Microscopic distance from tumor invasion front to serosa might be a useful predictive factor for peritoneal recurrence after curative resection of T3-gastric cancer.
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2020
2020
Historique:
received:
20
08
2019
accepted:
15
11
2019
entrez:
16
1
2020
pubmed:
16
1
2020
medline:
9
4
2020
Statut:
epublish
Résumé
Peritoneal recurrence is one of the most frequent recurrent diseases in gastric cancer. Although the exposure of cancer cells to the serosal surface is considered a common risk factor for peritoneal recurrence, there are some cases of peritoneal recurrence without infiltration to the serosal surface even after curative surgery. This study sought to clarify the risk factors of peritoneal recurrence in the absence of invasion to the serosal surface. Ninety-six patients with gastric cancer who underwent curative surgery were enrolled. In all 96 cases, the depth of tumor invasion was subserosal (T3). The microscopic distance from the tumor invasion front to the serosa (DIFS) was measured using tissue slides by H&E staining and pan-cytokeratin staining. E-cadherin expression was evaluated by immunohistochemical staining. Among the 96 patients, 16 developed peritoneal recurrence after curative surgery. The DIFS of the tumors with peritoneal recurrence (156±220 μm) was significantly shorter (p = 0.011) than that without peritoneal recurrence (360±478 μm). Peritoneal recurrence was significantly correlated with DIFS ≤234 μm (p = 0.023), but not with E-cadherin expression. The prognosis of DIFS ≤234 μm was significantly poorer than that of DIFS >234 μm (log rank, p = 0.007). A multivariate analysis of the patients' five-year overall survival revealed that DIFS ≤234 μm and lymph node metastasis were significantly correlated with survival (p = 0.005, p = 0.032, respectively). The measurement of the DIFS might be useful for the prediction of peritoneal recurrence in T3-gastric cancer patients after curative surgery.
Sections du résumé
BACKGROUND
Peritoneal recurrence is one of the most frequent recurrent diseases in gastric cancer. Although the exposure of cancer cells to the serosal surface is considered a common risk factor for peritoneal recurrence, there are some cases of peritoneal recurrence without infiltration to the serosal surface even after curative surgery. This study sought to clarify the risk factors of peritoneal recurrence in the absence of invasion to the serosal surface.
MATERIALS AND METHODS
Ninety-six patients with gastric cancer who underwent curative surgery were enrolled. In all 96 cases, the depth of tumor invasion was subserosal (T3). The microscopic distance from the tumor invasion front to the serosa (DIFS) was measured using tissue slides by H&E staining and pan-cytokeratin staining. E-cadherin expression was evaluated by immunohistochemical staining.
RESULTS
Among the 96 patients, 16 developed peritoneal recurrence after curative surgery. The DIFS of the tumors with peritoneal recurrence (156±220 μm) was significantly shorter (p = 0.011) than that without peritoneal recurrence (360±478 μm). Peritoneal recurrence was significantly correlated with DIFS ≤234 μm (p = 0.023), but not with E-cadherin expression. The prognosis of DIFS ≤234 μm was significantly poorer than that of DIFS >234 μm (log rank, p = 0.007). A multivariate analysis of the patients' five-year overall survival revealed that DIFS ≤234 μm and lymph node metastasis were significantly correlated with survival (p = 0.005, p = 0.032, respectively).
CONCLUSION
The measurement of the DIFS might be useful for the prediction of peritoneal recurrence in T3-gastric cancer patients after curative surgery.
Identifiants
pubmed: 31940352
doi: 10.1371/journal.pone.0225958
pii: PONE-D-19-23016
pmc: PMC6961828
doi:
Substances chimiques
Cadherins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0225958Commentaires et corrections
Type : ErratumIn
Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
Références
JAMA Oncol. 2015 Jul;1(4):505-27
pubmed: 26181261
N Engl J Med. 2007 Nov 1;357(18):1810-20
pubmed: 17978289
Surg Oncol. 2017 Dec;26(4):352-358
pubmed: 29113652
J Surg Oncol. 2012 Sep 1;106(3):304-10
pubmed: 22231933
Cancer Microenviron. 2010 Jan 26;3(1):127-35
pubmed: 21209779
Am J Surg. 1999 Sep;178(3):256-62
pubmed: 10527450
Br J Cancer. 1995 Nov;72(5):1200-10
pubmed: 7577468
Oncol Lett. 2017 Dec;14(6):6991-6998
pubmed: 29344127
Br J Surg. 2000 Mar;87(3):353-7
pubmed: 10718807
Gastric Cancer. 2018 Jan;21(1):144-154
pubmed: 28417260
Gan To Kagaku Ryoho. 1995 Apr;22(5):703-8
pubmed: 7717727
Surg Today. 2006;36(9):835-8
pubmed: 16937291
Br J Cancer. 1996 Nov;74(9):1406-12
pubmed: 8912536
Int J Hematol Oncol Stem Cell Res. 2017 Apr 1;11(2):158-164
pubmed: 28875011
Gastric Cancer. 2011 Jun;14(2):101-12
pubmed: 21573743
Oncol Lett. 2015 Sep;10(3):1527-1532
pubmed: 26622703
Virchows Arch. 2016 Aug;469(2):155-61
pubmed: 27220762
Oncotarget. 2016 Dec 20;7(51):85502-85514
pubmed: 27907907
J Clin Oncol. 2011 Nov 20;29(33):4387-93
pubmed: 22010012
J Surg Oncol. 2000 Nov;75(3):165-71
pubmed: 11088047
Lancet. 2012 Jan 28;379(9813):315-21
pubmed: 22226517
Lancet Oncol. 2014 Nov;15(12):1389-96
pubmed: 25439693
Oncol Rep. 1997 Jul-Aug;4(4):743-8
pubmed: 21590132