ISSN:8756-0437    

DOI:10.1002/ssu.2980110602

出版商:John Wiley&Sons, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractAdenomas of the colon and rectum are perhaps the most commonly encountered of human benign epithelial neoplasms. Evidence of their relationship to the development of colorectal carcinoma has mounted over the years. They represent a phase present for significant duration in many fated to develop colon cancer. Because of this, and because of the technical advances in endoscopy, a great deal of effort has been expended on identifying and removing these lesions. Subsequent care of the patient is heavily dependent on the pathologic analysis of these lesions. They must be properly classified; the presence of cancer must be carefully sought. If present, the character and location of the cancer arising in the polyp must be carefully described. Communication between clinician and pathologist is of paramount importance. Attention must be paid to the precise meaning of such terms as dysplasia, carcinoma, and invasion. The pathologist's report needs to detail parameters important in determining prognosis and further therapy. © 1995 Wiley‐Liss, I

ISSN:8756-0437    

DOI:10.1002/ssu.2980110603

出版商:John Wiley&Sons, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractColitis‐associated carcinoma is often associated with, or preceded by, noninvasive epithelial neoplastic changes termed dysplasia. Surveillance colonoscopy with biopsies looking for dysplasia is now standard practice in the management of the cancer problem in ulcerative colitis. However, this practice continues to have a number of limitations and problems that need to be understood by surgeons who may be referring such patients. A number of recent reports indicate that colitis associated carcinoma is predominantly left‐sided and incorporation of this distribution in the surveillance methods merits consideration. The molecular and genetic abnormalities involved in the pathogenesis of colitis associated neoplasia are being actively investigated and may yield supplementary methods to better define individual patient risk. © 1995 Wiley‐Lis

ISSN:8756-0437    

DOI:10.1002/ssu.2980110604

出版商:John Wiley&Sons, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractRecognition of the mendelian dominant inherited syndrome of familial polyposis coli in the 1930s has been followed by the recognition of many inherited colonic polyposis syndromes. The recognition of different histological types of colon polyps was associated by the gradual recognition that some, such as the hamartomatous polyps, do not progress into adenocarcinoma, and others, such as various adenomas have a greater or lesser propensity to eventually give rise to invasive cancer.As the host of inherited syndromes expanded and were more widely recognized, additional inherited characteristics became apparent: such tumors as breast and thyroid associated with Cowden's syndrome, ovarian cysts and sex cord tumors with Peutz‐Jeghers syndrome, and, of course, the soft tissue, bony tumors, ampullary cancers, and fi‐broadenomas associated with Gardner's syndrome.In recent years, genetic markers for the various syndromes have been studied, and in some cases confirmed. This whole field is rapidly developing and is briefly covered. All the steps and influencing factors in cancer development are shown in one phase or another of the polyp‐cancer sequence in these inherited syndromes. © 1995 Wiley‐L

ISSN:8756-0437    

DOI:10.1002/ssu.2980110605

出版商:John Wiley&Sons, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractFrom a histologic and endoscopic standpoint, colon and rectal cancer (CRC) begins as a small neoplastic polyp which progressively enlarges and transforms through a dysplasia stage into invasive cancer. Recently, molecular abnormalities underlying the adenomacarcinoma progression have been defined. The adenomatous polyposis coli (APC) gene and mismatch repair genes are found to be dysfunctional early in the neoplastic process; either as inherited or somatic mutations. Subsequently, polyps progress to cancer along one of two paths depending on which gene is abnormal. When theAPCgene is the initial mutation tumor development follows the “loss of hetero‐zygocity” (LOH) pathway. If mismatch repair genes are altered, the “replication error” (RER) pathway is followed. Somatic mutations of the K‐rasoncogene and theMCC, DCC, andp53tumor suppressor genes accumulate in the LOH pathway and mark the progression through polyp stages. Microsatellite instability is a characteristic of the RER pathway but the precise genes involved in this pathway currently are not known. Defining these pathways has led to a new classification scheme for CRC with resultant changes in our clinical approach to screening, surveillance, and treatment. © 1995 Wil

