While, p53 overexpression was high and similar in carcinomas with and without anomalous union. CONCLUSIONS: These results suggest that there are three distinct pathways in gallbladder carcinogenesis; that is, de novo carcinoma develops from a predominant p53 alteration with low K-ras mutation, de novo carcinoma with anomalous union from K-ras mutation and p53 mutation, and carcinoma-in-adenoma from K-ras-, p53-, and probably APC-gene-related, as yet unknown, alteration.

Adenoma↗
PubMed2001

Lessons learned from colorectal model of tumourigenesis.

Genetic analytical techniques were carried out to identify mutations in adenomatous polyposis coli (APC) gene and K-ras oncogene in colorectal tumourigenesis. These two genes are said to be early mutation genes among other mutation genes that constitute the model for colorectal tumourigenesis. To do this analysis, DNA was isolated from colorectal formalin fixed paraffin-embedded tumour tissue sections. The sections were deparaffinised, digested in proteinase-K, followed by DNA isolation. The DNA was amplified by Polymerase Chain Reaction (PCR), screened by using Denaturing Gradient Gel Electrophoresis (DGGE) or Single Strand Conformation Polymorphism (SSCP) and then sequenced. These results lend support to the fact that colorectal cancer and indeed cancer in general develops through a multi-step process; also that accumulation of genetic mutations underlie the development of neoplasia. We are in the process of extending this study to cancer of oesophagus to see if a similar or parallel model of carcinogenesis holds and in what sequence it is.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

The clinical [corrected] background of familial adenomatous polyposis. History, epidemiology, diagnosis and treatment.

Familial adenomatous polyposis (FAP) is a dominantly inherited genetic disorder predisposing to colon cancer through the early development of multiple adenomatous polyps in the large bowel. FAP is not restricted to the colon and rectum, but is a more complex disease which can potentially affect almost any organ not only with benign tumours but also with life threatening carcinomas. Desmoid tumours and gastroduodenal polyps and cancer are the two more worrying extracolonic manifestations of FAP. Recent advances in FAP knowledge, such as the report of congenital hypertrophy of the retinal pigment epithelium (CHRPE) or the APC gene identification, are very useful for screening and long-term follow-up of the patients through regional or national registries. Nutritional and pharmacological intervention trials are under way to assess potential new medical treatments of FAP. Surgery is still the only effective treatment for colorectal cancer prevention in FAP. The choice of a surgical procedure is controversial, but the introduction of total proctocolectomy with ileal pouch-anal anastomosis can be considered as a major advance in surgical treatment of FAP during the last decade.

Abnormalities, Multiple↗
PubMed1997

Genetic alterations and epithelial dysplasia in juvenile polyposis syndrome and sporadic juvenile polyps.

Juvenile polyps are regarded as hamartomatous polyps and occur in sporadic and familial syndromic settings. There is increased risk of gastrointestinal neoplasia in patients with juvenile polyposis syndrome, but the molecular mechanisms are not known. We therefore studied 78 colorectal juvenile polyposis from 12 patients with juvenile polyps syndrome and 34 sporadic juvenile polyps for epithelial dysplasia and genetic changes associated with colorectal neoplasia. Dysplasia occurred in 31% of syndromic juvenile polyps but not in sporadic juvenile polyps (P < 0.0001). Topographic control of proliferation and expression of the cyclin-dependent kinase inhibitor p21(WAFI/CIP1) seen in native colorectal epithelium was lost in 79% of dysplastic juvenile polyps and in 8% of nondysplastic juvenile polyps (P < 0.000001). Somatic mutations in the adenomatous polyposis coli (APC) gene were demonstrated in 50% of dysplastic juvenile polyps (3 of 6) but not in any of 16 juvenile polyps without dysplasia (P = 0.01). Both sporadic and syndromic juvenile polyps had K-ras mutations (14%) and there was no relationship to dysplasia. p53 gene product overexpression identified by immunohistochemical staining occurred rarely in dysplastic juvenile polyps (2 of 24, 8%). Our results indicate that the multiple genetic alterations involved in usual colorectal neoplasia also play a role in neoplastic transformation of juvenile polyps, predominantly in juvenile polyposis syndrome.

