Cell Death & Disease, volume 9, Article number: 1151 (2018)
The ubiquitin carboxyl terminal BAP1 is a member of deubiquitinating enzymes superfamily, which are responsible for coordinating ubiquitin-signaling processes through the removal of ubiquitin from protein substrates. Studies of families with high incidence of mesothelioma led to the discovery that all affected family members carried heterozygous BAP1 mutations (BAP1+/−), a condition that was named “the BAP1 cancer syndrome”.
Since the initial discovery in 2011, over 100 families have been identified worldwide affected by the BAP1 cancer syndrome.
Authors: El Bachir Affar, Michele Carbone
We hypothesized that four criteria could help identify malignant mesotheliomas (MMs) most likely linked to germline mutations of BAP1 or of other genes: family history of MM, BAP1-associated cancers, or multiple malignancies; or age younger than 50 years old.
Authors: Sandra Pastorino, Yoshie Yoshikawa, Harvey I. Pass, Mitsuru Emi, Masaki Nasu, Ian Nasu, Ian Pagano, Yasutaka Takinishi, Ryuji Yamamoto, Michael Manaai, Tomoko Hashimoto-Tamaoki, Masaki Ohmuraya, Keisuke Goto, Chandra Goparaju, Kavita Y. Sarin, Mika Tanji, Angela Bononi, Andrea Napolitano, Giovanni Gaudino, Mary Hesdorffer, and Michele Carbone.
For the past 10 years, the Virginia & Barry Weinman Foundation, in conjunction with the University of Hawaii Cancer Center, has sponsored an annual meeting of top researchers from around the world. This publication in Cell Death & Differentiation (6 August 2018) is a consensus report about the role of genes and environment in carcinogenesis.
Inhibition of the spindle assembly checkpoint kinase Mps-1 as a novel therapeutic strategy in malignant mesothelioma
CFI-402257 is a promising novel therapeutic agent to improve the efficacy of the current chemotherapeutic regimens for MM patients.
Cell Death and Differentiation, June 30, 2017 (doi: 10.1038/cdd.2017.95)
Aerobic glycolysis, also known as the ‘Warburg effect’, does not necessarily occur as an adaptive process that is consequence of carcinogenesis, but rather that it may also predate malignancy by many years and facilitate carcinogenesis.