The Experts below are selected from a list of 439632 Experts worldwide ranked by ideXlab platform
Anders Mellemgaard - One of the best experts on this subject based on the ideXlab platform.
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Metachronous Colorectal Cancer in young patients: Expression of the hereditary nonpolyposis Colorectal Cancer syndrome?
Diseases of the Colon & Rectum, 1991Co-Authors: Lars Bo Svendsen, Steffen Bülow, Anders MellemgaardAbstract:The cumulative incidence rate of metachronous Colorectal Cancer in patients younger than 40 years of age at diagnosis of the primary Cancer has been shown to be 30 percent. Metachronous Colorectal Cancer is predominantly located in the right colon with a decreasing frequency toward the rectum. The risk of developing a metachronous Colorectal Cancer was found to be 16–29 times increased when compared with the risk of having a primary Colorectal Cancer. Because of the resemblance between characteristics of metachronous Colorectal Cancer and the features of hereditary nonpolyposis Colorectal Cancer (HNPCC), it is proposed that young Colorectal Cancer patients developing metachronous Colorectal Cancer could in fact be HNPCC patients .
Hans Clevers - One of the best experts on this subject based on the ideXlab platform.
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mathematical model of Colorectal Cancer initiation
Proceedings of the National Academy of Sciences of the United States of America, 2020Co-Authors: Chay Paterson, Hans Clevers, Ivana BozicAbstract:Quantifying evolutionary dynamics of Cancer initiation and progression can provide insights into more effective strategies of early detection and treatment. Here we develop a mathematical model of Colorectal Cancer initiation through inactivation of two tumor suppressor genes and activation of one oncogene, accounting for the well-known path to Colorectal Cancer through loss of tumor suppressors APC and TP53 and gain of the KRAS oncogene. In the model, we allow mutations to occur in any order, leading to a complex network of premalignant mutational genotypes on the way to Colorectal Cancer. We parameterize the model using experimentally measured parameter values, many of them only recently available, and compare its predictions to epidemiological data on Colorectal Cancer incidence. We find that the reported lifetime risk of Colorectal Cancer can be recovered using a mathematical model of Colorectal Cancer initiation together with experimentally measured mutation rates in Colorectal tissues and proliferation rates of premalignant lesions. We demonstrate that the order of driver events in Colorectal Cancer is determined primarily by the fitness effects that they provide, rather than their mutation rates. Our results imply that there may not be significant immune suppression of untreated benign and malignant Colorectal lesions.
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mathematical model of Colorectal Cancer initiation
bioRxiv, 2020Co-Authors: Chay Paterson, Hans Clevers, Ivana BozicAbstract:ABSTRACT Quantifying evolutionary dynamics of Cancer initiation and progression can provide insights into more effective strategies of early detection and treatment. Here we develop a mathematical model of Colorectal Cancer initiation through inactivation of two tumor suppressor genes and activation of one oncogene, accounting for the well-known path to Colorectal Cancer through loss of tumor suppressors APC and TP53, and gain of the KRAS oncogene. In the model, we allow mutations to occur in any order, leading to a complex network of incomplete mutational genotypes on the way to Colorectal Cancer. We parametrize the model using experimentally measured parameter values, many of them only recently available, and compare its predictions to epidemiological data on Colorectal Cancer incidence. We find that the reported incidence of Colorectal Cancer can be recovered using a mathematical model of Colorectal Cancer initiation together with experimentally measured mutation rates in Colorectal tissues and proliferation rates of premalignant lesions. We demonstrate that the order of driver events in Colorectal Cancer is determined by the combined effect of the rates at which driver genes are mutated and the fitness effects they provide. Our results imply that there may not be significant immune suppression of untreated benign and malignant Colorectal lesions.
Michiko Miyaki - One of the best experts on this subject based on the ideXlab platform.
