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Adenomatous Polyposis Coli clinical trials

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NCT ID: NCT03649971 Completed - Clinical trials for Adenomatous Polyposis Coli

A Study of Guselkumab in Participants With Familial Adenomatous Polyposis

Start date: November 19, 2018
Phase: Phase 1
Study type: Interventional

The purpose of this study is to determine the effect of treatment with guselkumab in participants with familial adenomatous polyposis (FAP) on rectal/pouch polyp burden.

NCT ID: NCT03494543 Completed - Clinical trials for Familial Adenomatous Polyposis

Endoscopic Papillectomy for Ampullary Adenomas

Papillectomy
Start date: January 1, 2005
Phase:
Study type: Observational

In this single-center experience we retrospectively evaluated principal clinical outcomes of endoscopic papillectomy in all patients referred to our unit. The same evaluation was then performed dividing sproradic ampullary adenoma from familial adenomatous polyposis associated adenomas, and resulting outcomes were compared.

NCT ID: NCT03471403 Recruiting - Clinical trials for Familial Adenomatous Polyposis

Cold Snare Polypectomy for Duodenal Adenomas in Familial Adenomatous Polyposis

COPDA
Start date: October 10, 2017
Phase:
Study type: Observational

The purpose of this study is to collect prospective observational data regarding patients with diagnosed Familial Adenomatous Polyposis (FAP) undergoing cold snare polypectomy for duodenal adenomas

NCT ID: NCT03346980 Completed - Duodenal Cancer Clinical Trials

Endoscopic Evaluation of Duodenal Polyposis in Patients With Familial Adenomatous Polyposis (FAP)

Start date: December 1, 2017
Phase:
Study type: Observational [Patient Registry]

Familial adenomatous polyposis (FAP) is an autosomal dominant genetic disorder that predisposes to a number or malignant disorders [1,2]. Clinically, FAP presents with an abnormal number of colorectal polyps (100-5000), while it genetically is defined by mutations in the APC-gene [1]. Historically, colorectal cancer has been the major cause of deaths for FAP patient. However, as the incidence of colorectal cancer has decreased with the use of prophylactic colectomy, the incidence of duodenal cancer has increased [3,4]. It is estimated that the cumulative lifetime risk of duodenal polyposis exceeds 95% [1,5]. The predictor of duodenal cancer is duodenal polyposis, which is almost inevitable in patients with FAP. In 1989 the Spigelman score was introduced in order to assess the severity of duodenal polyposis and stratify patients according to risk of duodenal cancer (Table 1) [6]. It is a composite score that includes two endoscopic parameters (number and maximum size of polyps, respectively) and two histopathological parameters (histological subtype and grade of dysplasia). The score ranges from 0-12 and it has been classified in four stages. The 10-year risk of developing duodenal cancer corresponds with the Spigelman stage ranging from ≈0 for stage 0-1 to 36% for stage 4 [7]. Besides duodenal cancer, the indications of cancer prophylactic surgical resection are debatable, but generally recommended in the case of Spigelman stage 4 or high-grade dysplasia. Table 1 Spigelman Classification for duodenal polyposis Criterion 1 point 2 points 3 points Polyp number 1-4 5-20 >20 Polyp size (mm) 1-4 5-10 >20 Histology Tubular Tubulovillous Villous Dysplasia Low grade* High grade* Stage 0: 0 points; stage I: 1-4 points; stage II: 5-6 points; stage III: 7-8 points; stage IV: 9-12 points. *Originally, 3 grades of dysplasia were incorporated. While the correlation to cancer has been explored in several studies, the validation and the reproducibility of the Spigelman score remains somewhat unclear. The primary aim of this study is to assess the inter- and intra-observer agreement of the Spigelman score for experienced endoscopists using state-of-the-art high-definition (HD) endoscopes. Hypothesis: The Spigelman score has perfect reproducibility for endoscopic experts (κ>0.80 with 95% CI.).

NCT ID: NCT03333265 Completed - Colorectal Adenomas Clinical Trials

Primary Chemoprevention of Familial Adenomatous Polyposis With Berberine Hydrochloride

Start date: September 1, 2017
Phase: Phase 2/Phase 3
Study type: Interventional

In recent years, Berberine hydrochloride has been reported to inhibit cancer cell proliferation and to be cytotoxic towards cancer cells. Patients with familial adenomatous polyposis have a nearly 100 percent risk of colorectal cancer. The aim of this study is to investigate the chemopreventive effects Berberine hydrochlorid on the regression of colorectal adenomas.

