The Tasmanian Devil's tumor has subsided naturally, bringing the light of day to the fight against cancer in mankind.

Read: RASL11A activation provides a potential target for cancer treatment as a natural mechanism for tumor suppression.
have you seen the Tasmanian Devil movie? The film tells the story of a group of daredevil snow enthusiasts who break into the Tasmanian mountains, triggering the curse of the land's ancient indigenous people, and the huge Tasmanian devil attacking them.
the original shape of this "devil" in the film, in fact, is a small animal - the kangaroo.
has the nickname "Tasmanian Devil" because of the animal's grumpy temper and good fighting.
however, a disease called "Bag Facial Tumor (DFTD)" has caused the kangaroo population to almost suffer from "extinction".
DFTD is a type of bite-borne cancer in which infected animals have a 100% mortality rate in 12-18 months.
amazing, less than 20 cases of tumors have been found to subside naturally in the kangaroo population infected with the cancer.
this spontaneous tumor subsidy is also reported in a small number of human cancer patients, what is the specific mechanism by which the tumor self-subsidies? Can Tasmanian devil's tumour snage provide new insights into the fight against cancer in humanity? Recently, a team led by the School of Biological Sciences at Washington State University published an article in the journal "Sein Regression Tumor in Tasmanian DevilS Associated with RASL11A Activation" in the journal Genetics.
they found that the receding tumor represented a gene that slows the growth of tumor cells, ras-like protein family member 11A (RASL11A), but in non-fading tumors, the gene was silenced.
specifically, researchers initially attributed the spontaneous decline of DFTD to causal mutations.
However, no relevant variants were found in the kangaroo genome after comparative genomics analysis of receding and non-fading tumors.
but one of the results caught the attention of the team - a single mutation appeared in the 5' non-translation al-translation area of RASL11A in the receding tumor, where as a regulator for rDNA transcription and a recognized tumor suppressor.
So, is the expression of RASL11A associated with tumor decline? The researchers sequenced transcription groups of two receding tumors and two non-fading tumors and showed that RASL11A was expressed in degenerative tumors, but not in non-degraded (i.e. wild) tumors, consistent with their low expression in human prostate cancer and colon cancer cell lines.
this suggests that a single-point mutation in the 5' non-translated area of RASL11A may cause this tumor suppressor to be expressed in a degenerative tumor and eventually cause the tumor to subside.
the genetic differentiation of tumors in malignant facial tumors to further verify the results, the researchers directly tested whether the expression of RASL11A had a negative impact on tumor cell proliferation or survival.
results showed that the expression of RASL111A significantly reduced the overall proliferation frequency of tumor cells, which confirmed the important role of RASL11A expression in tumor subsidy.
RASL11A activation inhibits the proliferation of tumor cells in vitro, like many tumor phenotypes, tumor subsidies in DFTD may involve multiple genes, but interference with a single gene mutation product is sufficient to prevent tumor growth.
a recent meta-analysis of human cancer found that a mutation is strong enough to affect the function of the RAS pathway.
in addition, about 30% of all human cancers have the RAS allelerate mutation.
, RASL111A activation provides a potential target for cancer treatment as a natural mechanism to suppress tumors.
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