A dualistic model of primary anal canal adenocarcinoma with distinct cellular origins, etiologies, inflammatory microenvironments and mutational signatures: implications for personalised medicine-Reference-Cited by-同舟云学术

A dualistic model of primary anal canal adenocarcinoma with distinct cellular origins, etiologies, inflammatory microenvironments and mutational signatures: implications for personalised medicine

Published:2018-04-27 Issue:10 Volume:118 Page:1302-1312
ISSN:0007-0920
Container-title:British Journal of Cancer
language:en
Short-container-title:Br J Cancer

Author:

Herfs Michael,Roncarati Patrick,Koopmansch Benjamin,Peulen Olivier,Bruyere Diane,Lebeau Alizee,Hendrick Elodie,Hubert Pascale,Poncin Aurelie,Penny William,Piazzon Nathalie,Monnien Franck,Guenat David,Mougin Christiane,Prétet Jean-Luc,Vuitton Lucine,Segers Karin,Lambert Frederic,Bours Vincent,de Leval Laurence,Valmary-Degano Severine,Quick Charles M,Crum Christopher P,Delvenne Philippe

Publisher

Springer Science and Business Media LLC

Subject

Cancer Research,Oncology

Link

http://www.nature.com/articles/s41416-018-0049-2.pdf

Reference49 articles.

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2. Herfs, M. et al. Proteomic signatures reveal a dualistic and clinically relevant classification of anal canal carcinoma. J. Pathol. 241, 522–533 (2017).

3. Yang, E. J. et al. Microanatomy of the cervical and anorectal squamocolumnar junctions: a proposed model for anatomical differences in HPV-related cancer risk. Mod. Pathol.: Off. J. US Can. Acad. Pathol. Inc. 28, 994–1000 (2015).

4. Valmary-Degano, S. et al. Signature patterns of human papillomavirus type 16 in invasive anal carcinoma. Hum. Pathol. 44, 992–1002 (2013).

5. Meulendijks, D. et al. HPV-negative squamous cell carcinoma of the anal canal is unresponsive to standard treatment and frequently carries disruptive mutations in TP53. Br. J. Cancer 112, 1358–1366 (2015).

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