WASHINGTON (Reuters) - Researchers have found a stem cell, a kind of master cell, that may cause at least some types of prostate cancer.
Their findings are only experimental — the stem cells were found in mice — but could explain at least some types of prostate cancer and eventually offer new ways to treat it, they reported on Wednesday in the journal Nature.
The findings also show a potential new source for prostate tumors — so-called luminal cells, which secrete various compounds used in the prostate.
“The role of stem cells in the development of prostate cancer has been a focus of speculation for many years,” Dr. Helen Rippon of Britain’s Prostate Cancer Charity said in a statement.
“Importantly, this new stem cell does not rely on androgens — the male sex hormones that control prostate growth — to survive and grow. This may give a clue as to why prostate cancer often becomes resistant to treatments designed to regulate these androgens in the later stages of the disease,” added Rippon, who was not involved in the research.
“This improved knowledge will also be a step forward in learning how we might help to prevent the disease from developing in men in the first place.”
Michael Shen of Columbia University Medical Center and colleagues named the new stem cells CARNs, for castration-resistant Nkx3.1-expressing cells.
They normally regenerate part of the tissue that lines the inside of the gland, which produces semen. But the cells can also form tumors if certain genes meant to stop out-of-control growth get turned off.
Shen said researchers had believed that tumors arise from a different layer of cells in the prostate, called basal cells.
“Previous research suggested that prostate cancer originates from basal stem cells, and that during cancer formation these cells differentiate into luminal cells,” Shen said in a statement. “Instead, CARNs may represent a luminal origin for prostate cancer.”
Prostate cancer is the second most common cancer in men worldwide after lung cancer, killing 254,000 men a year globally.
Writing by Maggie Fox; Editing by Philip Barbara