Evidence map›Paper›PMID 17387143›Full record

ArticleGenome research2007

The modifier of Min 2 (Mom2) locus: embryonic lethality of a mutation in the Atp5a1 gene suggests a novel mechanism of polyp suppression.

Amy A Baran, Karen A Silverman, Joseph Zeskand, Revati Koratkar, Ashley Palmer, Kristen McCullen, Walter J Curran, Tina Bocker Edmonston, Linda D Siracusa, Arthur M Buchberg

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Dominant-Negative Form of SIGIRR: SIGIRRJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022
    Article
  3. Article
  4. Article
  5. Article
  6. Identification of ATP synthase α subunit as a new maternal factor capable of protecting zebrafish embryos from bacterial infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  7. The gut microbiota modulates differential adenoma suppression by B6/J and B6/N genetic backgrounds in ApcMammalian genome : official journal of the International Mammalian Genome Society · 2019
    Article
  8. Article
  9. Colitis-associated colon cancer: Is it in your genes?World journal of gastroenterology · 2015
    Review
  10. Genetic dissection of the Mom5 modifier locus and evaluation of Mom5 candidate genes.Mammalian genome : official journal of the International Mammalian Genome Society · 2015
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. More than two decades of Apc modeling in rodents.Biochimica et biophysica acta · 2013
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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

10 authors at 1 institution in 1 country.

Amy A BaranKimmel Cancer Center, Thomas Jefferson University, Jefferson Medical College, Philadelphia, Pennsylvania 19107, USA.
Karen A Silverman
Joseph Zeskand
Revati Koratkar
Ashley Palmer
Kristen McCullen
Walter J Curran
Tina Bocker Edmonston
Linda D Siracusa
Arthur M Buchberg
Thomas Jefferson University · US

Funding

TRAINING PROGRAMS IN MOLECULAR GENETICS OF CANCERT32CA009678 · NCI · THOMAS JEFFERSON UNIVERSITY · PI BUCHBERG, ARTHUR M. · 1992 to 2008
$2.3M
NCI NIH HHS T32 CA009678NCI NIH HHS T32-CA09678
6 · The paper itself

Abstract

Inactivation of the APC gene is considered the initiating event in human colorectal cancer. Modifier genes that influence the penetrance of mutations in tumor-suppressor genes hold great potential for preventing the development of cancer. The mechanism by which modifier genes alter adenoma incidence can be readily studied in mice that inherit mutations in the Apc gene. We identified a new modifier locus of ApcMin-induced intestinal tumorigenesis called Modifier of Min 2 (Mom2). The polyp-resistant Mom2R phenotype resulted from a spontaneous mutation and linkage analysis localized Mom2 to distal chromosome 18. To obtain recombinant chromosomes for use in refining the Mom2 interval, we generated congenic DBA.B6 ApcMin/+, Mom2R/+ mice. An intercross revealed that Mom2R encodes a recessive embryonic lethal mutation. We devised an exclusion strategy for mapping the Mom2 locus using embryonic lethality as a method of selection. Expression and sequence analyses of candidate genes identified a duplication of four nucleotides within exon 3 of the alpha subunit of the ATP synthase (Atp5a1) gene. Tumor analyses revealed a novel mechanism of polyp suppression by Mom2R in Min mice. Furthermore, we show that more adenomas progress to carcinomas in Min mice that carry the Mom2R mutation. The absence of loss of heterozygosity (LOH) at the Apc locus, combined with the tendency of adenomas to progress to carcinomas, indicates that the sequence of events leading to tumors in ApcMin/+ Mom2R/+ mice is consistent with the features of human tumor initiation and progression.

Indexed as

MutationAnimalsChromosome MappingFetal DeathGenetic LinkageIntestinal PolyposisMaleMiceMice, Inbred C57BLMice, Inbred DBAMitochondrial Proton-Translocating ATPasesPhenotypePolypsTumor Suppressor ProteinsMitochondrial Proton-Translocating ATPasesTumor Suppressor Proteins

Identifiers

PMID17387143
PMCPMC1855180
OpenAlexW2167708547

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.