Evidence map›Paper›PMID 23665203›Full record

ArticleThe American journal of pathology2013

FAM190A deficiency creates a cell division defect.

Kalpesh Patel, Francesca Scrimieri, Soma Ghosh, Jun Zhong, Min-Sik Kim, Yunzhao R Ren, Richard A Morgan, Christine A Iacobuzio-Donahue, Akhilesh Pandey, Scott E Kern

Open access · hybridAbstract read
In one paragraph

Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.6field-weighted citation impact, top 32% of its field
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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  3. Identification ofFrontiers in veterinary science · 2026
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  6. Polymorphisms ofFoods (Basel, Switzerland) · 2023
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  9. Genetic Elements at the Alpha-Synuclein Locus.Frontiers in neuroscience · 2022
    Review
  10. Article
  11. Article
  12. The genetics of ductal adenocarcinoma of the pancreas in the year 2020: dramatic progress, but far to go.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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.

Kalpesh PatelDepartment of Oncology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA.
Francesca Scrimieri
Soma Ghosh
Jun Zhong
Min-Sik Kim
Yunzhao R Ren
Richard A Morgan
Christine A Iacobuzio-Donahue
Akhilesh Pandey
Scott E Kern
Johns Hopkins University · US

Funding

Tumor Antigens for Individual Signatures and TherapyP50CA062924 · NCI · JOHNS HOPKINS UNIVERSITY · PI LENNON, ANNE MARIE · 1993 to 2022
$54.6M
Zebrafish CoreP01CA134292 · NCI · JOHNS HOPKINS UNIVERSITY · PI LEACH, STEVEN D · 2009 to 2013
$7.4M
High-throughput analysis of pancreatic cancer mutationsR01CA128920 · NCI · JOHNS HOPKINS UNIVERSITY · PI KERN, SCOTT E · 2009 to 2012
$1.0M
NCI NIH HHS P01 CA134292NCI NIH HHS P50 CA062924NCI NIH HHS P50 CA62924NCI NIH HHS R01 CA128920
6 · The paper itself

Abstract

Like the p16, SMAD4, and RB1 genes, FAM190A (alias CCSER1) lies at a consensus site of homogeneous genomic deletions in human cancer. FAM190A transcripts in 40% of cancers also contain in-frame deletions of evolutionarily conserved exons. Its gene function was unknown. We found an internal deletion of the FAM190A gene in a pancreatic cancer having prominent focal multinuclearity. The experimental knockdown of FAM190A expression by shRNA caused focal cytokinesis defects, multipolar mitosis, and multinuclearity as observed in time-lapse microscopy. FAM190A was localized to the γ-tubulin ring complex of early mitosis and to the midbody in late cytokinesis by immunofluorescence assay and was present in the nuclear fraction of unsynchronized cells by immunoblot. FAM190A interacted with EXOC1 and Ndel1, which function in cytoskeletal organization and the cell division cycle. Levels of FAM190A protein peaked 12 hours after release from thymidine block, corresponding to M-phase. Slower-migrating phosphorylated forms accumulated toward M-phase and disappeared after release from a mitotic block and before cytokinesis. Studies of FAM190A alterations may provide mechanistic insights into mitotic dysregulation and multinuclearity in cancer. We propose that FAM190A is a regulator or structural component required for normal mitosis and that both the rare truncating mutations and common in-frame deletion alteration of FAM190A may contribute to the chromosomal instability of cancer.

Indexed as

Biomarkers, TumorCell Cycle ProteinsCell DivisionCell Line, TumorChromosomal InstabilityFlow CytometryFluorescent Antibody TechniqueHumansImmunoblottingMutationNeoplasmsBiomarkers, TumorCCSER1 protein, humanCell Cycle Proteins

Identifiers

PMID23665203
PMCPMC3702746
OpenAlexW1973225825

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.