Titlebook: Hereditary Colorectal Cancer; Genetic Basis and Cl Laura Valle,Stephen B. Gruber,Gabriel Capellá Book 2018 Springer International Publishin

abandon

書目名稱Hereditary Colorectal Cancer影響因子(影響力)




書目名稱Hereditary Colorectal Cancer影響因子(影響力)學(xué)科排名




書目名稱Hereditary Colorectal Cancer網(wǎng)絡(luò)公開度




書目名稱Hereditary Colorectal Cancer網(wǎng)絡(luò)公開度學(xué)科排名




書目名稱Hereditary Colorectal Cancer被引頻次




書目名稱Hereditary Colorectal Cancer被引頻次學(xué)科排名




書目名稱Hereditary Colorectal Cancer年度引用




書目名稱Hereditary Colorectal Cancer年度引用學(xué)科排名




書目名稱Hereditary Colorectal Cancer讀者反饋




書目名稱Hereditary Colorectal Cancer讀者反饋學(xué)科排名

乞討

The Molecular Basis of Lynch-like Syndromepathogenic germline mutation has been identified. Patients and their first-degree relatives are considered to have an intermediate risk of developing cancer between LS and the general population..In this chapter, we aimed to review the most promising work in the area. Double somatic variants in MMR

interpose

Constitutional Mismatch Repair Deficiency malignancies in childhood. This recessively inherited condition is named CMMRD for constitutional mismatch repair deficiency. The spectrum of tumours is distinct from LS. Malignant brain tumours are at least as frequent as gastrointestinal tumours, and in more than a third of cases, haematological

暫時(shí)過來

Mismatch Repair-Proficient Hereditary Nonpolyposis Colorectal Cancerle defects in the DNA mismatch repair (MMR) system; more specifically, these patients have no germline mutations in the MMR genes and, therefore, no tumor microsatellite instability or loss of immunohistochemical staining of MMR proteins. The proportion of nonpolyposis CRC families without MMR defec

leniency

Genetic and Environmental Modifiers of Cancer Risk in Lynch Syndromeximately 1 in 280 (0.35%) of the population are estimated to carry a pathogenic mutation in one of these genes. However, penetrance (age-specific cancer risk) estimates for mutation carriers have been found to vary substantially depending on person’s sex and which gene is mutated. Further, penetranc

LEER

Adenomatous Polyposis Syndromes: Introductionancer (CRC), unless detected early. Currently, at least five different inherited forms can be delineated by molecular genetic analyses. Although all types are defined by multiple adenomas which result in a similar diagnostic and therapeutic approach, a significant clinical variability in terms of nu

不法行為

拖網(wǎng)

Adenomatous Polyposis Syndromes: Polymerase Proofreading-Associated Polyposisnd . have been found to be a rare cause of multiple colorectal adenomas and carcinomas. This condition is known as polymerase proofreading-associated polyposis (PPAP). The EDM of . is also somatically mutated in ~1% of colorectal cancers (CRCs) and ~8% of endometrial cancers. In this chapter we will

窒息

畸形

Adenomatous Polyposis Syndromes: NTHL1-Associated Polyposis / Tumor Syndromeed individuals have been described. Most had between 10 and 50 adenomas and two thirds had already developed CRC. Other cancers described include breast and endometrial cancer. In this chapter the clinical characteristics, genetics, tumor characteristics, and prevalence will be discussed.