Meylan, E. et al. Requirement for NF-κB signalling in a mouse model of lung adenocarcinoma.
Gibbons, D. L. et al. Expression signatures of metastatic capacity in a genetic mouse model of lung adenocarcinoma.
We injected these liposomes into a mouse model of lung cancer.
Conversely, TTF-1 counters epithelial to mesenchymal transition in cell-based studies and inhibits progression of primary lung adenocarcinomas to metastases in an animal model of lung adenocarcinomas.
MIT biologists have now identified a major switch that occurs as adenomas transition to adenocarcinomas in a mouse model of lung cancer.
A new computer model of lung injury by the Boston University scientists, described in May in the journal Nature, shows how the lung pops open in sudden bursts that expose large surface areas available for gas exchange, or breathing.
Cheung AF, DuPage M, Dong HK, Chen J, Jacks T. Regulated expression of a tumor-associated antigen reveals multiple levels of T-cell tolerance in a mouse model of lung cancer.
Here we report that Tks5, which has been linked to the formation of proteolytic cellular protrusions known as invadopodia, undergoes an isoform switch during metastatic progression in a genetically engineered mouse model of lung adenocarcinoma.
Further characterization of these isoforms by knockdown and overexpression experiments demonstrated that Tks5long promoted invadopodia in vitro and increased metastasis in transplant models and an autochthonous model of lung adenocarcinoma.
Using cells derived from a genetically engineered mouse model of lung adenocarcinomas, we observed that silenced TTF-1 expression down-regulated occludin, which we supported with additional siRNA experiments.
The researchers, led by Tyler Jacks, director of the David H. Koch Institute for Integrative Cancer Research at MIT, found the alteration while studying a mouse model of lung cancer.
