Not exact matches
Testing each of these factors for their ability to return differentiated tumor cells to a stem -
like state, identified a combination of four — POU3F2, SOX2, SALL2 and OLIG2 — that was able to reprogram differentiated tumor cells back into
glioblastoma stem cells, both in vitro and in an animal model.
During a conversation this month in his office at Weill Cornell Medicine in New York City, Fine rattled off more dismal stats,
like the many failed clinical trials of experimental drugs for
glioblastoma;
like the paltry increase in life expectancy for people with
glioblastoma from 12 months in 1990 to 15 today;
like the stupid (in hindsight) assumptions about how
glioblastomas grow and how to study them in mice.
According to his unpublished findings, when he puts
glioblastoma cells from patients into lab dishes with brain organoids, the cells attach to the surface of the organoids, burrow into them, and within 24 to 48 hours grow into a mass that eventually «looks exactly
like what happened in the patient's own brain,» Fine said.
Another is that the transplanted bits of tumor act nothing
like cancers in actual human brains, Fine and colleagues reported in 2006: Real - life
glioblastomas grow and spread and resist treatment because they contain what are called tumor stem cells, but tumor stem cells don't grow well in the lab, so they don't get transplanted into those mouse brains.
«In principle, both these features make GA11 an attractive drug candidate to target glioma stem -
like cells in
glioblastoma multiforme tumors,» said Ichiro Nakano, M.D., Ph.D., and colleagues in the paper.
In addition, a growing number of immunotherapy clinical trials are in place to test this groundbreaking approach on other cancers
like lymphoma, multiple myeloma, and for solid tumors, through trials in
glioblastoma, mesothelioma, and ovarian and pancreatic cancer.