Adenomatous Polyposis Coli↗
PubMed1999

Dominant negative effect of the APC1309 mutation: a possible explanation for genotype-phenotype correlations in familial adenomatous polyposis.

Inactivation of the adenomatous polyposis coli (APC) gene product initiates colorectal tumorigenesis. Patients with familial APC (FAP) carry germ-line mutations in the APC gene and develop multiple colorectal adenomas and subsequent carcinomas early in life. The severity of the disease correlates with the position of the inherited APC mutation (genotype-phenotype correlation). Together with the fact that both germ-line and sporadic APC mutations cluster in the central region of the APC gene, this points to a dominant negative effect of certain APC mutants. Loss of APC function was recently shown to result in enhanced beta-catenin-/Tcf-mediated transcription in colon epithelial cells. Here, we provide experimental evidence for a dominant negative effect of APC gene products associated with severe polyposis. Wild-type APC activity in beta-catenin-/Tcf-mediated transcription was strongly inhibited by a mutant APC that is truncated at codon 1309. In contrast, mutant APC gene products that are associated with attenuated polyposis (codon 386 or 1465) interfered only weakly with wild-type APC activity. These results suggest a molecular explanation for the genotype-phenotype correlation in FAP patients and support the idea that colorectal tumor growth might be, in part, driven by selection for a mutation in the mutation cluster region.

Adenomatous Polyposis Coli↗
PubMed2002

Low frequency of beta-catenin gene mutations in pilomatricoma.

We investigated beta-catenin and adenomatous polyposis coli (APC) gene abnormalities in human pilomatricoma, in which a high incidence of beta-catenin gene mutations has been reported. Nucleated tumour cells were microdissected from 20 paraffin-embedded pilomatricomas. Exon 3 of the beta-catenin gene was amplified using polymerase chain reaction and sequencing analysis was performed. Immunostaining for beta-catenin and lymphoid-enhancer factor-1 was performed using the avidin-biotin-peroxidase method. Dinucleotide repeat markers D5S409 and D5S299 were used for polymerase chain reaction-based microsatellite analysis of the APC gene. The mutation cluster region of the APC gene was amplified using polymerase chain reaction and sequenced. Sequencing analysis revealed beta-catenin gene mutations in 30%. All studied samples showed nuclear lymphoid-enhancer factor-1 and cytoplasmic/nuclear beta-catenin expression. Loss of heterozygosity was observed in the APC gene, but no mutations in the mutation cluster region were found in seven tumours without beta-catenin mutations. The frequency of beta-catenin gene mutations was remarkably low, thus suggesting (i) the presence of mutations in other than exon 3 of the beta-catenin gene, (ii) a possible role of APC gene abnormalities, or (iii) involvement of other components of the Wingless-type MMTV integration site family pathway.

Adolescent↗
PubMed1998

APC mutations in human colorectal adenomas: analysis of the mutation cluster region with temperature gradient gel electrophoresis and clinicopathological features.

To date, the earliest mutations in colorectal adenomas have been found in the adenomatous polyposis coli (APC) gene, considered the 'gatekeeper' in tumourigenesis. To study the types of APC gene mutations and their relation to clinicopathological features which are associated with malignant potential, the mutation cluster region of the APC gene was analysed in a series of 32 human sporadic colorectal adenomas from 22 patients. DNA was extracted from frozen sections and two overlapping fragments which cover the mutation cluster region were amplified using the polymerase chain reaction (PCR). Mutations were screened with temperature gradient gel electrophoresis and identified by DNA sequencing. Mutations were found in 14 samples (44 per cent) from 11 patients. The changes could be characterized as point mutations (n = 7), deletions of one or more nucleotides (n = 6), and insertions (n = 1). From five patients, multiple adenoma samples were obtained and the adenomas from two of these patients showed a heterogeneous mutation pattern in the APC gene. All detected mutations are predicted to result in a truncated APC protein. Genetic alterations in the mutation cluster region of the APC gene occurred significantly more frequently in large adenomas and showed a trend towards an increase in villous adenomas and adenomas with moderate and severe dysplasia. It is concluded that an increased proportion of APC gene mutations were found in the adenomas showing clinicopathological features associated with increased proliferation but not with characteristics of malignant potential. The results suggest that in a significant proportion of adenomas, other (genetic) alterations are involved in early tumourigenesis.

