ArticleGene expression1999
Changes in levels of normal ML-1 gene transcripts associated with the conversion of human nontumorigenic to tumorigenic phenotypes.
Article in Gene expression, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 9 citations in OpenAlex.
- Consensus, controversies, and conundrums of P4-ATPases: The emerging face of eukaryotic lipid flippases.The Journal of biological chemistry · 2024Review
- Disruption of the ATP8A2 gene in a patient with a t(10;13) de novo balanced translocation and a severe neurological phenotype.European journal of human genetics : EJHG · 2010Article
- Metastatic conversion of chemically transformed human cells.Gene expression · 1999Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Evaluation of malignant human tumors in a xenobiotic nude mouse system has demonstrated that not all cells in tumors exhibit the capacity to form progressively growing tumors. However, nontumorigenic cells isolated from human tumors can be converted to a tumorigenic phenotype in nude mice by treatment with chemical carcinogens or by transfection with antisense to tumor suppressor genes. A newly discovered gene, designated ML-1, appears to be associated with tumorigenesis, because an ML-1 antisense cDNA construct, transfected into nontumorigenic, anchorage-independent growth (AIG) cells, was sufficient to convert these cells into a tumorigenic phenotype. The AIG cells transfected with ML-1 antisense cDNA constructs and converted to tumorigenic cells did not exhibit expression of normal ML-1 mRNA transcripts in the converted cells when evaluated by Northern analysis, whereas premalignant and normal cells expressed ML-1 transcripts at a high level. The converted cells exhibited a loss of growth control and produced tumors in a surrogate nude mouse that were greater than 2.0 cm in less than 2 months. The ML-1 gene has a DNA sequence that is 2177 bp in size and is located on chromosome number 13 on the q arm at site 12-14. Sequence analysis and investigation of GenBank sequences indicate that this is a newly described human gene.
Indexed as
Identifiers
10551800PMC6157390W126348691What 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.