Evidence map›Paper›PMID 30730996›Full record

ArticlePloS one2019

Clinicopathological characterization of SMAD4-mutated intestinal adenocarcinomas: A case-control study.

Xiaoyan Liao, Yansheng Hao, Xiaofei Zhang, Stephen Ward, Jane Houldsworth, Alexandros D Polydorides, Noam Harpaz

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 2 pooled it
2.2field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. SMAD4 mutation correlates with poor prognosis in non-small cell lung cancer.Laboratory investigation; a journal of technical methods and pathology · 2021
    Article
  9. Article
  10. SMAD4 mutations identified in Iranian patients with colorectal cancer and polyp.Gastroenterology and hepatology from bed to bench · 2021
    Article
  11. Driver mutations of the adenoma-carcinoma sequence govern the intestinal epithelial global translational capacity.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Frontiers in oncology · 2019
    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

7 authors at 1 institution in 1 country.

Xiaoyan LiaoDepartment of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Yansheng HaoDepartment of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Xiaofei ZhangDepartment of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Stephen WardDepartment of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Jane HouldsworthDepartment of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Alexandros D PolydoridesDepartment of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Noam HarpazDepartment of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Icahn School of Medicine at Mount Sinai · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The SMAD4 tumor suppressor gene product inhibits transforming growth factor-β-mediated signaling and is mutated in ~10% of colorectal carcinomas. The prognostic significance of SMAD4 mutations has been controversial. We studied the pathological and clinical characteristics of SMAD4-mutated intestinal adenocarcinomas using a retrospective case-control study design. Cases and controls were identified among 443 primary adenocarcinomas that had undergone next generation DNA sequencing (NGS) with the Ion AmpliSeq Cancer Hotspot Panel v2, which evaluates 50 cancer-related genes. Twenty-eight SMAD4-mutated (SMAD4m) patients were matched 1:2 with 56 consecutive SMAD4 wild-type (SMAD4wt) control patients from the same analysis stream. Compared with the SMAD4wt controls, the SMAD4m tumors were of higher stage (P = 0.026) and were more likely to feature mucinous differentiation (P = 0.0000), to occur in the setting of Crohn's disease (P = 0.0041), and to harbor concurrent RAS mutations (P = 0.0178). Tumor mucin content was significantly correlated with mutations involving the MH2 domain of the SMAD4 protein (P = 0.0338). Correspondence between mutation sites and morphology was demonstrated directly in a mixed adenocarcinoma and neuroendocrine tumor where SMAD4 mutations involving different protein domains were found in histologically disparate tumor regions despite both containing identical KRAS and TP53 mutations.

Indexed as

AdenocarcinomaCarcinoma, NeuroendocrineIntestinal NeoplasmsMutationAdultAgedAged, 80 and overCase-Control StudiesDNA Mutational AnalysisFemaleHigh-Throughput Nucleotide SequencingHumansMaleMiddle AgedProto-Oncogene Proteins p21(ras)Smad4 ProteinKRAS protein, humanProto-Oncogene Proteins p21(ras)Smad4 ProteinSMAD4 protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID30730996
PMCPMC6366887
OpenAlexW2912839464

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.