A Prospective Study of the Clinical, Genetic, Screening, and Pathologic Features of a Family With Hereditary Mixed Polyposis Syndrome
Tel Aviv University, Tell Afif, Tel Aviv, IsraelThe American Journal of Gastroenterology (Impact Factor: 10.76). 11/2003; 98(10):2317-20. DOI: 10.1111/j.1572-0241.2003.07714.x
In 1997, hereditary mixed polyposis syndrome (HMPS) was described in an Ashkenazi pedigree having colorectal polyps with mixed histology and risk for colorectal cancer (CRC). The mutation is now localized to 15q13-14. Since 1980, compliant relatives of an HMPS family were seen annually, tested genetically, and had colonoscopy offered every 1 to 2 yr from age 20 yr. The Israeli pedigree has 37 members (17 clinically affected by CRC or polyps), and seven of 13 available relatives entered our screening program. The others, followed-up elsewhere, provided clinical information. Half of our screened group had rectal bleeding; others were asymptomatic. Colonoscopy, performed a mean of four times, identified polyps in all seven patients (mean age 28 yr). Polyps were removed and included juvenile adenomas, mixed juvenile adenomas, hyperplastic polyps, mixed hyperplastic adenomas, serrated adenomas, and tubular adenomas. None of our screened patients developed CRC or extracolonic neoplasia. Linkage analysis localized their mutation to 15q13-14. This high-penetrance founder mutation so far is described only in Ashkenazim. The CRC pathway seems to be through juvenile and hyperplastic polyps. Mutation identification will aid screening for and evaluation of HMPS prevalence in Jewish and non-Jewish populations. Meanwhile, a cancer pedigree and correct classification of polyps will identify HMPS families. They require early and frequent colonoscopy, polypectomy, and elective extensive colectomy when indicated.
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ABSTRACT: In this paper, we present a new discrete cosine transform (DCT) processor architecture using computation sharing multiplication (CSHM). We introduce a computation sharing multiplier based DCT architecture to achieve image quality and hardware complexity trade-off and analyze the performance. Comparison of the performance, area and power consumption with a DA (distributed arithmetic) based DCT architecture is performed. The result shows that the proposed architecture improves power consumption by 14% and area by 41% with acceptable image quality degradation.
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ABSTRACT: Hereditary mixed polyposis syndrome (HMPS), characterized by hyperplastic, juvenile, admixed, serrated adenomas and eventually colorectal cancer, is managed by repeated polypectomy and surgery. We determined if HMPS polyps express cyclooxygenase-2 (COX-2). Nineteen recent HMPS polyps, from five family members, were stained for COX-2. Polyps' epithelium and stroma and comparison tissues (normal colonic mucosa , sporadic juvenile polyps , colorectal cancers ) were quantified for COX-2 by: area of staining (0-3) x intensity (0-3). Epithelial, stromal, and total scores were evaluated in relationship to histology and dysplasia. HMPS polyps COX-2 mean epithelial (5.0+/-3.0), stromal (6.9+/-1.9), and total (11.8+/-4.6) scores were significantly higher (P < 0.01) than sporadic juvenile polyps (0.6+/-0.7, 3.1+/-2.2, and 3.6+/- 2.2 respectively), while colorectal cancer scored 9, 9, and 18. There was a positive association (P < 0.01) among histology, degree of dysplasia, and COX-2 expression. COX-2 expression in HMPS polyps and its association with dysplasia suggest that chemoprevention might be a useful adjunct therapy.
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ABSTRACT: Ashkenazi Jews, as compared to non-European Jews and non-Jews, are at increased risk for colorectal cancer (CRC), this is attributed to genetic susceptibility and/or lifestyle. Aims: To follow Israeli long-term trends in CRC incidence and mortality and their associations with ethnicity. All Israeli CRC data accumulated 1970-2001 was used, age standardized rates (adjusted to world standard population) was computed by cancer site, US Surveillance, Epidemiology and End Results Program (SEER) Stage and ethnic group (continent of birth: Europe-America, Asia, Africa, Israel). From 1970, CRC incidence increased 190% in males and 140% in females; mainly colon cancer (270% and 185% respectively) (P < 0.01), while rectal cancer incidence decreased and is now stable. Stage 3 CRC increased while stage 4 decreased significantly (P < 0.01 for both). In 2001, CRC incidence per 100,000 in European-American-born males was 48.3, Asian and African born 35.5 and Israeli born 32.7 (relative risk (RR) 1.36, P = 0.03), while European-American female rates were 35 and all the others 26 (RR 1.35, P < 0.01). Overall survival increased 9% over 30 years (P < 0.01), 5 years survival since 1988-1996 for European-American born was 43.1%, Asian 46.7%, African 47.5% and Israeli 55.8%. Stage-2 CRC 5 years survivals for 1970-1996 (most had no post surgical treatment) for European-American born were 41.7%, Asian and African 44.8% and Israeli 53.4% (P < 0.05). Stage-3 CRC survivals (most received adjuvant therapy in addition to surgery) for European-American born was 38.8%, Asian and African 43.3% and Israeli 45.1% (P < 0.01). Colon cancer has increased in Israel, mainly in males and European-American born. Israeli-born Jews (of 20 to 60% mixed ethnicity and lifestyle habits) have the lowest incidence and best survival data for stages-2 and -3 CRC. There is evidence of ethnic survival advantage and possibly in response to adjuvant oncological therapy.