Evidence map›Paper›PMID 15693618›Full record

ArticleJournal of molecular evolution2004

Evolution of the exon-intron structure and alternative splicing of the MAGE-A family of cancer/testis antigens.

Irena I Artamonova, Mikhail S Gelfand

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Article in Journal of molecular evolution, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed.

  1. Cancer regression and neurological toxicity following anti-MAGE-A3 TCR gene therapy.Journal of immunotherapy (Hagerstown, Md. : 1997) · 2013
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Irena I ArtamonovaShemyakin-Ovchinnikov Institute of Bioorganic Chemistry RAS, Miklukho-Maklaya 16/10, Moscow 117997, Russia.
Mikhail S Gelfand

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer/testis antigens (CT-antigens) are proteins that are predominantly expressed in cancer and testis and thus are possible targets for immunotherapy. Most of them form large multigene families. The evolution of the MAGE-A family of CT-antigens is characterized by four processes: (1) gene duplications; (2) duplications of the initial exon; (3) point mutations and short insertions/deletions inactivating splicing sites or creating new sites; and (4) deletions removing sites and creating chimeric exons. All this concerns the genomic regions upstream of the coding region, creating a wide diversity of isoforms with different 5'-untranslated regions. Many of these isoforms are gene-specific and have emerged due to point mutations in alternative and constitutive splicing sites. There are also examples of chimeric mRNAs, likely produced by splicing of read-through transcripts. Since there is consistent use of homologous sites for different genes and no random, indiscriminant use of preexisting cryptic sites, it is likely that most observed isoforms are functional, and do not result from relaxed control in transformed cells.

Indexed as

Evolution, MolecularAlternative SplicingAnimalsAntigensAntigens, NeoplasmBase SequenceBiomarkers, TumorExonsGenome, HumanHumansInternetIntronsMaleMelanoma-Specific AntigensMiceMolecular Sequence DataAntigensAntigens, NeoplasmBiomarkers, TumorMAGEA1 protein, humanMelanoma-Specific AntigensNeoplasm ProteinsProtein IsoformsRecombinant Fusion Proteins

Identifiers

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

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.