Colonic Stent as Bridge to Surgery for Malignant Obstruction Induces Gene Expressional Changes Associated with a More Aggressive Tumor Phenotype.


Journal

Annals of surgical oncology
ISSN: 1534-4681
Titre abrégé: Ann Surg Oncol
Pays: United States
ID NLM: 9420840

Informations de publication

Date de publication:
Dec 2021
Historique:
received: 09 03 2021
accepted: 25 04 2021
pubmed: 2 9 2021
medline: 18 11 2021
entrez: 1 9 2021
Statut: ppublish

Résumé

Colonic stent is recommended as a bridge to elective surgery for malignant obstruction to improve short-term clinical outcomes for patients with colorectal cancer. However, since the oncological outcomes remain controversial, this study aimed to investigate the impact of self-expandable metallic stent (SEMS) on the tumor microenvironment. Patients treated with colonic stent as a bridge to surgery from 2010 to 2015 were identified from hospital records. Tumor biopsies and resected tumor samples of the eligible patients were retrieved retrospectively. Gene expression analysis was performed using the NanoString nCounter PanCancer IO 360 gene expression panel. Of the 164 patients identified, this study included 21 who underwent colonic stent placement as a bridge to elective surgery. Gene expression analysis revealed 82 differentially expressed genes between pre- and post-intervention specimens, of which 72 were upregulated and 10 downregulated. Among the significantly upregulated genes, 46 are known to have protumor functions, of which 26 are specifically known to induce tumorigenic mechanisms such as proliferation, migration, invasion, angiogenesis, and inflammation. In addition, ten differentially expressed genes were identified that are known to promote antitumor functions. SEMS induces gene expressional changes in the tumor microenvironment that are associated with tumor progression in colorectal cancer and may potentiate a more aggressive phenotype. Future studies are warranted to establish optimal timing of surgery after SEMS insertion in patients with obstructive colorectal cancer.

Sections du résumé

BACKGROUND BACKGROUND
Colonic stent is recommended as a bridge to elective surgery for malignant obstruction to improve short-term clinical outcomes for patients with colorectal cancer. However, since the oncological outcomes remain controversial, this study aimed to investigate the impact of self-expandable metallic stent (SEMS) on the tumor microenvironment.
METHODS METHODS
Patients treated with colonic stent as a bridge to surgery from 2010 to 2015 were identified from hospital records. Tumor biopsies and resected tumor samples of the eligible patients were retrieved retrospectively. Gene expression analysis was performed using the NanoString nCounter PanCancer IO 360 gene expression panel.
RESULTS RESULTS
Of the 164 patients identified, this study included 21 who underwent colonic stent placement as a bridge to elective surgery. Gene expression analysis revealed 82 differentially expressed genes between pre- and post-intervention specimens, of which 72 were upregulated and 10 downregulated. Among the significantly upregulated genes, 46 are known to have protumor functions, of which 26 are specifically known to induce tumorigenic mechanisms such as proliferation, migration, invasion, angiogenesis, and inflammation. In addition, ten differentially expressed genes were identified that are known to promote antitumor functions.
CONCLUSION CONCLUSIONS
SEMS induces gene expressional changes in the tumor microenvironment that are associated with tumor progression in colorectal cancer and may potentiate a more aggressive phenotype. Future studies are warranted to establish optimal timing of surgery after SEMS insertion in patients with obstructive colorectal cancer.

Identifiants

pubmed: 34467497
doi: 10.1245/s10434-021-10226-4
pii: 10.1245/s10434-021-10226-4
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

8519-8531

Informations de copyright

© 2021. Society of Surgical Oncology.

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Auteurs

Malene Broholm (M)

Center for Surgical Science, Department of Surgery, Zealand University Hospital, Køge, Denmark. malenebroholm87@gmail.com.
Department of Science and Environment, Roskilde University, Roskilde, Denmark. malenebroholm87@gmail.com.

Thea Helene Degett (TH)

Center for Surgical Science, Department of Surgery, Zealand University Hospital, Køge, Denmark.

Sara Furbo (S)

Center for Surgical Science, Department of Surgery, Zealand University Hospital, Køge, Denmark.

Anne-Marie Kanstrup Fiehn (AK)

Center for Surgical Science, Department of Surgery, Zealand University Hospital, Køge, Denmark.
Department of Pathology, Zealand University Hospital, Køge, Denmark.
Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.

Mustafa Bulut (M)

Center for Surgical Science, Department of Surgery, Zealand University Hospital, Køge, Denmark.
Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.

Thomas Litman (T)

Department of International Health, Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.

Jens Ole Eriksen (JO)

Department of Pathology, Zealand University Hospital, Køge, Denmark.

Jesper T Troelsen (JT)

Department of Science and Environment, Roskilde University, Roskilde, Denmark.

Lise Mette Rahbek Gjerdrum (LMR)

Department of Pathology, Zealand University Hospital, Køge, Denmark.
Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.

Ismail Gögenur (I)

Center for Surgical Science, Department of Surgery, Zealand University Hospital, Køge, Denmark.
Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.

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