ArticleOncogene2008
Atm is a negative regulator of intestinal neoplasia.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- The path to metastatic mouse models of colorectal cancer.Oncogene · 2018Review
- The importance of p53 pathway genetics in inherited and somatic cancer genomes.Nature reviews. Cancer · 2016Review
- Loss of ATM accelerates pancreatic cancer formation and epithelial-mesenchymal transition.Nature communications · 2015Article
- ATM signalling and cancer.Oncogene · 2014Review
- Tug of war between survival and death: exploring ATM function in cancer.International journal of molecular sciences · 2014Review
- Functional variations in the ATM gene and susceptibility to differentiated thyroid carcinoma.The Journal of clinical endocrinology and metabolism · 2012Article
- A bioinformatical and functional approach to identify novel strategies for chemoprevention of colorectal cancer.Oncogene · 2011Article
- Limited role of murine ATM in oncogene-induced senescence and p53-dependent tumor suppression.PloS one · 2009Article
- Widespread hyperplasia induced by transgenic TGFalpha in ApcMin mice is associated with only regional effects on tumorigenesis.Carcinogenesis · 2008Article
- Tumor suppression by p53 in the absence of Atm.Molecular cancer research : MCR · 2008Article
- The pro-apoptotic K-Ras 4A proto-oncoprotein does not affect tumorigenesis in the ApcMin/+ mouse small intestine.BMC gastroenterology · 2008Article
- Trial Watch: Targeting ATM-CHK2 and ATR-CHK1 pathways for anticancer therapy.Molecular & cellular oncologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The ataxia telangiectasia-mutated (ATM) gene has been implicated as an early barrier to the growth and progression of incipient solid tumors. Here, we show that germ-line nullizygosity for the mouse Atm gene significantly increases the proliferative index, net growth rate and multiplicity of intestinal adenomas in two distinct models of familial colon cancer: Apc(Min/+) and Apc(1638N/+). These effects of Atm deficiency are quantitatively different from deficiency for either of the genomic stability genes Bloom's syndrome helicase or DNA ligase 4, and the effect of Atm loss on tumor multiplicity is largely independent of the effect of ionizing radiation. Furthermore, the loss of heterozygosity rates at the adenomatous polyposis coli (Apc) locus are unaffected by Atm loss. Taken together, these data implicate the Atm gene product as a barrier to dysplastic growth in the early stages of intestinal tumor progression, independent of its effects on genomic stability.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.