Rob describes a recent paper in Nature that casts some doubt on the cancer stem cell hypothesis - or at least the scarcity of these cells - though he doesn't think it's that serious a blow.
Part of the evidence for the cancer stem cell hypothesis is that when human tumour cells are implanted into an immunocompromised host mouse only a small percentage of these cells are capable of reproducing a tumour. This new paper demonstrates that if the host is more immunocompromised then a larger number of cells are capable of reproducing a tumour, instead of only as low as one in a million cells to as many as one in four.Alexey at Hematopoiesis follows that up with a pair of research blogging posts also about stem cells and cancer. First off, he describes the complexity of the cell cycle and stem cell self-renewal, how disruptions in these processes can lead to hematological malignancies and how the complexity adds a layer of protection
So, on one hand, downregulation of those genes promotes stem cells to exit from a quiescent state and enter into cell cycle, leading to their expansion, exhaustion and cancer development, but on the another hand, the involvement of multiple genes could protect them from it.This is followed with a post about age related changes in gene expression. Cancer is fairly well recognized as a disease of aging, but Alexey takes a closer look at specifics
Now, let’s get close to cancer. Bmi-1 is known as a tumor promotor, and genes that it repress - Ink4a/Arf are tumor suppressors. Hmga2 is anti-aging, but is a tumor promotor. So, aging of adult stem cell system actually protects us from cancer.Abel Pharmboy at Terra Sigillata has another piece about the link between aging and cancer. This one focuses on a recent PLoS Biology paper discussing senescence-associated secretory phenotype and how it may complicated therapies taking advantage of the senescence pathways.
Cells induced to undergo senescence with DNA-damaging agents exhibit a secretory phenotype, termed the senescence-associated secretory phenotype (SASP), whereby molecules involved in inflammation and metastasis are released into the local environment. In younger individuals, thisAbel Pharmboy was also able to talk to one of the authors directly about the significance of the paper.
mechanism could prevent the development of cancer but in older individuals could increase the risk of cancer. In cancer, for example, therapies that causes cellular growth arrest and senescence may be of limited utility unless those senescent cells are removed. My takehome message from this paper is that we may have to rethink the benefit of cancer therapies that are cytostatic.
While on the topic of unintended consequences, Philip Smith has sent us a story by dsantore at Sociology Eye. The brief piece describes the story of a New York Times editor taking testosterone suppressants as cancer treatment and found them gender blurring.
Among the more notable side effects are Jennings’ shrinking testicles, hot flashes, and potentially enlarged breasts. The gendered implications of these bodily changes are not lost on JenningsThe original story in the NYT is an interesting cap on the month of Movember, and a reminder of some of the lesser thought of aspects of prostate cancer.
With that concludes the 16th edition of the Cancer Research Blog Carnival. The next one will appear Jan 2, but is still in need of a host. If you're sick of seeing it here at the Bayblab all the time, send us an email and we'll set you up as a future host. In the meantime, start writing posts for the next edition and submit them here. You can check out previous editions here.