Age alone no longer should be considered a defining factor when determining whether an older patient with blood cancer is a candidate for stem cell transplantation. That’s the conclusion of the first study summarizing long-term outcomes from a series of prospective clinical trials of patients age 60 and over who were treated with the mini-transplant, a “kinder, gentler” form of allogeneic (donor cell) stem cell transplantation developed at Fred Hutchinson Cancer Research Center. The findings are published Nov. 2 in JAMA, The Journal of the American Medical Association.
“Age is no longer a barrier to allogeneic transplant,” said Mohamed Sorror,
Bond strengthened: Eight-year-old Thamirabharuni, holding her brother who donated the stem cells, did not suffer from rejection or graft versus host disease as the tissue match was perfect – Photo: V. Ganesan
Eight-year-old Thamirabharuni and her one-year-old brother Pugazhendhi share a special kind of bond not commonly seen among siblings. Thanks to her brother, Thamirabharuni no longer suffers from thalassemia disease.
The stem cells transplanted in March helped her get rid of thalassemia. And hundred days after the procedure, one can safely say that her disease has been cured.
The stem cells that were transplanted came from two different sources
If there’s one single image that universally connotes death, it’s that of a skeleton. But in the living human body, bones are a beehive of activity that, at the cellular level, is as lively and intricate as any dance troupe could perform.
Within the hollows of the long bones dwells a spongy tissue called marrow, which hosts stem cells responsible for the production of both red and a variety of white blood cells. The latter are the warriors, messengers, sentries and medics that compose our immune system. White blood cells defend against microbial invaders and scour our bodies for suspicious
Bone marrow stromal cells [BMSCs; also known as mesenchymal stem cells (MSCs)] effectively suppress inflammatory responses in acute graft-versus-host disease in humans and in a number of disease models in mice. Many of the studies concluded that BMSC-driven immunomodulation is mediated by the suppression of proinflammatory Th1 responses while rebalancing the Th1/Th2 ratio toward Th2.