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Thématique :
- Pancréas/Voies biliaires
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Originalité :
Très original
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| Doit faire évoluer notre pratique : |
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Dans certains cas
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Nom du veilleur :
Professeur Vinciane REBOURS
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Gut
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2018/09
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2018 Sep;67(9):1652-1662.
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doi: 10.1136/gutjnl-2017-315062.
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IPMNs with co-occurring invasive cancers: neighbours but not always relatives
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Felsenstein M, Noë M, Masica DL, Hosoda W, Chianchiano P, Fischer CG, Lionheart G, Brosens LAA, Pea A, Yu J, Gemenetzis G, Groot VP, Makary MA, He J, Weiss MJ, Cameron JL, Wolfgang CL, Hruban RH, Roberts NJ, Karchin R, Goggins MG, Wood LD
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https://www.ncbi.nlm.nih.gov/pubmed/29500184
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Abstract
OBJECTIVE:
Intraductal papillary mucinous neoplasms (IPMNs) are precursor lesions that can give rise to invasive pancreatic carcinoma. Although approximately 8% of patients with resected pancreatic ductal adenocarcinoma have a co-occurring IPMN, the precise genetic relationship between these two lesions has not been systematically investigated.
DESIGN:
We analysed all available patients with co-occurring IPMN and invasive intrapancreatic carcinoma over a 10-year period at a single institution. For each patient, we separately isolated DNA from the carcinoma, adjacent IPMN and distant IPMN and performed targeted next generation sequencing of a panel of pancreatic cancer driver genes. We then used the identified mutations to infer the relatedness of the IPMN and co-occurring invasive carcinoma in each patient.
RESULTS:
We analysed co-occurring IPMN and invasive carcinoma from 61 patients with IPMN/ductal adenocarcinoma as well as 13 patients with IPMN/colloid carcinoma and 7 patients with IPMN/carcinoma of the ampullary region. Of the patients with co-occurring IPMN and ductal adenocarcinoma, 51% were likely related. Surprisingly, 18% of co-occurring IPMN and ductal adenocarcinomas were likely independent, suggesting that the carcinoma arose from an independent precursor. By contrast, all colloid carcinomas were likely related to their associated IPMNs. In addition, these analyses showed striking genetic heterogeneity in IPMNs, even with respect to well-characterised driver genes.
CONCLUSION:
This study demonstrates a higher prevalence of likely independent co-occurring IPMN and ductal adenocarcinoma than previously appreciated. These findings have important implications for molecular risk stratification of patients with IPMN.
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Quelle est la signature génomique des TIPMP et des cancers du pancréas concomitants chez un même patient ?
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Un analyse génomique par séquençage des lésions d’adénocarcinome et de TIPMP à distance et à proximité chez un même patient. Dans 51% des cas, un lien existait entre les 2 lésions mais dans 18% les 2 lésions étaient complètement différentes.
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Au final les cancers du pancréas qui se développent à distance des lésions de TIPMP que nous surveillons (!), ont souvent des anomalies génétiques très différentes (et donc un précurseur différent !). Cela souligne que l’intérêt d’une politique de surveillance qui serait basée sur des recherches altérations génétiques sur du liquide de TIPMP ponctionné est très limité !
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