Evidence map›Paper›PMID 26563151›Full record

ArticleClinical & experimental metastasis2016

Genomic gain of the PRL-3 gene may represent poor prognosis of primary colorectal cancer, and associate with liver metastasis.

N Nakayama, K Yamashita, T Tanaka, H Kawamata, A Ooki, T Sato, T Nakamura, M Watanabe

Abstract read
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In one paragraph

Article in Clinical & experimental metastasis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 37% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Observational
  6. 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

8 authors at 1 institution in 1 country.

N NakayamaDepartment of Surgery, Kitasato University School of Medicine, Asamizodai 2-1-1, Minami-ku, Sagamihara, Kanagawa, 252-0380, Japan.
K YamashitaDepartment of Surgery, Kitasato University School of Medicine, Asamizodai 2-1-1, Minami-ku, Sagamihara, Kanagawa, 252-0380, Japan. keishi23@med.kitasato-u.ac.jp.
T TanakaDepartment of Surgery, Kitasato University School of Medicine, Asamizodai 2-1-1, Minami-ku, Sagamihara, Kanagawa, 252-0380, Japan.
H KawamataDepartment of Surgery, Kitasato University School of Medicine, Asamizodai 2-1-1, Minami-ku, Sagamihara, Kanagawa, 252-0380, Japan.
A OokiDepartment of Surgery, Kitasato University School of Medicine, Asamizodai 2-1-1, Minami-ku, Sagamihara, Kanagawa, 252-0380, Japan.
T SatoDepartment of Surgery, Kitasato University School of Medicine, Asamizodai 2-1-1, Minami-ku, Sagamihara, Kanagawa, 252-0380, Japan.
T NakamuraDepartment of Surgery, Kitasato University School of Medicine, Asamizodai 2-1-1, Minami-ku, Sagamihara, Kanagawa, 252-0380, Japan.
M WatanabeDepartment of Surgery, Kitasato University School of Medicine, Asamizodai 2-1-1, Minami-ku, Sagamihara, Kanagawa, 252-0380, Japan.
Kitasato University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PRL-3 genomic copy number is increased in colorectal cancer (CRC), and PRL-3 expression is closely associated with lymph node and liver metastasis of CRC. However, the clinical significance of PRL-3 genomic gain for CRC remains obscure. Here, PRL-3 genomic status in 109 primary CRC tumors and in 44 CRC tumors that had metastasized to the liver, was quantified using real time PCR. Association of PRL-3 genomic status with clinicopathological factors and prognosis was assessed in detail. PRL-3 genomic gain was identified in 31 primary CRC (27.4 %) and was more frequently seen in stage III than in stage II (p = 0.025). Among the clinicopathological factors assessed, PRL-3 genomic gain was significantly associated with poorly differentiated histology (p = 0.0039). Moreover, CRC patients with PRL-3 genomic gain exhibited poorer prognosis than those with no gain in stage II-IV CRC (p = 0.017). PRL-3 genomic gain was identified in 18 (41 %) of the liver metastasis tumors, and this frequency of gain was significantly increased as compared to that of the corresponding primary CRCs (11 %) (p = 0.001). Our findings suggested that PRL-3 genomic gain may represent an aggressive phenotype of primary CRC, and may associate with liver metastasis.

Indexed as

Colorectal NeoplasmsFemaleGene DosageHumansImmunohistochemistryKaplan-Meier EstimateLiver NeoplasmsMaleNeoplasm ProteinsPrognosisProportional Hazards ModelsProtein Tyrosine PhosphatasesReal-Time Polymerase Chain ReactionNeoplasm ProteinsProtein Tyrosine PhosphatasesPTP4A3 protein, humanColorectal cancerGenomic gainLiver metastasisPRL-3Prognosis

Identifiers

PMID26563151
OpenAlexW2178132182

What OpenQuestion holds

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Registered trials

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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.