Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The adaptive imbalance in base excision–repair enzymes generates microsatellite instability in chronic inflammation

15 Dec 2003

Abstract excerpt

Chronic infection and associated inflammation are key contributors to human carcinogenesis. Ulcerative colitis (UC) is an oxyradical overload disease and is characterized by free radical stress and colon cancer proneness. Here we examined tissues from noncancerous colons of ulcerative colitis patients to determine (a) the activity of two base excision-repair enzymes, AAG, the major 3-methyladenine DNA...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Acute Lymphoblastic Leukemia research
Share to DNA Repair Mechanisms
Share to Genetic factors in colorectal cancer

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 14679184
DOI: 10.1172/jci19757

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The adaptive imbalance in base excision–repair enzymes generates microsatellite instability in chronic inflammationPMID 14679184Read ↗

DNA repair is indispensable for survival after acute inflammation.Semantic proximity Read ↗

Oxidative stress in ulcerative colitis: an old concept but a new concernSemantic proximity Read ↗

The Pivotal Role of DNA Repair in Infection Mediated-Inflammation and CancerSemantic proximity Read ↗

DNA Repair Protein Expression and Oxidative/Nitrosative Stress in Ulcerative Colitis and Sporadic Colorectal CancerSemantic proximity Read ↗

Pathogenesis and biomarkers of carcinogenesis in ulcerative colitis.Semantic proximity Read ↗

Oxidative Stress and DNA DamageSemantic proximity Read ↗

DNA glycosylase NEIL2 prevents <i>Fusobacterium</i> -mediated inflammation and DNA damage in colonic epithelial cellsSemantic proximity Read ↗

Increased susceptibility of chronic ulcerative colitis-induced carcinoma development in DNA repair enzyme Ogg1 deficient mice.Semantic proximity Read ↗

The DNA Glycosylase NEIL2 Suppresses Fusobacterium-Infection-Induced Inflammation and DNA Damage in Colonic Epithelial CellsSemantic proximity Read ↗

DNA damage induced by chronic inflammation contributes to colon carcinogenesis in mice.Semantic proximity Read ↗

Tumbling down a different pathway to genetic instability.Semantic proximity Read ↗

Inflammation-mediated genomic instability: roles of activation-induced cytidine deaminase in carcinogenesis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.