ReviewDer Pathologe2012
[Molecular pathology of gastric cancer].
Review in Der Pathologe, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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.
Who cites it
7 citing papers in PubMed.
- MDM2 amplification is rare in gastric cancer.Virchows Archiv : an international journal of pathology · 2023Article
- Hypericin Induces Apoptosis in AGS Cell Line with No Significant Effect on Normal Cells.Iranian journal of pharmaceutical research : IJPR · 2020Article
- Knockdown of long noncoding RNA GHET1 inhibits cell‑cycle progression and invasion of gastric cancer cells.Molecular medicine reports · 2018Article
- Binding of the Helicobacter pylori OipA causes apoptosis of host cells via modulation of Bax/Bcl-2 levels.Scientific reports · 2017Article
- Enhanced expression of long non-coding RNA NEAT1 is associated with the progression of gastric adenocarcinomas.World journal of surgical oncology · 2016Article
- Hematopoietic pre-B cell leukemia transcription factor interacting protein is overexpressed in gastric cancer and promotes gastric cancer cell proliferation, migration, and invasion.Cancer science · 2015Article
- Knockdown of Rab9 Suppresses the Progression of Gastric Cancer Through Regulation of Akt Signaling Pathway.Technology in cancer research & treatmentArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer is one of the most common cancers worldwide. In recent decades, major advancements in the understanding of the epidemiology, pathology and pathogenesis of gastric cancer have been witnessed. Infections with Helicobacter pylori or Epstein-Barr virus, dietary and lifestyle factors contribute to the risk of developing gastric cancer. With respect to pathogenesis at least three distinct types of gastric cancer exist, (1) proximal, (2) distal diffuse and (3) distal non-diffuse types. Genetic and epigenetic alterations are related to oncogene mutations and tumor suppressor gene inactivation. Canonical oncogenic pathways such as the WNT/β-catenin signaling pathway are de-regulated in gastric cancer. Hereditary and familial type gastric cancers are currently linked to CDH1 gene mutations and various genetic polymorphisms determining disease susceptibility. Molecular subtypes of gastric cancer have been identified which separate diffuse from intestinal type gastric cancer and are not entirely congruent with the histopathological phenotype according to Laurén but may influence chemosensitivity. Putative cancer stem cell markers of gastric cancer have been found (e.g. ADAM17, CD133, FZD7, LGR5) and correlate with patient prognosis. Thus, molecular phenotyping of gastric cancer is still in its infancy and the search for novel diagnostic, prognostic and predictive biomarkers continues.
Indexed as
Identifiers
22983100What OpenQuestion holds
Registered trials
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.