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Suspected hereditary nonpolyposis Colorectal Cancer
Diseases of the Colon & Rectum, 1999Co-Authors: Jae-gahb Park, Hans F. A. Vasen, Kyu Joo Park, Paivi Peltomaki, Maurizio Ponz De Leon, Miguel A. Rodriguez-bigas, Jan Lubinski, Nicholas E. Beck, Marie-luise Bisgaard, Michiko MiyakiAbstract:PURPOSE: The aim of this study was to determine the frequency of mutations in the mismatch repair genes in families suspected of having hereditary nonpolyposis Colorectal Cancer. METHODS: We devised two criteria for families suspected of having hereditary nonpolyposis Colorectal Cancer (Criteria I and II). Criteria I consist of at least two first-degree relatives affected with Colorectal Cancer with at least one of the following: development of multiple Colorectal tumors including adenomatous polyp, at least one Colorectal Cancer case diagnosed before the age of 50, and occurrence of a hereditary nonpolyposis Colorectal Cancer extracolonic Cancer (endometrium, urinary tract, small intestine, stomach, hepatobiliary system, or ovary) in family members. Criteria II consist of one Colorectal Cancer patient with at least one of the following: early age of onset (
Lars Bo Svendsen - One of the best experts on this subject based on the ideXlab platform.
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Metachronous Colorectal Cancer in young patients: Expression of the hereditary nonpolyposis Colorectal Cancer syndrome?
Diseases of the Colon & Rectum, 1991Co-Authors: Lars Bo Svendsen, Steffen Bülow, Anders MellemgaardAbstract:The cumulative incidence rate of metachronous Colorectal Cancer in patients younger than 40 years of age at diagnosis of the primary Cancer has been shown to be 30 percent. Metachronous Colorectal Cancer is predominantly located in the right colon with a decreasing frequency toward the rectum. The risk of developing a metachronous Colorectal Cancer was found to be 16–29 times increased when compared with the risk of having a primary Colorectal Cancer. Because of the resemblance between characteristics of metachronous Colorectal Cancer and the features of hereditary nonpolyposis Colorectal Cancer (HNPCC), it is proposed that young Colorectal Cancer patients developing metachronous Colorectal Cancer could in fact be HNPCC patients .
Hans F. A. Vasen - One of the best experts on this subject based on the ideXlab platform.
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survival of mutyh associated polyposis patients with Colorectal Cancer and matched control Colorectal Cancer patients
Journal of the National Cancer Institute, 2010Co-Authors: Maartje Nielsen, Hans Morreau, Hans F. A. Vasen, Stefan Aretz, Julian R. Sampson, Liza N Van Steenbergen, Natalie Jones, Stefanie Vogt, Olaf M Dekkers, Maryska L G JanssenheijnenAbstract:Background MUTYH-associated polyposis is a recessively inherited disorder characterized by a lifetime risk of Colorectal Cancer that is up to 100%. Because specific histological and molecular genetic features of MUTYH-associated polyposis Colorectal Cancers might influence tumor behavior and patient survival, we compared survival between patients with MUTYH-associated polyposis Colorectal Cancer and matched control patients with Colorectal Cancer from the general population.
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Suspected hereditary nonpolyposis Colorectal Cancer
Diseases of the Colon & Rectum, 1999Co-Authors: Jae-gahb Park, Hans F. A. Vasen, Kyu Joo Park, Paivi Peltomaki, Maurizio Ponz De Leon, Miguel A. Rodriguez-bigas, Jan Lubinski, Nicholas E. Beck, Marie-luise Bisgaard, Michiko MiyakiAbstract:PURPOSE: The aim of this study was to determine the frequency of mutations in the mismatch repair genes in families suspected of having hereditary nonpolyposis Colorectal Cancer. METHODS: We devised two criteria for families suspected of having hereditary nonpolyposis Colorectal Cancer (Criteria I and II). Criteria I consist of at least two first-degree relatives affected with Colorectal Cancer with at least one of the following: development of multiple Colorectal tumors including adenomatous polyp, at least one Colorectal Cancer case diagnosed before the age of 50, and occurrence of a hereditary nonpolyposis Colorectal Cancer extracolonic Cancer (endometrium, urinary tract, small intestine, stomach, hepatobiliary system, or ovary) in family members. Criteria II consist of one Colorectal Cancer patient with at least one of the following: early age of onset (