NCT ID: NCT03095703 Completed - Clinical trials for Adenomatous Polyposis Coli

Sirolimus and Familial Adenomatous Polyposis (FAP)

Start date: October 3, 2017
Phase: Phase 2
Study type: Interventional

The aim of the study is to investigate the effect of sirolimus on the progression of intestinal adenomas in patients with FAP and to assess the safety of this treatment.

NCT ID: NCT03061591 Not yet recruiting - Clinical trials for Familial Adenomatous Polyposis

Turmeric Supplementation on Polyp Number and Size in Patients With Familial Adenomatous Polyposis.

Start date: April 2017
Phase: Phase 2
Study type: Interventional

A Phase 2, randomized, double blind, placebo controlled trial for the effectivness of wholistic turmeric supplementation on polyp burden mong patients with Familial Adenomatouse Polyposis (FAP). Fourty Patients will be randomly assigned in a 1:1 ratio to recieve treatment with 8 capsuls (2*4 capsuls/day) of wholistic Turmeric capsules (Pukka herbs) or placebo for six months.

NCT ID: NCT03050268 Recruiting - Pancreatic Cancer Clinical Trials

Familial Investigations of Childhood Cancer Predisposition

SJFAMILY
Start date: April 6, 2017
Phase:
Study type: Observational

NOTE: This is a research study and is not meant to be a substitute for clinical genetic testing. Families may never receive results from the study or may receive results many years from the time they enroll. If you are interested in clinical testing please consider seeing a local genetic counselor or other genetics professional. If you have already had clinical genetic testing and meet eligibility criteria for this study as shown in the Eligibility Section, you may enroll regardless of the results of your clinical genetic testing. While it is well recognized that hereditary factors contribute to the development of a subset of human cancers, the cause for many cancers remains unknown. The application of next generation sequencing (NGS) technologies has expanded knowledge in the field of hereditary cancer predisposition. Currently, more than 100 cancer predisposing genes have been identified, and it is now estimated that approximately 10% of all cancer patients have an underlying genetic predisposition. The purpose of this protocol is to identify novel cancer predisposing genes and/or genetic variants. For this study, the investigators will establish a Data Registry linked to a Repository of biological samples. Health information, blood samples and occasionally leftover tumor samples will be collected from individuals with familial cancer. The investigators will use NGS approaches to find changes in genes that may be important in the development of familial cancer. The information gained from this study may provide new and better ways to diagnose and care for people with hereditary cancer. PRIMARY OBJECTIVE: - Establish a registry of families with clustering of cancer in which clinical data are linked to a repository of cryopreserved blood cells, germline DNA, and tumor tissues from the proband and other family members. SECONDARY OBJECTIVE: - Identify novel cancer predisposing genes and/or genetic variants in families with clustering of cancer for which the underlying genetic basis is unknown.

NCT ID: NCT03027401 Withdrawn - Neoplasms Clinical Trials

Clinical Sequencing of Cancer and Tissue Repository: OncoGenomics

Start date: January 10, 2017
Phase:
Study type: Observational

Background: Saliva, blood, tissue, and cancer contain DNA. DNA makes the "instruction book" for the cells in the body. Cancer is caused by changes in DNA that affect cell function. Researchers want to test DNA of people with tumors. They want to look for genetic changes in tumors that could be targets for treatment. Because DNA can change as cancer changes, more testing may be done at different times. Objectives: To find the DNA changes in cancer that may help guide treatment. To collect samples and data to be used in future studies. Eligibility: People any age with cancer or a pre-cancerous tumor Design: - Participants will be screened with a medical history, physical exam, and blood tests. Participants will give a sample of their tumor. This is usually from a previous procedure. Participants will give a saliva or blood sample. They cannot eat, drink, smoke, or chew gum for 30 minutes before giving saliva. They will spit about 1 teaspoon of saliva into a tube. - Some participants may have a punch biopsy instead. A small instrument will take a small piece of skin. - Researchers will collect data from participants medical records. - Participants will answer questions about their family health history. They will also answer questions about their views on the study, including possible unexpected results. - Extra blood or tissue samples may be taken at other times during the participants' treatment. All samples will be saved in secure ClinOmics freezers to be used in future studies. - Participants will be told by their doctors if any test results affect their health or their cancer treatment.

NCT ID: NCT02961374 Completed - Clinical trials for Familial Adenomatous Polyposis

Erlotinib Hydrochloride in Reducing Duodenal Polyp Burden in Patients With Familial Adenomatous Polyposis at Risk of Developing Colon Cancer

Start date: October 27, 2017
Phase: Phase 2
Study type: Interventional

This phase II trial studies the side effects of erlotinib hydrochloride and how well it works in reducing duodenal polyp burden in patients with familial adenomatous polyposis at risk of developing colon cancer. Erlotinib hydrochloride may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.