ArticleCancer science2017
Esophageal adenocarcinoma microenvironment: Peritumoral adipose tissue effects associated with chemoresistance.
Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 17 citations in OpenAlex.
- Intratumoral and peritumoral radiomics for preoperative prediction of pathological complete response to neoadjuvant immunochemotherapy in patients with esophageal squamous cell carcinoma.European journal of radiology open · 2026Article
- Intratumoral and peritumoral CT radiomics combined with clinical and hematologic inflammatory markers for predicting lymph node metastasis in esophageal squamous cell carcinoma: a retrospective single-center study.La Radiologia medica · 2026Article
- AKR1C3 enhances radioresistance in esophageal adenocarcinoma via inhibiting ferroptosis through suppressing TRIM21-mediated ubiquitination of HSPA5.Cell death & disease · 2025Article
- Bone health and body composition in prostate cancer: Meet-URO and AIOM consensus about prevention and management strategies.ESMO open · 2024Article
- Mitochondrial CaScientific reports · 2024Article
- Article
- Obesity, the Adipose Organ and Cancer in Humans: Association or Causation?Biomedicines · 2023Review
- Pathological Responses of the Primary Tumor and Locoregional Lymph Nodes After Neoadjuvant Immunochemotherapy in Esophageal Squamous Cell Cancer.World journal of oncology · 2022Article
- Comparative genomic analysis of esophageal squamous cell carcinoma and adenocarcinoma: New opportunities towards molecularly targeted therapy.Acta pharmaceutica Sinica. B · 2022Review
- Adipogenic progenitors in different organs: Pathophysiological implications.Reviews in endocrine & metabolic disorders · 2022Review
- Prognostic value of stem cell markers in esophageal and esophagogastric junction cancer: a meta-analysis.Journal of Cancer · 2020Article
- Squamous cell carcinoma antigen 1 is associated to poor prognosis in esophageal cancer through immune surveillance impairment and reduced chemosensitivity.Cancer science · 2019Article
- Esophageal adenocarcinoma microenvironment: Peritumoral adipose tissue effects associated with chemoresistance.Cancer science · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peritumoral microenvironment affects cancer development and chemoresistance, and visceral adipose tissue may play a critical role. We aimed to identify depot-specific adipose characteristics associated with carcinogenesis and resistance to neoadjuvant therapy in esophageal adenocarcinoma (EAC). We analyzed: (i) the peritumoral adipose tissue of rats following the induction of esophageal carcinogenesis; (ii) the peritumoral and distal (omental) adipose tissue of patients affected by EAC; (iii) adipose-derived stem cells (ADSC) isolated from healthy patients and treated with conditioned medium (CM), collected from tumoral and adipose tissue of patients with EAC. In peritumoral adipose tissue of rats, CD34, CD31 and vascular endothelial growth factor (VEGF) expression increased progressively during EAC development. In patients with EAC, expression of CD34, CD45, CD90 and nucleostemin (NSTM) was higher in peritumoral than in distal adipose tissue and decreased in the presence of neoadjuvant therapy. Moreover, expression of NSTM, octamer-binding transcription factor 4 (OCT-4) and VEGF was higher in peritumoral (but not in distal) adipose tissue of chemoresistant patients. In ADSC, treatment with peritumoral adipose tissue CM increased the adipogenic potential and the expression of CD34, CD90, NSTM and OCT-4. These effects were similar to those induced by cancer-derived CM, but were not observed in ADSC treated with distal adipose tissue CM and were partially reduced by a leptin antagonist. Last, ADSC treated with peritumoral CM of chemoresistant patients displayed increased expression of NSTM, OCT-4, leptin, leptin receptor, alpha-smooth muscle actin (α-SMA), CD34 and VEGF. These results suggest that peritumoral adipose tissue may promote, by paracrine signaling, the expression of depot-specific factors associated with therapeutic resistance.
Indexed as
Identifiers
What 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.