Oncogenic mutations drive intestinal cancer initiation through paracrine remodeling

Cancer Cell ◽  
2021 ◽  
Vol 39 (7) ◽  
pp. 913-915
Author(s):  
Helen H.N. Yan ◽  
April S. Chan ◽  
Suet Yi Leung
Cancers ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2168
Author(s):  
Ludivine Raby ◽  
Pamela Völkel ◽  
Xuefen Le Bourhis ◽  
Pierre-Olivier Angrand

Zebrafish (Danio rerio) is an excellent model to study a wide diversity of human cancers. In this review, we provide an overview of the genetic and reverse genetic toolbox allowing the generation of zebrafish lines that develop tumors. The large spectrum of genetic tools enables the engineering of zebrafish lines harboring precise genetic alterations found in human patients, the generation of zebrafish carrying somatic or germline inheritable mutations or zebrafish showing conditional expression of the oncogenic mutations. Comparative transcriptomics demonstrate that many of the zebrafish tumors share molecular signatures similar to those found in human cancers. Thus, zebrafish cancer models provide a unique in vivo platform to investigate cancer initiation and progression at the molecular and cellular levels, to identify novel genes involved in tumorigenesis as well as to contemplate new therapeutic strategies.


2015 ◽  
Vol 13 (02) ◽  
pp. 1571002
Author(s):  
Chao Liu ◽  
Chi Zhang ◽  
Jing Su ◽  
Dongsheng Zhang ◽  
Sha Cao

"Cancer Bioinformatics" is a new book published in 2014 by Springer. This 14-chapter book offers a quite unique and potentially controversial view about what drives a cancer to initiate, progress, metastasize and develop in an accelerated manner in metastatic sites. The book treats cancer as an evolutionary process of a diseased tissue (rather than cells) in an increasingly more challenging microenvironment; and discusses the various stresses encountered by a neoplastic tissue and their roles in (driving) cancer initiation, progression, metastasis and post-metastatic development. Most of the discussions are made based on discoveries through mining cancer tissue omic data. In contrast to the on-going theories that cancers are the result of genomic mutations, the book clearly downplays the roles of genomic mutations, particularly oncogenic mutations, in cancer formation and progression. Throughout the book, the authors made special efforts in conveying their overarching view that cancer is a pathway to cell survival under certain stresses, and cell proliferation is either the result or a side-effect of survival processes when evolving to overcome the stresses. While the book is presented in an informatics style, it is actually a book of cancer biology focused on how information can be derived from cancer omic data to address a variety of basic cancer biology questions. Compared to other cancer biology books, this book is clearly less detail-oriented but more holistic and spans the entire range of cancer evolution.


2016 ◽  
Vol 9 (7) ◽  
pp. 534-546 ◽  
Author(s):  
Karyn L. Sheaffer ◽  
Ellen N. Elliott ◽  
Klaus H. Kaestner

Nature Cancer ◽  
2021 ◽  
Vol 2 (12) ◽  
pp. 1292-1292
Author(s):  
Ioanna Pavlaki

1955 ◽  
Vol 29 (4) ◽  
pp. 507-514 ◽  
Author(s):  
Madge T. Macklin
Keyword(s):  

2012 ◽  
Vol 24 (4) ◽  
pp. 309-318 ◽  
Author(s):  
Koji NOGAKI ◽  
Nobuyuki OHIKE ◽  
Manabu TAKAHASHI ◽  
Genki TSUKUDA ◽  
Yusuke WADA ◽  
...  

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