Evidence map›Paper›PMID 8385096›Full record

ArticleIn vitro cellular & developmental biology : journal of the Tissue Culture Association1993

Characterization of the DiFi rectal carcinoma cell line derived from a familial adenomatous polyposis patient.

M Olive, S Untawale, R J Coffey, M J Siciliano, D M Wildrick, H Fritsche, S Pathak, L M Cherry, M Blick, P Lointier

Abstract read
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In one paragraph

Article in In vitro cellular & developmental biology : journal of the Tissue Culture Association, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 46 citations in OpenAlex.

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  9. Antibody targeting of claudin-1 as a potential colorectal cancer therapy.Journal of experimental & clinical cancer research : CR · 2017
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  16. Molecular imaging of therapeutic response to epidermal growth factor receptor blockade in colorectal cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2008
    Article
  17. Digital karyotyping.Proceedings of the National Academy of Sciences of the United States of America · 2002
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  18. Article
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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

10 authors at 3 institutions in 1 country.

M OliveUniversity of Texas M. D. Anderson Cancer Center, Section of Gastrointestinal Oncology and Digestive Diseases, Houston 77030.
S Untawale
R J Coffey
M J Siciliano
D M Wildrick
H Fritsche
S Pathak
L M Cherry
M Blick
P Lointier
The University of Texas MD Anderson Cancer Center · USBaylor Genetics · USVanderbilt University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The DiFi human colorectal cancer cell line was recently established from a familial adenomatous polyposis patient with extracolonic features characteristic of the Gardner syndrome. These cells have now been propagated for 150 passages in standard culture media and vessels without feeder layers or collagen coatings. They retain features of colonic epithelial cells such as surface microvilli, secretory vesicles, and desmosomes. Cytosol of DiFi cells contains a high level (502 U/mg protein) of the mucin CA 19-9. In addition, DiFi cells produce carcinoembryonic antigen, and induce tumors in athymic mice. Cytoskeleton analysis of DiFi cells by fluorescence microscopy showed a pronounced disorganization of actin cable structure. The isozyme genetic signature of DiFi cells is unique (0.01 probability of finding the same genetic signature in a different cell line), differs from that of HeLa cells, and has expressional features seen in other colorectal cell lines. The DiFi cell karyotype is tetraploid, contains many marker chromosomes, and shows numerous episomal particles. Two copies of chromosome 18 were absent, and only a single normal chromosome 17 was found. This parallels detection of allelic losses from DiFi cell DNA at loci on chromosomes 17p and 18 using molecular (cDNA) probes. DiFi cells clearly express transcripts for the c-myc proto-oncogene, the c-myb proto-oncogene, and the p53 tumor suppressor gene. Transforming growth factor beta inhibits DiFi cell growth in soft agar and suppresses c-myc expression in these cells. The value of this cell line in the study of genetic alterations in colorectal cancer is discussed.

Indexed as

ActinsAdenocarcinoma, MucinousAnimalsAntigens, Tumor-Associated, CarbohydrateCell CycleCell LineCytoplasmic GranulesDesmosomesFemaleGene Expression Regulation, NeoplasticGenotypeHumansKaryotypingMiceMice, NudeMicroscopy, FluorescenceActinsAntigens, Tumor-Associated, CarbohydrateMAS1 protein, humanProto-Oncogene MasProto-Oncogene Proteins c-mycTransforming Growth Factor beta

Identifiers

PMID8385096
OpenAlexW2046445045

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.