ISSN:8756-0437    

DOI:10.1002/ssu.2980110606

出版商:John Wiley&Sons, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractHereditary nonpolyposis colorectal cancer (HNPCC) results from an inherited defect in one of the genes responsible for repair of errors that occur during DNA replication. Affected individuals have high risk for cancers of the colon and certain extracolonic sites. It appears that HNPCC patients form adenomas at about the same rate as the general population and there is circumstantial evidence that adenoma is the precursor to colorectal carcinoma in the syndrome. It is hypothesized that HNPCC features accelerated progression from colonie adenoma to carcinoma, a process theoretically driven by the inability to repair DNA mismatches. Evidence in support of the “Aggressive Adenoma” in HNPCC is provided. We discuss our recommendations for colono‐scopic surveillance on an annual basis for HNPCC gene‐positive individuals, and for genetic counseling. © 1995 Wiley

ISSN:8756-0437    

DOI:10.1002/ssu.2980110607

出版商:John Wiley&Sons, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractClinical trials in colorectal cancer prevention are based on carcino‐genesis research and epidemiologic observations that relate certain macronutrients, micronutrients, non‐nutritive factors in foods, and synthetic chemicals to colon neoplasms. These factors appear to act at various points along the putative normal mucosa → adenomatous polyp → cancer sequence. This gives an opportunity to develop innovative clinical trials, both in agent selection and in the use of intermediate markers. Clinical colorectal cancer prevention trials are now in progress that employ dietary fiber, a variety of vitamins and minerals and several synthetic drugs, especially the NSAIDs. Most of these trials use the adenomatous polyp as a surrogate marker for colon cancer, thereby reducing trial duration, number of subjects required and overall expense. This paper is a brief review of the basic and epidemiologic background for colorectal cancer prevention trials and their current status. © 1995 Wiley

ISSN:8756-0437    

DOI:10.1002/ssu.2980110608

出版商:John Wiley&Sons, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractThe flexible fibroscopic colonoscope has changed the way we approach colonie disease. The technique of safe, effective colonoscopy is discussed including the indications and contraindications for therapeutic intervention via the colonoscope. The techniques of polypectomy is described, including some tips for methodology gained by the broad experience of the author, and admonition against the possible complications which can be life‐threatening. The application for polypectomy in the presence of in‐situ or invasive cancer is presented. The possible future development of colonoscopic and laparoscopic techniques are presented. The article concludes with a discussion of the monumental work of the National Polyp Study documenting that patients undergoing polypectomy have a significant reduction in the incidence of colon cancer. Application of the knowledge to the general population requires the identification of at‐risk populations. © 1995 Wiley‐L

ISSN:8756-0437    

DOI:10.1002/ssu.2980110609

出版商:John Wiley&Sons, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractFamilial adenomatous polyposis (FAP) is a genetic disorder transmitted in an autosomal dominant pattern. One‐half of members of an affected family will carry the gene, and all carriers will succumb to colon cancer or extracolonic manifestations if not detected and treated early. When the diagnosis is made, surgery is indicated. Surgical options include total proctocolectomy with ileostomy, continent ileos‐tomy, total colectomy with ileorectal anastomosis, and total proctocolectomy with ileal pouch anal anastomosis. Many diverse factors, such as extent of rectal disease, the presence and extent of carcinoma, sphincter function, and extracolonic disease, influence which surgical procedure is most appropriate for the individual patient with FAP. This article reviews the surgical options for treating FAP, with emphasis on specific indications, contraindications, and anticipated outcomes. © 1995 Wiley‐Lis

ISSN:8756-0437    

DOI:10.1002/ssu.2980110610

出版商:John Wiley&Sons, Inc.    

年代:1995

数据来源: WILEY

ISSN:8756-0437    

DOI:10.1002/ssu.2980110601

出版商:John Wiley&Sons, Inc.    

年代:1995

数据来源: WILEY