Results 31 to 40 of about 10,129 (212)

Updates in the field of hereditary nonpolyposis colorectal cancer [PDF]

open access: yesExpert Review of Gastroenterology & Hepatology, 2020
Up to one third of colorectal cancers show familial clustering and 5% are hereditary single-gene disorders. Hereditary non-polyposis colorectal cancer comprises DNA mismatch repair-deficient and -proficient subsets, represented by Lynch syndrome (LS) and familial colorectal cancer type X (FCCTX), respectively.
Paivi, Peltomäki   +2 more
openaire   +2 more sources

Analysis of colorectal cancers in British Bangladeshi identifies early onset, frequent mucinous histotype and a high prevalence of RBFOX1 deletion [PDF]

open access: yes, 2013
Background Prevalence of colorectal cancer (CRC) in the British Bangladeshi population (BAN) is low compared to British Caucasians (CAU). Genetic background may influence mutations and disease features.
Sengupta, N   +69 more
core   +1 more source

Alcohol consumption, alcohol dehydrogenase 3 polymorphism, and colorectal adenomas. [PDF]

open access: yes, 2003
Alcohol is a probable risk factor with regard to colorectal neoplasm and is metabolized to the carcinogen acetaldehyde by the genetically polymorphic alcohol dehydrogenase 3 (ADH3) enzyme.
Ocké, Marga C   +18 more
core   +2 more sources

HISTORY OF HEREDITARY NONPOLYPOSIS COLORECTAL CANCER OR “LYNCH SYNDROME”

open access: yesRevista Médica Clínica Las Condes, 2017
Hereditary Nonpolyposis Colorectal Cancer (HNPCC or “Lynch syndrome”), involving pathogenic variants in the Mismatch Repair (MMR) genes, is the most common inherited condition that predisposed to colorectal adenomas and colorectal cancer. In this chapter
Patrick M Lynch, JD, MD
doaj   +1 more source

Ovarian Cancer: Epidemiology, Disease Mechanisms, New Diagnosis and Treatment Strategies, and Research Directions

open access: yesiNew Medicine, EarlyView.
ABSTRACT Ovarian cancer (OC) continues to be the deadliest gynecological malignancy and a significant cause of cancer‐related mortality among women worldwide. Standard treatment strategies typically entail platinum‐based chemotherapy in conjunction with cytoreductive surgery.
Zunera Khalid   +4 more
wiley   +1 more source

The Genomics of colorectal cancer: State of the art

open access: yes, 2008
The concept of the adenoma-carcinoma sequence, as first espoused by Morson et al. whereby the development of colorectal cancer is dependent on a stepwise progression from adenomatous polyp to carcinoma is well documented.
Hodgson, SV   +3 more
core   +1 more source

Molecular diagnosis of hereditary nonpolyposis colorectal cancer (Lynch syndrome)

open access: yesRevista de la Facultad de Medicina, 2016
Lynch syndrome is the most common cause of inherited colorectal cancer, totaling 5 to 8% of all the cases with high susceptibility to this type of cancer and extracolonic cancer.
David Serrano, Clara Eugenia Arteaga
doaj   +1 more source

DNA content analysis of colorectal cancer defines a distinct ‘microsatellite and chromosome stable’ group but does not predict response to radiotherapy [PDF]

open access: yes, 2014
Colorectal cancers (CRC) are thought to have genetic instability in the form of either microsatellite instability (MSI) or chromosomal instability (CIN).
Ilyas, Mohammad   +13 more
core   +1 more source

Familial Adenomatous Polyposis—Risk of Cancer, Cancer Prevention, and Long‐Term Consequences: Learnings from Five Decades with the Danish Polyposis Register

open access: yesAPMIS, Volume 134, Issue 5, May 2026.
ABSTRACT Familial adenomatous polyposis (FAP) is a hereditary condition marked by the growth of hundreds to thousands of adenomatous polyps in the colon and rectum, significantly elevating the risk of colorectal cancer (CRC) if left untreated. Caused by pathogenic variants in the APC gene, FAP is typically identified in adolescence, often leading to ...
John Gásdal Karstensen
wiley   +1 more source

Numbers of mutations to different types of colorectal cancer

open access: yesBMC Cancer, 2005
Background The numbers of oncogenic mutations required for transformation are uncertain but may be inferred from how cancer frequencies increase with aging. Cancers requiring more mutations will tend to appear later in life.
Tavaré Simon   +5 more
doaj   +1 more source

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