Evidence map›Paper›PMID 22321641›Full record

ReviewFEBS letters2012

Two sides of the story? Smad4 loss in pancreatic cancer versus head-and-neck cancer.

Stephen P Malkoski, Xiao-Jing Wang

Abstract readReview
In one paragraph

Review in FEBS letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing 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

40 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. HPV-mediated regulation of SMAD4 modulates the DNA damage response in head and neck cancer.Journal of experimental & clinical cancer research : CR · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Whole-exome sequencing of cervical carcinomas identifies activating ERBB2 and PIK3CA mutations as targets for combination therapy.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  15. Review
  16. Article
  17. Smad7 Promotes Healing of Radiotherapy-Induced Oral Mucositis without Compromising Oral Cancer Therapy in a Xenograft Mouse Model.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  18. Review
  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

2 authors at 1 institution in 1 country.

Stephen P MalkoskiDivision of Pulmonary Sciences and Critical Care Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, United States.
Xiao-Jing Wang
University of Colorado Anschutz Medical Campus · US

Funding

Tissue Bank and Biomarkers CoreP50CA058187 · NCI · UNIVERSITY OF COLORADO DENVER · PI MILLER, YORK E · 1992 to 2018
$43.8M
Role of TGFbeta signaling in HNSCC progressionR01DE015953 · NIDCR · UNIVERSITY OF COLORADO DENVER · PI WANG, XIAO-JING · 2004 to 2014
$3.6M
ROLE OF SMADS IN THE EPIDERMIS AND SKIN CARCINOGENESISR01CA087849 · NCI · UNIVERSITY OF COLORADO DENVER · PI WANG, XIAO-JING · 2000 to 2011
$2.7M
TGF BETA SIGNALING AND SKIN CARCINOGENESISR01CA079998 · NCI · UNIVERSITY OF COLORADO DENVER · PI WANG, XIAO-JING · 1999 to 2009
$2.1M
Effects of Altering TGF Beta Signaling on Wound HealingR01AR061792 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI WANG, XIAO-JING · 2011 to 2015
$1.9M
Identification of normal and cancer stem cells and their niche in oral mucosaRC1DE020649 · NIDCR · UNIVERSITY OF COLORADO DENVER · PI WANG, XIAO-JING · 2009 to 2010
$869k
TGFbeta and lung squamous cell carcinomaK08CA131483 · NCI · UNIVERSITY OF COLORADO DENVER · PI MALKOSKI, STEPHEN P · 2008 to 2012
$685k
NCI NIH HHS CA131483NCI NIH HHS CA79998NCI NIH HHS CA87849NCI NIH HHS K08 CA131483NCI NIH HHS P50 CA058187NCI NIH HHS R01 CA079998NCI NIH HHS R01 CA087849NIAMS NIH HHS R01 AR061792NIDCR NIH HHS DE15953NIDCR NIH HHS DE20649NIDCR NIH HHS R01 DE015953NIDCR NIH HHS RC1 DE020649
6 · The paper itself

Abstract

TGFβ signaling Smads (Smad2, 3, and 4) were suspected tumor suppressors soon after their discovery. Nearly two decades of research confirmed this role and revealed other divergent and cancer-specific functions including paradoxical tumor promotion effects. Although Smad4 is the most potent tumor suppressor, its functions are highly context-specific as exemplified by pancreatic cancer and head-and-neck cancer: in pancreatic cancer, Smad4 loss cannot initiate tumor formation but promotes metastases while in head-and-neck cancer Smad4 loss promotes cancer progression but also initiates tumor formation, likely through effects on genomic instability. The differing consequences of impaired Smad signaling in human cancers and the molecular mechanisms that underpin these differences will have important implications for the design and application of novel targeted therapies.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCarcinoma, Squamous CellCholangiocarcinomaColonic NeoplasmsDisease ProgressionFanconi AnemiaFemaleHead and Neck NeoplasmsHumansIntestinal PolyposisMaleMiceModels, BiologicalNeoplastic Syndromes, HereditaryPancreatic NeoplasmsSmad4 ProteinSMAD4 protein, humanTransforming Growth Factor beta

Identifiers

PMID22321641
PMCPMC3285395
OpenAlexW2114008428

What OpenQuestion holds

Textmetadata
LicenceTDM
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.