Adenoma↗
PubMed2002

Genetic predisposition to clinical manifestations in familial adenomatous polyposis with special reference to duodenal lesions.

OBJECTIVES: In familial adenomatous polyposis (FAP), genetic predisposition for duodenal adenomatosis has not been investigated precisely. The aim of this study was to investigate the correlation between adenomatous polyposis coli (APC) gene mutation and duodenal adenomatosis in FAP. METHODS: APC gene mutation was determined by means of a protein truncation test in 34 patients from 25 families with FAP. The prevalence and grade of duodenal adenomatosis were compared among the proximal mutation group (exons 1-9), the distal mutation group (exons 10-15), and the undetermined groups. The correlation between the course of duodenal adenomatosis and APC gene mutation was retrospectively investigated in 19 patients. RESULTS: The prevalence of duodenal adenomatosis was lower in the proximal mutation group (44%) than in the distal mutation (100%) and undetermined (83%) groups. In patients with positive duodenal adenomatosis, the endoscopic grade did not differ among the groups. The endoscopic grade increased in two of the four patients with the proximal mutation group (50%), in three of 10 patients with the distal mutation group (30%), and in two of five patients (40%) with the undetermined group. CONCLUSIONS: Truncating APC gene mutation proximal to exon 9 may contribute to the less frequent development of duodenal adenomatosis in FAP, but severity and progression of duodenal adenomatosis do not seem to be determined by APC gene mutation alone.

Adenomatous Polyposis Coli↗
PubMed2000

Loss of heterozygosity of adenomatous polyposis coli gene in cutaneous tumors as determined by using polymerase chain reaction and paraffin section preparations.

It has been suggested that an alteration in the adenomatous polyposis coli (APC) gene, which is a tumor suppressor gene, is one of the earlier events in carcinogenesis of some adenocarcinomas. We undertook this study to determine the prevalence of loss of heterozygosity (LOH) of the APC gene in several kinds of cutaneous tumors. Fifty-seven unrelated Japanese patients were examined for analysis of the APC gene. The 57 cases consisted of extramammary Paget's disease, squamous cell carcinoma (SCC), eccrine poroma and porocarcinoma, metastatic tumor of rectal adenocarcinoma and malignant melanoma. DNA was extracted from the tumor and normal portions dissected from the formalin-fixed paraffin-embedding sections and amplified with the use of the PCR. The amplified DNA was examined for LOH in the APC gene. Seven samples of 32 heterozygous persons of APC gene (three out of seven eccrine poromas, two eccrine porocarcinomas and two metastatic tumors of rectal adenocarcinoma) showed for LOH in the APC gene. None of the heterozygous samples from the extramammary Paget's disease (11), SCC (five) and melanoma (five) showed LOH. These results suggest that tumor or tumor suppressor genes, other than the APC gene, may be responsible for extramammary Paget's disease and SCC and that LOH involving APC may have some relevance to the formation and progression of eccrine tumors as in rectal tumors.

Adenomatous Polyposis Coli Protein↗
PubMed2005

Loss of heterozygosity of APC and CDH1 genes in laryngeal squamous cell carcinoma.

The molecular mechanisms involved in the development and progression of laryngeal cancer, specifically squamous cell carcinoma, still need further investigation and elucidation. Twenty-two laryngeal squamous cell carcinomas were analyzed in our study regarding genetic changes of two tumor suppressor genes: Adenomatous polyposis coli (APC) and E-cadherin (CDH1). APC gene instability was tested by polymerase chain reaction (PCR)/loss of heterozygosity (LOH) using the restriction fragment length polymorphism (RFLP) method. The samples were also screened for mutations using the heteroduplex method. E-cadherin gene was analyzed by PCR amplification of tetranucleotide marker (D16S752) linked to E-cadherin gene. The results of our analysis showed three samples with LOH of the APC gene out of 15 heterozygous patients (20%). Only one LOH of the CDH1 gene (5.5%) out of 18 heterozygous patients was discovered. D16S752 marker did not reveal any replication error-positive samples. There were six samples showing heteroduplexes (33%) encompassed in APC's exon 11. Altogether, nine samples (41%) showed alterations of the APC gene. Our results suggest that alterations of APC gene may have a role in squamous cell carcinoma development. Detected LOH of the E-cadherin gene indicates that genetic changes of this gene are not very frequent, but that other components of the wnt signaling cascade may also be involved.

