Zobrazeno 1 - 10
of 15
pro vyhledávání: '"Jill D. Brensinger"'
Autor:
Francis M. Giardiello, Karen A. Johnson, Constance A. Griffin, Lynne S. Rosenblum-Vos, Gloria M. Petersen, Jill D. Brensinger
Publikováno v:
American Journal of Medical Genetics. 91:207-211
The APC I1307K gene mutation is associated with increased colorectal cancer (CRC) risk in Ashkenazi Jews. Factors predicting acceptance of this and other hereditary colon cancer mutation tests in a clinical setting are unknown. We analyzed sex, age,
Autor:
Susan V. Booker, Steven N. Goodman, Jill D. Brensinger, Francis M. Giardiello, Johan Offerhaus, Marcia Cruz-Correa, Gloria M. Petersen, Anne C. Tersmette
Publikováno v:
Gastroenterology, 119(6), 1447-1453. W.B. Saunders Ltd
Background & Aims: The Peutz–Jeghers syndrome (PJS) is an autosomal dominant polyposis disorder with increased risk of multiple cancers, but literature estimates of risk vary. Methods: We performed an individual patient meta-analysis to determine t
Publikováno v:
Cancer. 86:1720-1730
The discovery of genes responsible for inherited forms of colorectal cancer have the potential to improve cancer risk assessment and counseling. Germline mutations (nonsense, frameshift) of APC are associated with familial adenomatous polyposis, an a
Publikováno v:
Annals of Oncology. 8:1151-1156
Colorectal cancer is a leading cause of cancer related death in both Europe and the United States. Approximately 20% of cases occur in familial aggregations making this disorder the most frequent form of hereditary neoplasia [1]. Consequently, patien
Autor:
Stanley R. Hamilton, Linda M. Hylind, Gloria M. Petersen, Francis M. Giardiello, Rodger D. Parker, Judith A. Bacon, Jill D. Brensinger, Michael C. Luce, Susan V. Booker
Publikováno v:
New England Journal of Medicine. 336:823-827
The use of commercially available tests for genes linked to familial cancer has aroused concern about the impact of these tests on patients. Familial adenomatous polyposis is an autosomal dominant disease caused by a germ-line mutation of the adenoma
Autor:
Stanley R. Hamilton, J. A. Offerhaus, Anne J. Krush, Francis M. Giardiello, Linda M. Hylind, Jill D. Brensinger, Susan V. Booker, A. C. Tersmette
Publikováno v:
Gut, 38(4), 578-581. BMJ Publishing Group
BACKGROUND--Sulindac, a non-steroidal anti-inflammatory drug, causes regression of colorectal adenomas in patients with familial adenomatous polyposis (FAP) but the response is variable. Specific clinical factors predictive of sulindac induced regres
Autor:
Jill D. Brensinger, Renata Laxova
Publikováno v:
Journal of Genetic Counseling. 4:27-47
Previous studies of the closed Amish population have proven to be valuable in the field of genetics, however they have not explored the Amish parents' opinions and attitudes concerning genetic conditions and services. This exploration is necessary in
Autor:
Stanley R. Hamilton, Gloria M. Petersen, Susan V. Booker, M. C. Luce, Judy Bacon, Jill D. Brensinger, M C Cayouette, Francis M. Giardiello
Publikováno v:
Gut. 39:867-869
BACKGROUND: Hepatoblastoma is a rare, rapidly progressive, usually fatal childhood malignancy, which if confined to the liver can be cured by radical surgical resection. An association between hepatoblastoma and familial adenomatous polyposis (FAP),
Publikováno v:
Gastroenterology. 121(1)
This literature review and the recommendations therein were prepared for the American Gastroenterological Association (AGA) Clinical Practice and Practice Economics Committee. The paper was approved by the Committee on March 20, 2001, and by the AGA
Autor:
Francis M. Giardiello, Bert Vogelstein, Gloria M. Petersen, Stephen B. Gruber, Jill D. Brensinger, Nickolas Papadopoulos, Kenneth W. Kinzler, Stanley R. Hamilton, Steven J. Laken
Publikováno v:
Proceedings of the National Academy of Sciences of the United States of America. 96(5)
Familial adenomatous polyposis (FAP) is an autosomal-dominant disease characterized by the development of hundreds of adenomatous polyps of the colorectum. Approximately 80% of FAP patients can be shown to have truncating mutations of the APC gene. T