Adult↗
PubMed2000

Fundic gland polyps in familial adenomatous polyposis: neoplasms with frequent somatic adenomatous polyposis coli gene alterations.

Fundic gland polyps (FGPs) are the most common gastric polyps in patients with familial adenomatous polyposis (FAP). FGPs have traditionally been regarded as nonneoplastic, possibly hamartomatous lesions, but the pathogenesis of FGPs in both FAP and sporadic patients remains unclear. FGPs in FAP can show foveolar dysplasia, and rarely invasive gastric adenocarcinoma has been reported in patients with FAP and fundic gland polyposis. Using direct gene sequencing and allelic loss assays at 5q, we analyzed somatic adenomatous polyposis coli (APC) gene alterations in 41 FAP-associated FGPs (20 with foveolar dysplasia, six indefinite for dysplasia, and 15 nondysplastic) and 13 sporadic FGPs. The foveolar epithelium and dilated fundic glands of the polyps were separately microdissected and analyzed in 25 of 41 FAP-associated FGPs and 13 of 13 sporadic FGPs. Somatic APC gene alterations were identified frequently (21 of 41 cases, 51%) in FAP-associated FGPs. Both the foveolar epithelium and the dilated fundic gland epithelium comprising the FGPs were shown to carry the same somatic APC gene alteration in 24 (96%) of 25 cases. Furthermore, there was no difference in the frequency of somatic APC gene alterations between FGPs with foveolar dysplasia (10 of 20, 50%), indefinite for dysplasia (four of six, 67%), and nondysplastic (seven of 15, 47%) in FAP patients (P: = 0.697). In contrast, FGPs from non-FAP patients showed infrequent (one of 13, 8%) APC gene alterations (P: = 0.008). These results show that FGPs in FAP patients are pathogenetically distinct from sporadic FGPs. Somatic, second-hit APC gene alterations, which precede morphological dysplasia in many FAP-associated FGPs, indicate that FGPs arising in the setting of FAP are neoplastic lesions.

Adenomatous Polyposis Coli↗
PubMed1995

Effects of docosahexaenoic acid (DHA) on intestinal polyp development in Apc delta 716 knockout mice.

Epidemiological studies and animal experiments show an association of dietary intake of fish oils and low incidence of several types of cancers. The active ingredients of fish oils appear to be polyunsaturated fatty acids of omega-3 type such as eicosapentaenoic acid and docosahexaenoic acid (DHA). We have investigated chemopreventive effects of DHA on mouse intestinal polyposis using adenomatous polyposis coli (Apc) gene knockout mice. Damage to the human APC gene is responsible for not only familial adenomatous polyposis but also many sporadic cancers of the entire digestive tract. Using homologous recombination in embryonic stem cells, we recently constructed gene knockout mice containing a truncation mutation in the Apc gene at codon 716 (Apc delta 716). The heterozygous mice developed numerous intestinal polyps, and all microadenomas dissected from the earliest polyps had already lost the wild-type allele, indicating the loss of heterozygosity [Oshima et al. (1995), Proc. Natl Acad. Sci. USA, 92, 4482-4486]. We fed Apc delta 716 heterozygotes with AIN-76A purified diet containing 3% DHA for 7 weeks, and scored the number and size of intestinal polyps. Average DHA intakes per day were 4.1 and 4.3 g/kg body wt for males and females, respectively. DHA-fed females had only 31% of polyps compared with the control females that developed about 220 polyps, whereas DHA-fed females showed no significant decrease in the polyp number. As for the polyp size, the proportion of larger polyps decreased more significantly in females than in males. This is the first demonstration that DHA inhibits intestinal polyposis induced by an Apc mutation at both its formation and growth.

Animals↗